A cell surface receptor involved in regulation of cell growth and differentiation. It is specific for EPIDERMAL GROWTH FACTOR and EGF-related peptides including TRANSFORMING GROWTH FACTOR ALPHA; AMPHIREGULIN; and HEPARIN-BINDING EGF-LIKE GROWTH FACTOR. The binding of ligand to the receptor causes activation of its intrinsic tyrosine kinase activity and rapid internalization of the receptor-ligand complex into the cell.
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
A publication issued at stated, more or less regular, intervals.
A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form.
"The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.
The premier bibliographic database of the NATIONAL LIBRARY OF MEDICINE. MEDLINE® (MEDLARS Online) is the primary subset of PUBMED and can be searched on NLM's Web site in PubMed or the NLM Gateway. MEDLINE references are indexed with MEDICAL SUBJECT HEADINGS (MeSH).
Cancers or tumors of the LARYNX or any of its parts: the GLOTTIS; EPIGLOTTIS; LARYNGEAL CARTILAGES; LARYNGEAL MUSCLES; and VOCAL CORDS.
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)
A tubular organ of VOICE production. It is located in the anterior neck, superior to the TRACHEA and inferior to the tongue and HYOID BONE.
An EPIDERMAL GROWTH FACTOR related protein that is found in a variety of tissues including EPITHELIUM, and maternal DECIDUA. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form which binds to the EGF RECEPTOR.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A cell surface protein-tyrosine kinase receptor that is overexpressed in a variety of ADENOCARCINOMAS. It has extensive homology to and heterodimerizes with the EGF RECEPTOR, the ERBB-3 RECEPTOR, and the ERBB-4 RECEPTOR. Activation of the erbB-2 receptor occurs through heterodimer formation with a ligand-bound erbB receptor family member.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)
A cell line derived from cultured tumor cells.
Deacetylases that remove N-acetyl groups from amino side chains of the amino acids of HISTONES. The enzyme family can be divided into at least three structurally-defined subclasses. Class I and class II deacetylases utilize a zinc-dependent mechanism. The sirtuin histone deacetylases belong to class III and are NAD-dependent enzymes.
Screening techniques first developed in yeast to identify genes encoding interacting proteins. Variations are used to evaluate interplay between proteins and other molecules. Two-hybrid techniques refer to analysis for protein-protein interactions, one-hybrid for DNA-protein interactions, three-hybrid interactions for RNA-protein interactions or ligand-based interactions. Reverse n-hybrid techniques refer to analysis for mutations or other small molecules that dissociate known interactions.
Formation of an acetyl derivative. (Stedman, 25th ed)
Compounds that inhibit HISTONE DEACETYLASES. This class of drugs may influence gene expression by increasing the level of acetylated HISTONES in specific CHROMATIN domains.
A histone deacetylase subtype that is found along with HISTONE DEACETYLASE 2; RETINOBLASTOMA-BINDING PROTEIN 4; and RETINOBLASTOMA-BINDING PROTEIN 7 as core components of histone deacetylase complexes.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The ten-layered nervous tissue membrane of the eye. It is continuous with the OPTIC NERVE and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the CHOROID and the inner surface with the VITREOUS BODY. The outer-most layer is pigmented, whereas the inner nine layers are transparent.
Antibodies from non-human species whose protein sequences have been modified to make them nearly identical with human antibodies. If the constant region and part of the variable region are replaced, they are called humanized. If only the constant region is modified they are called chimeric. INN names for humanized antibodies end in -zumab.
Semisynthetic conjugates of various toxic molecules, including RADIOACTIVE ISOTOPES and bacterial or plant toxins, with specific immune substances such as IMMUNOGLOBULINS; MONOCLONAL ANTIBODIES; and ANTIGENS. The antitumor or antiviral immune substance carries the toxin to the tumor or infected cell where the toxin exerts its poisonous effect.
A protein phytotoxin from the seeds of Ricinus communis, the castor oil plant. It agglutinates cells, is proteolytic, and causes lethal inflammation and hemorrhage if taken internally.
Antibodies produced by a single clone of cells.
A conserved AMINO ACID SEQUENCE located in the intracellular domains of a family of transmembrane proteins involved in various IMMUNE RESPONSES. The CONSENSUS SEQUENCE of this motif is YXXL(or I)X(6-8)YXXL(or I) (where X denotes any amino acid). When phosphorylated ITAM motifs provide docking sites for PROTEIN TYROSINE KINASES of the Syk family thus forming signaling complexes which lead to activation of immune responses.
Tumors or cancer of the LUNG.
A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.
The proto-oncogene c-erbB-1 codes for the epidermal growth factor receptor. Its name originates from the viral homolog v-erbB which was isolated from an avian erythroblastosis virus (AEV) where it was contained as a fragment of the chicken c-ErbB-1 gene lacking the amino-terminal ligand-binding domain. Overexpression of erbB-1 genes occurs in a wide range of tumors, commonly squamous carcinomas of various sites and less commonly adenocarcinomas. The human c-erbB-1 gene is located in the chromosomal region 7p14 and 7p12.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.
A storage reservoir for BILE secretion. Gallbladder allows the delivery of bile acids at a high concentration and in a controlled manner, via the CYSTIC DUCT to the DUODENUM, for degradation of dietary lipid.
Series of ocean waves produced by geologic events or underwater LANDSLIDES. These waves can travel at speeds averaging 450 (and up to 600) miles per hour in the open ocean.
Sudden slips on a fault, and the resulting ground shaking and radiated seismic energy caused by the slips, or by volcanic or magmatic activity, or other sudden stress changes in the earth. Faults are fractures along which the blocks of EARTH crust on either side have moved relative to one another parallel to the fracture.
Tumors or cancer of the gallbladder.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
The taking of a blood sample to determine its character as a whole, to identify levels of its component cells, chemicals, gases, or other constituents, to perform pathological examination, etc.
Agents that inhibit PROTEIN KINASES.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
A radiological stereotactic technique developed for cutting or destroying tissue by high doses of radiation in place of surgical incisions. It was originally developed for neurosurgery on structures in the brain and its use gradually spread to radiation surgery on extracranial structures as well. The usual rigid needles or probes of stereotactic surgery are replaced with beams of ionizing radiation directed toward a target so as to achieve local tissue destruction.
Drugs that block nerve conduction when applied locally to nerve tissue in appropriate concentrations. They act on any part of the nervous system and on every type of nerve fiber. In contact with a nerve trunk, these anesthetics can cause both sensory and motor paralysis in the innervated area. Their action is completely reversible. (From Gilman AG, et. al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed) Nearly all local anesthetics act by reducing the tendency of voltage-dependent sodium channels to activate.
That portion of the electromagnetic spectrum from the UHF (ultrahigh frequency) radio waves and extending into the INFRARED RAYS frequencies.
Removal of tissue with electrical current delivered via electrodes positioned at the distal end of a catheter. Energy sources are commonly direct current (DC-shock) or alternating current at radiofrequencies (usually 750 kHz). The technique is used most often to ablate the AV junction and/or accessory pathways in order to interrupt AV conduction and produce AV block in the treatment of various tachyarrhythmias.

Immune responses to all ErbB family receptors detectable in serum of cancer patients. (1/11134)

Employing NIH3T3 transfectants with individual human ErbB receptor coding sequences as recombinant antigen sources, we detected by immunoblot analysis specific immunoreactivity against all four ErbB receptors among 13 of 41 sera obtained from patients with different types of epithelial malignancies. Overall, serum positivity was most frequently directed against ErbB2 followed by EGFR, ErbB3 and ErbB4. Specificity patterns comprised tumor patients with unique serum reactivity against ErbB2 or ErbB4. Moreover, approximately half of the positive sera exhibited concomitant reactivity with multiple ErbB receptors including EGFR and ErbB2, EGFR and ErbB4, ErbB2 and ErbB3 or EGFR, ErbB2 and ErbB3. Serum reactivity was confirmed for the respective ErbB receptors expressed by human tumor cells and corroborated on receptor-specific immunoprecipitates. Positive sera contained ErbB-specific antibodies of the IgG isotype. Representative immunohistochemical analysis of tumor tissues suggested overexpression of ErbB receptors for which serum antibodies were detectable in five of six patients. These findings implicate multiple ErbB receptors including ErbB3 and ErbB4 in addition to EGFR and ErbB2 in primary human cancer. Heterogeneity of natural ErbB-specific responses in cancer patients warrants their evaluation in light of immunotherapeutic approaches targeting these receptors.  (+info)

Growth inhibition of breast cancer cells by Grb2 downregulation is correlated with inactivation of mitogen-activated protein kinase in EGFR, but not in ErbB2, cells. (2/11134)

Increased breast cancer growth has been associated with increased expression of epidermal growth factor receptor (EGFR) and ErbB2 receptor tyrosine kinases (RTKs). Upon activation, RTKs may transmit their oncogenic signals by binding to the growth factor receptor bound protein-2 (Grb2), which in turn binds to SOS and activates the Ras/Raf/MEK/mitogen-activated protein (MAP) kinase pathway. Grb2 is important for the transformation of fibroblasts by EGFR and ErbB2; however, whether Grb2 is also important for the proliferation of breast cancer cells expressing these RTKs is unclear. We have used liposomes to deliver nuclease-resistant antisense oligodeoxynucleotides (oligos) specific for the GRB2 mRNA to breast cancer cells. Grb2 protein downregulation could inhibit breast cancer cell growth; the degree of growth inhibition was dependent upon the activation and/or endogenous levels of the RTKs. Grb2 inhibition led to MAP kinase inactivation in EGFR, but not in ErbB2, breast cancer cells, suggesting that different pathways might be used by EGFR and ErbB2 to regulate breast cancer growth.  (+info)

The Gab1 PH domain is required for localization of Gab1 at sites of cell-cell contact and epithelial morphogenesis downstream from the met receptor tyrosine kinase. (3/11134)

Stimulation of the hepatocyte growth factor (HGF) receptor tyrosine kinase, Met, induces mitogenesis, motility, invasion, and branching tubulogenesis of epithelial and endothelial cell lines in culture. We have previously shown that Gab1 is the major phosphorylated protein following stimulation of the Met receptor in epithelial cells that undergo a morphogenic program in response to HGF. Gab1 is a member of the family of IRS-1-like multisubstrate docking proteins and, like IRS-1, contains an amino-terminal pleckstrin homology domain, in addition to multiple tyrosine residues that are potential binding sites for proteins that contain SH2 or PTB domains. Following stimulation of epithelial cells with HGF, Gab1 associates with phosphatidylinositol 3-kinase and the tyrosine phosphatase SHP2. Met receptor mutants that are impaired in their association with Gab1 fail to induce branching tubulogenesis. Overexpression of Gab1 rescues the Met-dependent tubulogenic response in these cell lines. The ability of Gab1 to promote tubulogenesis is dependent on its pleckstrin homology domain. Whereas the wild-type Gab1 protein is localized to areas of cell-cell contact, a Gab1 protein lacking the pleckstrin homology domain is localized predominantly in the cytoplasm. Localization of Gab1 to areas of cell-cell contact is inhibited by LY294002, demonstrating that phosphatidylinositol 3-kinase activity is required. These data show that Gab1 is an important mediator of branching tubulogenesis downstream from the Met receptor and identify phosphatidylinositol 3-kinase and the Gab1 pleckstrin homology domain as crucial for subcellular localization of Gab1 and biological responses.  (+info)

Differential expression and translocation of protein tyrosine phosphatase 1B-related proteins in ME-180 tumor cells expressing apoptotic sensitivity and resistance to tumor necrosis factor: potential interaction with epidermal growth factor receptor. (4/11134)

Tumor necrosis factor (TNF)-induced apoptosis can be inhibited by overexpression of specific tyrosine kinases or activation of tyrosine kinase cascades, suggesting potential antagonism between apoptotic and tyrosine kinase signaling processes. In this report, the effects of TNF on EGF receptor tyrosine phosphorylation in ME-180 cell variants selected for apoptotic sensitivity (Sen) or resistance (Res) to TNF, previously shown to differentially express EGFr, were examined. Prior to the onset of apoptosis, TNF caused a significant reduction in the level of EGFr tyrosine phosphorylation in Sen cells but mediated only limited suppression of EGFr tyrosine phosphorylation in apoptotically resistant Res cells. In vitro incubation of cellular membranes with TNF derived from Sen cells stimulated a resident protein tyrosine phosphatase (PTP) activity which was able to dephosphorylate EGFr or tyrosine phosphopeptides mimicking an EGFr autophosphorylation site. In membrane preparations, PTPIB complexed with tyrosine phosphorylated EGFr and this association was disrupted by TNF through an apparent stimulation of PTP activity and turnover of phosphotyrosine. Intrinsic enzymatic activity of PTP1B was 2-3-fold higher in Sen versus Res cell lysates and a family of PTP1B-related proteins with altered C-termini was found to be highly expressed in Sen cells but absent or expressed at reduced levels in Res cells. Cytoplasmic extracts of Sen cells contained PTP1B-like proteins and TNF incubation resulted in the time dependent accumulation of PTP1B-like proteins in Sen cells but did not effect these proteins in Res cells. Together, these results suggest that specific changes in expression and subcellular distribution of phosphotyrosine modulatory proteins may play a role in conveying intrinsic apoptotic sensitivity to TNF in some tumor cell types.  (+info)

An intramembrane modulator of the ErbB2 receptor tyrosine kinase that potentiates neuregulin signaling. (5/11134)

The ErbB2 receptor tyrosine kinase plays a critical role in a variety of developmental processes, and its aberrant activation may contribute to the progression of some breast and ovarian tumors. ASGP2, a transmembrane glycoprotein found on the surface of the highly metastatic ascites 13762 rat mammary adenocarcinoma cell line, is constitutively associated with ErbB2 in these cells and in mammary tissue from pregnant rats. Expression studies indicate that ASGP2 interacts directly and specifically with ErbB2 through one of its epidermal growth factor-like domains and that the co-expression of the two proteins in the same cell dramatically facilitates their direct stable interaction. Ectopic expression of ASGP2 in human melanoma tumor cells potentiates the response of endogenous ErbB2 to the neuregulin-1 growth factor. These observations point to a novel intramembrane mechanism for the modulation of receptor tyrosine kinase activity.  (+info)

Transforming growth factor-alpha acting at the epidermal growth factor receptor reduces infarct volume after permanent middle cerebral artery occlusion in rats. (6/11134)

Transforming growth factor-alpha (TGF-alpha) is a ligand for the epidermal growth factor (EGF) receptor (EGFR), and is more abundant than EGF in the brain. The authors studied whether administration of exogenous TGF-alpha into the brain can protect neurons against ischemia in a model of permanent middle cerebral artery (MCA) occlusion in the rat, and whether any effect of TGF-alpha was mediated by EGFR by administering 4,5-dianilinophthalimide (DAPH), a protein-tyrosine kinase inhibitor with high selectivity for EGFR. Rats received either TGF-alpha (10 or 25 ng), DAPH (100 ng), DAPH plus TGF-alpha (25 ng), or vehicle in the ipsilateral first ventricle. Drugs were administered twice: 30 minutes before and 30 minutes after MCA occlusion, and infarct volume was evaluated 24 hours later. Transforming growth factor-alpha at the dose of 25 ng caused a statistically significant reduction of infarct volume (60%) in relation to ischemic rats administered vehicle. This reduction was no longer seen when TGF-alpha was administered in combination with DAPH. The present results show that TGF-alpha can protect neurons from ischemic damage, and that this effect is mediated by EGFR. It is suggested that activation of EGFR-mediated intracellular signalling pathways contributes to the survival of neural cells susceptible to ischemic injury.  (+info)

Elevation of the epidermal growth factor receptor and dependent signaling in human papillomavirus-infected laryngeal papillomas. (7/11134)

Laryngeal papillomas are benign tumors caused by human papillomaviruses types 6 and 11. This study addressed alterations in levels of signal transduction from the epidermal growth factor receptor (EGFR) in papillomas and cultured papilloma cells compared to normal tissue and cells. Mitogen-activated protein kinase (MAPK) was activated to a greater extent, phosphotyrosine was more abundant, and EGFR was overexpressed in laryngeal papillomas compared to normal laryngeal epithelium by Western blot analysis. The EGFR was 3 times more abundant in cultured papilloma cells than in normal laryngeal cells by Scatchard analysis and Western blot, without gene amplification or an increase in steady-state levels of mRNA. Following stimulation with EGF, a significant portion of the EGFR was recycled to the surface in papilloma cells, whereas in normal cells, it was not. Tyrosine kinase activity and activation of MAPK was more responsive to epidermal growth factor stimulation in papilloma cells than in uninfected primary laryngeal cells. PD153035, a specific inhibitor of the EGFR, and an EGFR-specific antibody that blocks ligand binding completely abrogated basal MAPK activation by endogenous ligands in laryngeal papilloma cells. These results demonstrated that infection of laryngeal epithelium by low-risk human papillomaviruses elevates the EGFR by posttranslational mechanisms, increasing its responsiveness to ligand-mediated activation. They also showed that MAPK activation in laryngeal papillomas depends upon ligand-mediated EGFR stimulation.  (+info)

Anti-epidermal growth factor receptor antibody C225 inhibits angiogenesis in human transitional cell carcinoma growing orthotopically in nude mice. (8/11134)

Epidermal growth factor receptor (EGFR) regulates the growth and progression of human transitional cell carcinoma (TCC) of the bladder. We have shown that therapy targeting EGFR inhibited the growth of human TCC established orthotopically in nude mice. The purpose of this study was to evaluate whether EGFR-directed therapy affects angiogenesis associated with the growth and metastasis of human TCC. We determined the cytostatic effect and the effect on production of angiogenic factors after in vitro treatment of the human TCC cell line 253J B-V with MAb C225, a chimerized monoclonal anti-EGFR antibody. The 253J B-V cells were implanted orthotopically into athymic nude mice, and established tumors (4 weeks) were treated with i.p. MAb C225. Expression of the angiogenic factors vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), and basic fibroblast growth factor (bFGF) was evaluated by immunohistochemistry and in situ mRNA hybridization analyses and correlated with microvessel density evaluated after immunohistochemical staining with anti-CD31. In vitro treatment with MAb C225 inhibited mRNA and protein production of VEGF, IL-8, and bFGF by 253J B-V cells in a dose-dependent manner. MAb C225 therapy of nude mice with established TCCs growing orthotopically resulted in inhibition of growth and metastasis compared with controls (P <0.0005). VEGF, IL-8, and bFGF expression was significantly lower in treated tumors than in controls. The down-regulation of these angiogenic factors preceded the involution of blood vessels. These studies indicate that therapy with anti-EGFR MAb C225 has a significant antitumor effect mediated, in part, by inhibition of angiogenesis.  (+info)

Epidermal growth factor receptors are present in some breast cancers in man, and there is an inverse relation to oestrogen receptor state. We assessed the presence of epidermal growth factor receptors as a single prognostic indicator in a series of breast tumours by comparing this with the Bloom and Richardson scores for these tumours. One hundred and eight ductal tumours were examined for epidermal growth factor receptors by radioligand binding. There was a significant (p less than 0.01) correlation between the presence of the growth factor receptor and poor prognosis as assessed by the Bloom and Richardson score, suggesting that epidermal growth factor receptor state could be a useful prognostic marker. Epidermal growth factor receptor state was not significantly correlated with the lymph node state but showed a tendency to be associated with large tumours.. ...
TY - JOUR. T1 - The role of MET activation in determining the sensitivity to epidermal growth factor receptor tyrosine kinase inhibitors. AU - Rho, Jin Kyung. AU - Choi, Yun Jung. AU - Lee, Jin Kyung. AU - Ryoo, Baek Yeol. AU - Na, Im Il. AU - Yang, Sung Hyun. AU - Lee, Seung Sook. AU - Kim, Cheol Hyeon. AU - Yoo, Young Do. AU - Lee, Jae Cheol. PY - 2009/10. Y1 - 2009/10. N2 - The development of resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) seems almost inevitable, even in patients with lung cancer that initially respond well to EGFR-TKIs. MET amplification was recently found to be a mechanism of escape from the anticancer effect of EGFR inhibitors. In the present study, we investigated the means whereby MET affects sensitivity to EGFR-TKIs in PC-9 cells. Gefitinib- or erlotinib-resistant sublines were established by exposing the parental PC-9 cell line to chronic, repeated treatments with these drugs. These resistant sublines showed more than 100-fold more ...
Epidermal growth factor receptor blockade with C225 plus gemcitabine results in regression of human pancreatic carcinoma growing orthotopically in nude mice by antiangiogenic mechanisms.
Malignant peritoneal mesotheliomas (MPM) are rare tumors representing 20% of all malignant mesothelioma cases. The median survival for these tumors is less than a year, and like other peritoneal surface malignancies, this is due primarily to intra-abdominal recurrence and progression. Currently there is a paucity of information about the biology of these tumors and molecular perturbations that are involved in tumor formation. Elucidation of mutations and biological pathways active in these tumors may identify valuable prognostic markers, as well as facilitate the development of novel therapies. In this study, we investigate the predictive value of epidermal growth factor receptor (EGFR) mutations in achieving optimal resectability. Twenty-nine patients with MPM were evaluated at a single tertiary care center and their tumors were probed for point mutations in the catalytic TK domain of epidermal growth factor receptor (mut+). All specimens were examined for somatic mutations by polymerase chain ...
Glioblastoma is a highly aggressive primary brain tumor in which the majority of cancer cells are undifferentiated. One of the most common oncogenic drivers for this malignancy is the epidermal...
TY - JOUR. T1 - Role of proneuregulin 1 cleavage and human epidermal growth factor receptor activation in hypertonic aquaporin induction. AU - Herrlich, Andreas. AU - Leitch, Virginia. AU - King, Landon S.. PY - 2004/11/2. Y1 - 2004/11/2. N2 - Mammalian cells are confronted with changes in extracellular osmolality at various sites, including the aqueous layer above the lung epithelium. Hypertonic shock induces the activation of mitogen-activated protein kinases and the expression of a defined set of genes, including aquaporins. We investigated upstream components of the response to hypertonicity in lung epithelial cells and found that before extracellular signal-regulated kinase activation and aquaporin synthesis, the membrane-bound prohormone neuregulin 1-β is cleaved and binds to human epidermal growth factor receptor 3 (HER3). The signaling is prevented by matrix metalloproteinase inhibition, inhibition of neuregulin 1-β binding to HER3, and inhibition of HER tyrosine kinase activity. ...
TY - JOUR. T1 - Epidermal growth factor receptor (EGFR)-tyrosine Kinase inhibitor treatment and salvage chemotherapy in EGFR-mutated elderly pulmonary adenocarcinoma patients. AU - Tseng, Yen Han. AU - Tseng, Yen Chiang. AU - Lin, Yi Hsuan. AU - Lee, Yu Chin. AU - Perng, Reury Perng. AU - Whang-Peng, Jacqueline. AU - Chen, Yuh Min. PY - 2015/6/8. Y1 - 2015/6/8. N2 - Background. Lung cancer is frequently a disease of elderly patients. However, these patients are often treated less actively owing to a higher comorbidity rate and poor performance status. The efficacy of different treatments in elderly patients with epidermal growth factor receptor (EGFR)-mutated lung cancer is still unknown. Materials and Methods. We retrospectively reviewed the records of our pulmonary adenocarcinoma patients treated between 2010 and 2013. Data on patient age, type of tumor EGFR mutation, response to first-line EGFR-tyrosine kinase inhibitor (TKI) treatment, type of salvage chemotherapy, and efficacy of EGFR-TKI ...
Monoclonal antibodies (MoAbs) were raised against epidermal growth factor (EGF) receptors on a human epidermoid carcinoma cell line, A431. Administration of anti-EGF receptor MoAbs inhibited tumor formation in athymic mice by A431 cells and by another epidermal carcinoma cell line, T222. When one of the same MoAbs was used in therapy against Li-7 (a human hepatoma) and HeLa cells (a cervical carcinoma), tumor growth was not affected. The number of EGF receptors on A431 cells was about 100-fold higher than on T222, Li-7, and HeLa cells, suggesting that the number of EGF receptors may not be an important determinant in suppressing tumor growth. Three anti-EGF receptor MoAbs were used in the present studies. MoAbs 528 (immunoglobulin G2a) and 225 (immunoglobulin G1) are capable of competing with EGF for receptor binding and inhibit proliferation of A431 cells in culture. The other MoAb, 455 (immunoglobulin G1), is incapable of blocking the binding of EGF to its receptors and has no effect on the ...
TY - JOUR. T1 - Disruption of ETV6 leads to TWIST1-dependent progression and resistance to epidermal growth factor receptor tyrosine kinase inhibitors in prostate cancer. AU - Tsai, Yuan Chin. AU - Zeng, Tao. AU - Abou-Kheir, Wassim. AU - Yeh, Hsiu Lien. AU - Yin, Juan Juan. AU - Lee, Yi Chao. AU - Chen, Wei Yu. AU - Liu, Yen Nien. N1 - Funding Information: This work was supported by the Ministry of Science and Technology of Taiwan to YCT (MOST104-2320-B-038-055-MY3), WYC (MOST106-2320-B-038-057), and YNL (MOST104-2314-B-038-045-MY3 and MOST105-2628-B-038 -006 -MY3), by Taipei Medical University-Wan Fang Hospital to WYC (105TMU-WFH-04), by the National Health Research Institutes of Taiwan to YNL (NHRI-EX107-10702BI), and by the Health and Welfare Surcharge of Tobacco Products to YNL (MOHW106-TDU-B-212-144001).. PY - 2018/2/19. Y1 - 2018/2/19. N2 - Background: ETS variant gene 6 (ETV6) is a putative tumor suppressor and repressed by epidermal growth factor receptor (EGFR) signaling in prostate ...
Title: Mechanisms of Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors and New Therapeutic Perspectives in Non Small Cell Lung Cancer. VOLUME: 12 ISSUE: 6. Author(s):Laura Bonanno, Antonio Jirillo and Adolfo Favaretto. Affiliation:Medical Oncology 2, Istituto Oncologico Veneto-IRCCS, Via Gattamelata, 64, 35128 Padova, Italy.. Keywords:EGFR, Tyrosine kinase inhibitors, resistance, mutations, amplifications, MET, VEGFR, NSCLC, Gefitinib, Erlotinib. Abstract: EGFR somatic mutations define a subset of NSCLCs that are most likely to benefit from EGFR tyrosine kinase inhibitors (TKIs). These tumors are dependent on EGFR-signaling for survival. Recently, tyrosine kinase domain somatic mutations have been approved as criterion to decide first-line therapy in this group of advanced NSCLCs. Anyway, all patients ultimately develop resistance to these drugs. Acquired resistance is linked to a secondary EGFR mutation in about a half of patients. Uncontrolled activation of ...
TY - JOUR. T1 - Receptor-mediated gene delivery using the Fab fragments of anti-epidermal growth factor receptor antibodies. T2 - Improved immunogene approach. AU - Chen, Jiabing. AU - Gamou, Shinobu. AU - Takayanagi, Atsushi. AU - Ohtake, Yuichiro. AU - Ohtsubo, Masafumi. AU - Shimizu, Nobuyoshi. PY - 1998. Y1 - 1998. N2 - We previously developed the immunogene approach toward cancer gene therapy using epidermal growth factor receptor (EGFR)-mediated endocytosis. Here, we describe an improved immunogene system, in which the antigen-binding (Fab) fragments of the monoclonal antibody (Ab) B4G7 against the human EGFR were conjugated with poly-L-lysine to form a gene delivery vehicle (designated Fab immunoporter). Within 12 hours, the β-galactosidase (β-gal) gene was transferred via the Fab immunoporter to virtually all of the nuclei of human squamous carcinoma A431 cells that overproduce the EGFR, and the β-gal enzyme activity was detected within 24 hours and retained for more than 3 days. ...
Intimal sarcoma (IS) is a rare, malignant, and aggressive tumor that shows a relentless course with a concomitant low survival rate and for which no effective treatment is available. In this study, 21 cases of large arterial blood vessel IS were analyzed by immunohistochemistry and fluorescence in situ hybridization and selectively by karyotyping, array comparative genomic hybridization, sequencing, phospho-kinase antibody arrays, and Western immunoblotting in search for novel diagnostic markers and potential molecular therapeutic targets. Ex vivo immunoassays were applied to test the sensitivity of IS primary tumor cells to the receptor tyrosine kinase (RTK) inhibitors imatinib and dasatinib. We showed that amplification of platelet-derived growth factor receptor α (PDGFRA) is a common finding in IS, which should be considered as a molecular hallmark of this entity. This amplification is consistently associated with PDGFRA activation. Furthermore, the tumors reveal persistent activati
TY - JOUR. T1 - Collaboration of RON and Epidermal Growth Factor Receptor in Human Bladder Carcinogenesis. AU - Hsu, Pei Yin. AU - Liu, Hsiao Sheng. AU - Cheng, Hong Lin. AU - Tzai, Tzong Shin. AU - Guo, How Ran. AU - Ho, Chung Liang. AU - Chow, Nan Haw. PY - 2006/11. Y1 - 2006/11. N2 - Purpose: Collaboration of heterologous receptor tyrosine kinases has emerged as an important paradigm in tumor progression. We recently proved that RON has an important role in human bladder carcinogenesis. Since epidermal growth factor receptor has been suggested to cross-talk with RON, we examined the significance of epidermal growth factor receptor in modulating RON associated tumorigenesis. Materials and Methods: The biological significance of collaboration between RON and epidermal growth factor receptor was examined in the TSGH8301, J82 and JR bladder cancer cell lines with different expression status. Immunoprecipitation and immunoblotting assays were done to investigate the interaction of RON with ...
Many epithelial cancers rely on enhanced expression of the epidermal growth factor receptor (EGFR) to drive proliferation and survival pathways. Development of therapeutics to target EGFR signaling has been of high importance, and multiple examples have been approved for human use. However, many of the current small molecule or antibody-based therapeutics are of limited effectiveness due to the inevitable development of resistance and toxicity to normal tissues. Recombinant immunotoxins are therapeutic molecules consisting of an antibody or receptor ligand joined to a protein cytotoxin, combining the specific targeting of a cancer-expressed receptor with the potent cell killing of cytotoxic enzymes. Over the decades, many bacterial- or plant-based immunotoxins have been developed with the goal of targeting the broad range of cancers reliant upon EGFR overexpression. Many examples demonstrate excellent anti-cancer properties in preclinical development, and several EGFR-targeted immunotoxins have
Epidermal growth factor (EGF) rapidly stimulates receptor autophosphorylation in A-431 cells. After 1 min the phosphorylated receptor can be identified at the plasma membrane using an anti-phosphotyrosine antibody. With further incubation at 37 degrees C, approximately 50% of the phosphorylated EGF receptor was internalized (t1/2 = 5 min) and associated with the tubulovesicular system and later with multivesicular bodies, but not the nucleus. During this period, there was no change in the extent or sites of phosphorylation. At all times the phosphotyrosine remained on the cytoplasmic side of the membrane, opposite to the EGF ligand identified by anti-EGF antibody. These data indicate that (a) the tyrosine-phosphorylated EGF receptor is internalized in its activated form providing a mechanism for translocation of the receptor kinase to substrates in the cell interior; (b) the internalized receptor remains intact for at least 60 min, does not associate with the nucleus, and does not generate any ...
After the intraportal injection of EGF, the EGF receptor (EGFR) is rapidly internalized into hepatic endosomes where it remains largely receptor bound (Lai et al., 1989. J. Cell Biol. 109:2751-2760). In the present study, we evaluated the phosphotyrosine content of EGFRs at the cell surface and in endosomes in order to assess the consequences of internalization. Quantitative estimates of specific radioactivity of the EGFR in these two compartments revealed that tyrosine phosphorylation of the EGFR was observed at the cell surface within 30 s of ligand administration. However, the EGFR was also highly phosphorylated in endosomes reaching levels of tyrosine phosphorylation significantly higher than those of the cell surface receptor at 5 and 15 min after EGF injection. A 55-kD tyrosine phosphorylated polypeptide (pyp55) was observed in association with the EGFR at the cell surface within 30 s of EGF injection. The protein was also found in association with the EGFR in endosomes as evidenced by ...
In the current study, we report on differences in outcome based on EGFR genotype after treatment with gefitinib or erlotinib in patients with NSCLC. A total of 36 eligible patients with EGFR mutations were identified. Of these, 32 (89%) patients had either an exon 19 deletion (n = 22) or the L858R point mutation (n = 10). This is the second study to compare patients with exon 19 deletions with those harboring an L858R point mutation and provides important independent validation to earlier observations (35). In a previously reported study, Riely et al. analyzed 34 NSCLC patients with either an exon 19 deletion (n = 23) or an L858R mutation (n = 11). Of these, 22 were treated with gefitinib and 12 were treated with erlotinib. The baseline characteristics of the patients in both studies are remarkably similar with respect to age, gender, smoking status, tumor histology, performance status, number of prior chemotherapy regimens, and EGFR-TKI administered.. Although the radiographic response rate in ...
This trial will investigate the efficacy and tolerability of epidermal growth factor receptor tyrosine kinase inhibitor, erlotinib, in combination with
This study was prospectively designed to evaluate a phase II study of gefitinib for non-small-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations. Clinical samples were tested for EGFR mutations by peptide nucleic acid-locked nucleic acid PCR clamp, and patients having EGFR mutations were given gefitinib 250 mg daily as the second treatment after chemotherapy. Poor PS patients omitted chemotherapy. Of 107 consecutive patients enrolled, samples from 100 patients were informative, and EGFR mutations were observed in 38 patients. Gefitinib was given to 27 patients with EGFR mutations, and the response rate was 78% (one complete response and 20 partial responses; 95% confidence interval: 58-93%). Median time to progression and median survival time (MST) from gefitinib treatment were 9.4 and 15.4 months, respectively. Grade 3 hepatic toxicity and skin toxicity were observed in one patient each. There were significant differences between EGFR mutations and wild-type
Purpose: To assess the cost-effectiveness of epidermal growth factor receptor (EGFR) gene mutation testing to guide the selection of gefitinib as first-line therapy in patients with advanced non-small cell lung cancer (NSCLC) in Ontario. Method: A decision analytic model was developed to conduct this cost-effectiveness analysis from the perspective of the Ontario Ministry of Health and Long-Term Care (MOHLTC). Under EGFR gene mutation testing strategy, tumour tissues from biopsy were assessed for EGFR gene mutation status. Patients with EGFR gene mutation would receive gefitinib as first-line therapy and conventional chemotherapy (platinum based chemotherapy and docetaxel (or pemetrexed)) before best supportive care (BSC). Patients without EGFR gene mutation would receive conventional chemotherapy and BSC. The other patients with undetermined EGFR gene mutation status would receive the same care as the patients under no testing strategy, who would receive conventional chemotherapy, erlotinib, ...
PDGFRs (platelet-derived growth factor receptors) are cell surface tyrosine kinase receptors for members of the platelet-derived growth factor(PDGF) family. PDGF subunits -A and -B are important factors regulating cell proliferation, cellular differentiation, cell growth, development and many diseases including cancer. There are two forms of the PDGFR: PDGFR alpha and PDGFR beta. PDGFRA has been shown to interact with PDGFRB, PLCG1, Sodium-hydrogen antiporter 3 regulator 1, Cbl gene, CRK, Caveolin 1 andPDGFC. PDGFRB has been shown to interact with PTPN11, NCK1, Grb2, Caveolin 1, PDGFRA, Sodium-hydrogen antiporter 3 regulator 1, RAS p21 protein activator 1, CRK, SHC1 and NCK2.
TY - JOUR. T1 - Developmental regulation of epidermal growth factor receptor kinase in rat intestine. AU - Thompson, John F.. AU - Van Den Berg, Merlijn. AU - Stokkers, Pieter C.F.. PY - 1994/11. Y1 - 1994/11. N2 - Background/Aims: Intraluminal epidermal growth factor (EGF) may regulate intestinal growth and function. The ontogeny, localization, and phosphorylation of the EGF receptor in rat small intestine were studied. Methods: EGF-receptor phosphorylation was assayed by antiphosphotyrosine Western blot after EGF administration in vivo and EGF incubation to everted sacs in vitro. EGF-receptor abundance and localization were assayed by Western blot and immunofluorescence using anti-EGF-receptor antibodies. Results: In vivo, orogastric EGF enhanced EGF-receptor phosphorylation in newborn rat jejunum and liver. However, intraluminal EGF had no effect on EGF-receptor phosphorylation in adult intestine or liver. In vitro, mucosal EGF stimulated a fourfold increase in EGF-receptor phosphorylation in ...
Title: Targeting Epidermal Growth Factor Receptor in Solid Tumors: Critical Evaluation of the Biological Importance of Therapeutic Monoclonal Antibodies. VOLUME: 16 ISSUE: 29. Author(s):Ch. Gialeli, D. Kletsas, D. Mavroudis, H. P. Kalofonos, G. N. Tzanakakis and N. K. Karamanos. Affiliation:Laboratory of Biochemistry, Department of Chemistry, University of Patras, 26110 Patras, Greece.. Keywords:Epidermal growth factor receptor, solid tumors, colorectal cancer, anti-EGFR therapy, monoclonal antibodies, cetuximab, panitumumab. Abstract: Numerous cellular pathways have a significant impact in the growth and metastatic potential of tumors. Essential element of such pathways is the epidermal growth factor receptor (EGFR), a member of the HER family of receptor tyrosine kinases. One of the most important issues in cancer, which attracted the attention of clinical oncologists, is the potential use of targeted therapies. EGFR signaling pathway is implicated in the control of cell survival, ...
Epidermal growth factor receptor-dependent mechanisms have been implicated in growth signal transduction pathways that contribute to cancer development, including dermal carcinogenesis. Detection of the extracellular domain of the epidermal growth factor receptor (EGFR ECD) in serum has been suggested as a potential biomarker for monitoring this effect in vivo. Arsenic is a known human carcinogen,
Background Clear cell renal cell carcinoma (ccRCC) is the most common histological subtype of renal cell carcinoma. In patients with ccRCC several prognostic markers have been suggested, enclosing epidermal growth factor receptor (EGFR) expression and chromosome 7 polysomy (C7p). Cancer cells addicted to EGFR bear activated mutations in the EGFR gene, and these mutations are useful in predicting susceptibility of ccRCC to EGFR inhibitors. The aim of this study was to evaluate the prognostic value of EGFR overexpression and C7p.. Patients and methods Archival specimens, coupled with clinical and survival data of 34 patients (20 men, 14 women, median age 58, range 42-79 years) who had undergone radical nephrectomy for ccRCC were analyzed. Immunohistochemistry and fluorescence in situ hybridization (FISH) specimens were sections of formalin-fixed paraffin-embedded tissue. EGFR expression was detected as membranous and cytoplasmic staining of neoplastic cells > 1%, and a ratio between ...
TY - JOUR. T1 - IL-13 induces mucin production by stimulating epidermal growth factor receptors and by activating neutrophils. AU - Shim, Jae Jeong. AU - Dabbagh, Karim. AU - Ueki, Iris F.. AU - Dao-Pick, Trang. AU - Burgel, Pierre Regis. AU - Takeyama, Kiyoshi. AU - Tam, Dominic Cheng Wei. AU - Nadel, Jay A.. PY - 2001/1. Y1 - 2001/1. N2 - Mucus hypersecretion contributes to the morbidity and mortality in acute asthma. Both T helper 2 (Th2) cytokines and epidermal growth factor receptor (EGFR) signaling have been implicated in allergen-induced goblet cell (GC) metaplasia. Present results show that a cascade of EGFR involving neutrophils is implicated in interleukin (IL)-13-induced mucin expression in GC. Treatment with a selective EGFR tyrosine kinase inhibitor prevented IL-13-induced GC metaplasia dose dependently and completely. Instillation of IL-13 also induced tumor necrosis factor-α protein expression, mainly in infiltrating neutrophils. Control airway epithelium contained few ...
Lung cancer with epidermal growth factor receptor (EGFR)-activating mutations responds favorably to the EGFR tyrosine kinase inhibitors gefitinib and erlotinib. However, 25% to 30% of patients with EGFR-activating mutations show intrinsic resistance, and the responders invariably acquire resistance to gefitinib. Here, we showed that hepatocyte growth factor (HGF), a ligand of MET oncoprotein, induces gefitinib resistance of lung adenocarcinoma cells with EGFR-activating mutations by restoring the phosphatidylinositol 3-kinase/Akt signaling pathway via phosphorylation of MET, but not EGFR or ErbB3. Strong immunoreactivity for HGF in cancer cells was detected in lung adenocarcinoma patients harboring EGFR-activating mutations, but no T790M mutation or MET amplification, who showed intrinsic or acquired resistance to gefitinib. The findings indicate that HGF-mediated MET activation is a novel mechanism of gefitinib resistance in lung adenocarcinoma with EGFR-activating mutations. Therefore, ...
The expression of mRNA for the epidermal growth factor (EGF) receptor, EGF and transforming growth factor alpha (TGF-alpha) was determined in 76 malignant, six borderline and 15 benign primary ovarian tumours using the reverse transcriptase-polymerase chain reaction and related to clinical and pathological parameters. Of the malignant tumours, 70% (53/76) expressed EGF receptor mRNA, 31% (23/75) expressed EGF mRNA and 35% (26/75) expressed TGF-alpha mRNA. For the borderline tumours, four of six (67%) expressed EGF receptor mRNA, 1/6 (17%) expressed TGF-alpha mRNA and none expressed EGF mRNA. Finally, 33% (5/15) of the benign tumours expressed EGF receptor mRNA, whereas 40% (6/15) expressed EGF mRNA and 7% (1/15) expressed TGF-alpha mRNA. The presence of the EGF receptor in malignant tumours was associated with that of TGF-alpha (P = 0.0015) but not with EGF (P = 1.00), whereas there was no relationship between the presence of EGF and TGF-alpha (P = 1.00). EGF receptor mRNA expression was significantly
Supplementary Material for: Role of Epidermal Growth Factor Receptor Expression on Patient Survival in Pancreatic Cancer: A Meta-Analysis
Close, J. L., Liu, J., Gumuscu, B. and Reh, T. A. (2006), Epidermal growth factor receptor expression regulates proliferation in the postnatal rat retina. Glia, 54: 94-104. doi: 10.1002/glia.20361 ...
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) will be the 1st\line treatment for individuals with mutant non\little\cell lung cancer (NSCLC). in the osimertinib group (= 41) vs the platinum\pemetrexed group (= 22; risk percentage 0.27; 95% self-confidence period, 0.13\0.56). The median PFS was 12.5 and 4.three months in the osimertinib and platinum\pemetrexed groups, respectively. Quality 3 adverse MK-5172 hydrate IC50 occasions determined to become linked to treatment happened in 5 individuals (12.2%) treated with osimertinib and 12 individuals (54.5%) treated with platinum\pemetrexed. The security and effectiveness leads to this subanalysis are in keeping with the outcomes of the entire AURA3 research, and support the usage of osimertinib in Japanese individuals with T790M mutation\positive NSCLC whose disease offers progressed following 1st\collection EGFR\TKI treatment. (ClinicalTrials.gov trial sign up zero. NCT02151981.) gene resulting in T790M is situated in ...
The aim of the present study was to investigate the mutation rate of the epidermal growth factor receptor (EGFR) in non-small cell lung cancer (NSCLC) patients and to apply logistic regression analysis to investigate the factors associated with EGFR gene mutation to provide data for the treatment of NSCLC. Paraffin tissue, bronchoscopy or pleural effusion specimens were collected from 176 NSCLC patients following pathological diagnosis. The EGFR gene exon 19 delL747-S75linss and delL747-S752ins deletion mutations, and the exon 20 T790M and exon 21 L858R mutations were identified using amplification refractory mutation system analysis. The clinical data and laboratory results of the patients were collected, and the total mutation rate of the EGFR gene in exons 19, 20 and 21 in the 176 NSCLC patients was found to be 48.3% (85/176). In addition, the EGFR gene mutation rate in adenocarcinoma was found to be significantly higher than that in squamous cell and large cell carcinoma (χ²=12.454; ...
The epidermal growth factor receptor (EGFR) is a widely expressed Ag that is successfully targeted in tumor patients by mAbs or tyrosine kinase inhibitors. A clinical study in non-small cell lung cancer patients demonstrated a positive correlation between EGFR expression levels and the therapeutic efficacy of the EGFR mAb cetuximab. However, the impact of EGFR expression on the different mechanisms of action (MoAs) triggered by the EGFR mAb has not been defined. In this study, BHK-21 cells were stably transfected to express different EGFR levels, which were quantified by immunofluorescence and immunohistochemistry and compared with EGFR levels of clinical non-small cell lung cancer samples. These cells were used to systematically investigate the impact of target Ag expression levels on Fab- or Fc-mediated MoAs of EGFR mAb. A negative correlation between EGFR levels and potency of Fab-mediated MoA was observed. Interestingly, Ab-dependent cell-mediated cytotoxicity (ADCC) by NK cells, monocytes, ...
Background. Epidermal Growth Factor Receptor (EGFR) is a key target molecule in current treatment of several neoplastic diseases. Hence, in order to develop and improve current drugs targeting EGFR signalling, an accurate understanding of how this signalling pathway is regulated is required. It has recently been demonstrated that inhibition of cAMP-dependent protein kinase (PKA) induces a ligand-independent internalization of EGFR. Cyclic-AMP-dependent protein kinase consists of a regulatory dimer bound to two catalytic subunits.. Results. We have investigated the effect on EGFR levels after ablating the two catalytic subunits, Cα and Cβ in two different models. The first model used targeted disruption of either Cα or Cβ in mice whereas the second model used Cα and Cβ RNA interference in HeLa cells. In both models we observed a significant reduction of EGFR expression at the protein but not mRNA level.. Conclusion. Our results suggest that PKA may represent a target that when manipulated ...
Activating mutations of the epidermal growth factor receptor (EGFR) confer sensitivity to the tyrosine kinase inhibitors (TKi), gefitinib and erlotinib. We analysed EGFR expression, EGFR mutation status and gene expression profiles of prostate cancer (PC) to supply a rationale for EGFR targeted therapies in this disease. Mutational analysis of EGFR TK domain (exons from 18 to 21) and immunohistochemistry for EGFR were performed on tumour tissues derived from radical prostatectomy from 100 PC patients. Gene expression profiling using oligo-microarrays was also carried out in 51 of the PC samples. EGFR protein overexpression (EGFRhigh) was found in 36% of the tumour samples, and mutations were found in 13% of samples. Patients with EGFRhigh tumours experienced a significantly increased risk of biochemical relapse (hazard ratio-HR 2.52, p=0.02) compared with patients with tumours expressing low levels of EGFR (EGFRlow). Microarray analysis did not reveal any differences in gene expression between EGFRhigh
TY - JOUR. T1 - Human epidermal growth factor receptor 2 (HER2) extracellular domain levels are associated with progression-free survival in patients with HER2-positive metastatic breast cancer receiving lapatinib monotherapy. AU - Lipton, Allan. AU - Leitzel, Kim. AU - Ali, Suhail M.. AU - Carney, Walter. AU - Platek, Greg. AU - Steplewski, Klaudia. AU - Westlund, Ron. AU - Gagnon, Robert. AU - Martin, Anne Marie. AU - Maltzman, Julie. PY - 2011/11/1. Y1 - 2011/11/1. N2 - BACKGROUND: Changes in serum human epidermal growth factor receptor 2 (HER2) levels associated with clinical outcomes, including objective response rate, progression-free survival (PFS), and overall survival have been reported in patients with metastatic breast cancer (MBC) receiving trastuzumab and chemotherapy. This study investigated whether baseline or changes in serum HER2 correlated with overall response rate (ORR) and/or PFS in patients with MBC receiving first-line lapatinib monotherapy. METHODS: The EGF20009 study ...
Conventional chemotherapeutic regimens have reached an efficacy plateau against most solid tumors and deal with significant toxicity. Recently, the goal of the oncologic research to improve outcome and reduce treatment-related side-effects has led to the development of novel anticancer treatments targeting specific proteins or genes involved in cancer growth and progression. In particular, the tyrosine-kinase inhibitors (TKIs) gefitinib and erlotinib targeting the epidermal growth factor receptor (EGFR) have been approved for the treatment of non-small-cell lung cancer (NSCLC). Their clinical activity has been related to different clinical and biological parameters, such as the presence of activating mutations in the kinase domain of the target. Disappointingly, their clinical efficacy is limited by the development of resistance which is caused in more than 50% of the cases by the emergence of a secondary point-mutation (T790M) in the ATP-binding cleft of EGFR. Several novel EGFR inhibitors, ...
TY - JOUR. T1 - Preoperative chemotherapy plus trastuzumab, lapatinib, or both in human epidermal growth factor receptor 2-positive operable breast cancer. T2 - Results of the randomized phase II CHER-LOB study. AU - Guarneri, Valentina. AU - Frassoldati, Antonio. AU - Bottini, Alberto. AU - Cagossi, Katia. AU - Bisagni, Giancarlo. AU - Sarti, Samanta. AU - Ravaioli, Alberto. AU - Cavanna, Luigi. AU - Giardina, Giovanni. AU - Musolino, Antonino. AU - Untch, Michael. AU - Orlando, Laura. AU - Artioli, Fabrizio. AU - Boni, Corrado. AU - Generali, Daniele Giulio. AU - Serra, Patrizia. AU - Bagnalasta, Michela. AU - Marini, Luca. AU - Piacentini, Federico. AU - DAmico, Roberto. AU - Conte, PierFranco. PY - 2012/6/1. Y1 - 2012/6/1. N2 - Purpose: This is a noncomparative, randomized, phase II trial of preoperative taxane-anthracycline in combination with trastuzumab, lapatinib, or combined trastuzumab plus lapatinib in patients with human epidermal growth factor receptor 2 (HER2) -positive, stage II ...
Epidermal growth factor receptors (EGF-Rs) are expressed at increasing levels on mouse preimplantation embryos. Immunofluorescence assays were used to show that unfertilized eggs and 2-cell embryos have a very low level of reactivity to antimouse EGF-R antibodies, but by the 4-cell stage and later t …
TY - JOUR. T1 - Molecular heterogeneity and response to neoadjuvant human epidermal growth factor receptor 2 targeting in CALGB 40601, a randomized phase III trial of paclitaxel plus trastuzumab with or without lapatinib. AU - Carey,Lisa A.. AU - Berry,Donald A.. AU - Cirrincione,Constance T.. AU - Barry,William T.. AU - Pitcher,Brandelyn N.. AU - Harris,Lyndsay N.. AU - Ollila,David W.. AU - Krop,Ian E.. AU - Henry,Norah Lynn. AU - Weckstein,Douglas J.. AU - Anders,Carey K.. AU - Singh,Baljit. AU - Hoadley,Katherine A.. AU - Iglesia,Michael. AU - Cheang,Maggie Chon U.. AU - Perou,Charles M.. AU - Winer,Eric P.. AU - Hudis,Clifford A.. PY - 2016/2/20. Y1 - 2016/2/20. N2 - Purpose Dual human epidermal growth factor receptor 2 (HER2) targeting can increase pathologic complete response rates (PCRs) to neoadjuvant therapy and improve progression-free survival in metastatic disease. CALGB 40601 examined the impact of dual HER2 blockade consisting of trastuzumab and lapatinib added to paclitaxel, ...
Targeted molecular therapy offers an exciting, new approach to treat human malignancy (1) and represents a fundamental change in cancer therapeutics (2) . Current treatment relies on cytotoxic drugs that, for the most part, lack specificity for tumor cells. A better understanding of the molecular pathogenesis of cancer has identified targets for therapeutic intervention that are specific against tumor cells and hence may reduce toxicity commonly associated with adjuvant treatment. The success of the TKI STI-571 in early clinical trials for the treatment of chronic myeloid leukemia (3) and gastrointestinal stromal tumors (4) highlights the unique potential for novel therapy based on specific molecular abnormalities present in a human cancer.. The EGFR3 pathway provides an attractive target for molecular therapy of HNSCC. Most work has focused on the use of anti-EGFR antibody preparations. Tumor proliferation in cell culture and tumor xenografts in athymic mice have been inhibited by these ...
Healthy individuals have few goblet cells in their airways, but in patients with hypersecretory diseases goblet-cell upregulation results in mucus hypersecretion, airway plugging, and death. Multiple stimuli produce hypersecretion via epidermal growth factor receptor (EGFR) expression and activation, causing goblet-cell metaplasia from Clara cells by a process of cell differentiation. These cells are also believed to be the cells of origin of non-small-cell lung cancer, but this occurs via cell multiplication. The mechanisms that determine which pathway is chosen are critical but largely unknown. Although no effective therapy exists for hypersecretion at present, the EGFR cascade suggests methods for effective therapeutic intervention.
TY - JOUR. T1 - Cetuximab and platinum-based chemoradio- or chemotherapy of patients with epidermal growth factor receptor expressing adenoid cystic carcinoma. T2 - A phase II trial. AU - Hitre, E.. AU - Budai, B.. AU - Takácsi-Nagy, Z.. AU - Rubovszky, G.. AU - Tóth, E.. AU - Remenár, É. AU - Polgár, C.. AU - Láng, I.. PY - 2013/9. Y1 - 2013/9. N2 - Background:Epidermal growth factor receptor (EGFR) is highly expressed in adenoid cystic carcinoma (ACC). The efficacy and toxicity of cetuximab with concomitant platinum-based chemoradio- or chemotherapy in patients with locally advanced or metastatic ACC, respectively, was evaluated.Methods:Eligible patients (9 with locally advanced tumour and 12 with metastases) had positive tumour EGFR expression. The cetuximab loading dose (400 mg m -2) was followed by 250 mg m -2 per week. Locally advanced tumours were irradiated (mean dose 65 Gy) and treated with concomitant cisplatin (75 mg m -2, intravenously). Patients with metastases received ...
Epidermal growth factor receptor (EGFR) is certainly a transmembrane glycoprotein encoded with a gene situated in the brief arm of chromosome 7. inhibitors (p=0.032). The outcomes of the existing study could be found in decision-making relating to the treating individuals with traditional EGFR exon mutations. solid course=kwd-title Keywords: lung adenocarcinoma, traditional EGFR mutations, micropapillary design, tyrosine kinase inhibitors Intro Lung cancer may be the most popular reason behind cancer-related death world-wide, with non-small cell lung malignancy (NSCLC) being the most frequent type [1, 2]. Improved knowledge of hereditary alteration in lung malignancy has resulted in the development of several onco-targeted medicines and significant accomplishments [3C5]. Activating mutations of epidermal development element receptor (EGFR) are recognized in about 20% of lung adenocarcinomas in Traditional western countries [6] and 40%C60% of lung adenocarcinomas in East Asia [7C9]. These ...
Aida, S., et al., Distribution of epidermal growth factor and epidermal growth factor receptor in human lung: immunohistochemical and immunoelectron-microscopic studies. Respiration, 1994. 61(3):161-166.. Allahverdian, S., et al., Sialyl Lewis X modification of the epidermal growth factor receptor regulates receptor function during airway epithelial wound repair. Clin Exp Allergy, 2010. 40(4):607-618.. Blanchet, S., et al., Fine particulate matter induces amphiregulin secretion by bronchial epithelial cells. Am J Resp Cell Mol Biol, 2004. 30(4):421-427.. Burgel, P.-R. and J.A. Nadel, Epidermal growth factor receptor-mediated innate immune responses and their roles in airway diseases. Eur Resp J, 2008. 32(4):1068-1081.. Ciardiello, F., and Tortora, G. (2008). EGFR antagonists in cancer treatment. N Engl J Med, 2008. 358(11):1160-1174.. Casalino-Matsuda, S.M., et al., Role of hyaluronan and reactive oxygen species in tissue kallikrein-mediated epidermal growth factor receptor activation in human ...
Specific, high affinity receptors for 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] have been demonstrated in human breast cancer cells. In addition, 1,25-(OH)2D3 has been shown to inhibit replication in some human breast cancer cell lines, although the mechanism(s) of this anti-tumor activity remain undefined. There is currently considerable interest in the role of autocrine growth factors in the control of breast cancer cell proliferation and the effects of steroid hormones on their production, receptor binding, and action. Since the epidermal growth factor (EGF) receptor mediates the effects of both EGF and the autocrine growth factor, alpha-transforming growth factor, we investigated the effect of 1,25-(OH)2D3 on EGF receptor levels in several human breast cancer cell lines. Preincubation of T-47D cells with 1,25-(OH)2D3 for 24 h resulted in a significant concentration-dependent decline in the specific binding of [125I]EGF. The effect was observed when EGF binding was assayed at either 0 or 37 degrees C,
Mutant epidermal growth factor receptor enhances induction of vascular endothelial growth factor by hypoxia and insulin-like growth factor-1 via a PI3 kinase dependent pathway
TY - JOUR. T1 - High EGFR mRNA expression is a prognostic factor for reduced survival in pancreatic cancer after gemcitabine-based adjuvant chemotherapy. AU - Fujita, Hayato. AU - Ohchida, Kenoki. AU - Mizumoto, Kazuhiro. AU - Itaba, Soichi. AU - Ito, Tetsuhide. AU - Nakata, Kohei. AU - Yu, Jun. AU - Kayashima, Tadashi. AU - Hayashi, Akifumi. AU - Souzaki, Ryota. AU - Tajiri, Tatsuro. AU - Onimaru, Manabu. AU - Manabe, Tatsuya. AU - OHTSuka, Takao. AU - Tanaka, Masao. PY - 2011/3. Y1 - 2011/3. N2 - Pancreatic ductal adenocarcinoma (PDAC) still presents a major therapeutic challenge and a phase III clinical trial has revealed that the combination of gemcitabine and a human epidermal growth factor receptor type I (HER1/EGFR) targeting agent presented a significant benefit compared to treatment with gemcitabine alone. The aim of this study was to investigate EGFR mRNA expression in resected PDAC tissues and its correlation with patient prognosis. We obtained formalin-fixed paraffin-embedded (FFPE) ...
Chai, C.S. and Liam, C (2017) Resistance mechanisms causing first-line epidermal growth factor receptor-tyrosine kinase inhibitor treatment failure. Annals of Oncology, 28 (10). ISSN 1569-8041 ...
MOESM12 of STAT3 induces G9a to exacerbate HER3 expression for the survival of epidermal growth factor receptor-tyrosine kinase inhibitors in lung cancers
TY - GEN. T1 - The epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 (Iressa) suppresses proliferation and invasion of human oral squamous carcinoma cells via p53 independent and MMP, uPAR dependent mechanism. AU - Eun, Ju Lee. AU - Jin, Ha Whang. AU - Nam, Kyeong Jeon. AU - Kim, Jin. PY - 2007/1. Y1 - 2007/1. N2 - Oral squamous cell carcinomas (OSCCs) are characterized by a marked propensity for local invasion and dissemination to cervical lymph nodes. Overexpression of the epidermal growth factor receptor (EGFR) and high levels of certain matrix metalloproteinases (MMPs) have been implicated in the development of squamous cell carcinoma of oral cancer. ZD1839 (Iressa) is a quinazoline derivative that selectively inhibits the EGFR tyrosine kinase activity and is clinically used for cancer patients. This article attempted to determine the mechanisms underlying the effects of ZD1839 on the cellular level, and to characterize the effects of ZD1839 with regard to human OSCC cell ...
TY - JOUR. T1 - Erlotinib (OSI-774, Tarceva™), a selective epidermal growth factor receptor tyrosine kinase inhibitor, in combination with chemotherapy for advanced non-small-cell lung cancer. AU - Hightower, Mary. AU - Belani, Chandra P.. AU - Jain, Vinay K.. PY - 2003/5. Y1 - 2003/5. UR - http://www.scopus.com/inward/record.url?scp=0038080166&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0038080166&partnerID=8YFLogxK. U2 - 10.1016/S1525-7304(11)70302-3. DO - 10.1016/S1525-7304(11)70302-3. M3 - Article. C2 - 14599299. AN - SCOPUS:0038080166. VL - 4. SP - 336. EP - 338. JO - Clinical Lung Cancer. JF - Clinical Lung Cancer. SN - 1525-7304. IS - 6. ER - ...
Panitumumab is the first human combinatorial antibody for the treatment of metastatic colorectal carcinoma. Dermatologic toxicity of all grades occurs in more than 90% of patients. However, there are few reports of purpura induced by anti-epidermal growth factor receptor antibody. Renal failure is also uncommon as an adverse event of anti-epidermal growth factor receptor antibody. A 67-year-old Japanese man with advanced colon cancer received monotherapy with panitumumab. General malaise, bilateral edema of his legs, and bilateral purpura of his forearms developed 2 days after the second cycle of panitumumab. A skin biopsy was performed to evaluate the purpuric lesions on his left leg and leukocytoclastic vasculitis was diagnosed. Blood tests showed grade III acute renal failure with a blood urea nitrogen level of 33.8 mg/dL and a creatinine level of 3.10 mg/dL. This is the first reported case of leukocytoclastic vasculitis followed by purpura and acute renal failure associated with panitumumab.
TY - JOUR. T1 - Epidermal growth factor receptor mutations and gene amplification in non-small-cell lung cancer. T2 - Molecular analysis of the IDEAL/INTACT gefitinib trials. AU - Bell, Daphne W.. AU - Lynch, Thomas J.. AU - Haserlat, Sara M.. AU - Harris, Patricia L.. AU - Okimoto, Ross A.. AU - Brannigan, Brian W.. AU - Sgroi, Dennis C.. AU - Muir, Beth. AU - Riemenschneider, Markus J.. AU - Iacona, Renee Bailey. AU - Krebs, Annetta D.. AU - Johnson, David H.. AU - Giaccone, Giuseppe. AU - Herbst, Roy S.. AU - Manegold, Christian. AU - Fukuoka, Masahiro. AU - Kris, Mark G.. AU - Baselga, José. AU - Ochs, Judith S.. AU - Haber, Daniel A.. PY - 2005/12/1. Y1 - 2005/12/1. N2 - Purpose: Most cases of non-small-cell lung cancer (NSCLC) with dramatic responses to gefitinib have specific activating mutations in the epidermal growth factor receptor (EGFR), but the predictive value of these mutations has not been defined in large clinical trials. The goal of this study was to determine the ...
Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are the standard first-line treatment for EGFR-mutant nonsmall cell lung cancer (NSCLC) patients. However, studies have reported that not all NSCLC patients harboring kinase domain mutations in epidermal growth factor receptor (EGFR) show significant clinical benefits from EGFR-targeted tyrosine kinase inhibitors (TKIs). Therefore, it is necessary to establish feasible biomarkers to predict the prognosis of EGFR-mutant NSCLC patients treated with EGFR-TKIs. This study aimed to determine biomarkers using inflammatory parameters from complete blood counts to predict the prognosis of EGFR-mutant NSCLC patients treated with EGFR-TKIs.We retrospectively investigated 127 stage IIIB/IV NSCLC patients with activating EGFR mutations who were treated with EGFR-TKIs. We used receiver operating characteristic (ROC) curves to determine the optimal cut-off for the inflammatory markers as prognostic factors. Additionally, univariate and ...
Over-expression of truncated epidermal growth factor receptor (EGFR) occurs in a variety of malignancies including glioblastoma multiforme, breast and lung cancer. The truncation deletes an extracellular domain and results in constitutive activation of the receptor. NIH3T3 cells were transfected with full length or truncated human EGFR and differences in growth rates in vivo and in vitro analysed. A growth advantage was seen for cells expressing mutant receptor compared to full length EGFR in vivo only. Administration of an anti-mutant EGFR antibody to mice transiently reduced the growth rates of mutant tumours, confirming that the mutant receptor itself was important in this enhanced tumorigenicity. This showed that stimuli present in vivo and not in vitro may be contributing to growth. We therefore analysed the regulation of the angiogenic factor vascular endothelial growth factor (VEGF). Although levels of secreted VEGF did not differ significantly between wild-type and mutant EGFR cell lines when
To determine the expression of nucleostemin (NS), epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) mRNA in human esophageal squamous cell carcinoma (ESCC) tissues and their association in a human ESCC cell line. The expression of NS, EGF and EGFR mRNA was determined in paired normal esophageal and ESCC tissues of 62 patients using in situ hybridization. The association between NS and EGF or EGFR was examined using immunoblotting and real time polymerase chain reaction in a human ESCC cell line transfected with NS siRNA or treated with a selective EGFR inhibitor. In normal esophageal and ESCC tissues, the positive detection rates were 21.0% (13/62) and 69.4% (43/62) for NS mRNA staining, 40.3% (25/62) and 77.4% (48/62) for EGF mRNA staining, and 30.6% (19/62) and 75.8% (41/62) for EGFR mRNA staining, respectively. These results indicated that NS, EGF and EGFR mRNA expression was upregulated mostly in ESCC tissues. Moreover, the expression of NS, EGF and EGFR mRNA was ...
Clinical trials have shown that epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) did not improve the survival of patients with EGFR-mutated non-small cell lung cancer (NSCLC) because of the high crossover of treatments. Realistically, the role of EGFR-TKIs in NSCLC with mutated EGFR is not well known. We retrospectively analysed data from patients with recurrent or metastatic NSCLC. Clinical prognostic factors were identified by Cox proportional hazards modelling. Among 503 patients, the median overall survival (OS) for all of patients was 11.7 months. Cox analysis showed that PS 0-1, recurrent disease, EGFR mutations, or EGFR-TKI treatment were associated with improved OS. In patients with EGFR-activating mutations, Cox analysis showed that patients with adenocarcinoma, recurrent disease, or EGFR-TKI treatment had significantly longer survival. Patients with EGFR-activating mutations who received EGFR-TKI therapy had a median OS of 24.3 months, which was significantly longer than
The epidermal growth factor receptor (EGFR/ERBB1) is the prototypical and first discovered member of the ERBB family of receptor tyrosine kinases. As transmembrane receptors, their primary function is to translate extracellular signals into cellular response. Signaling is initiated through binding by members of the EGF ligand family, which induces receptor homodimerization or heterodimerization with other ERBB receptors (ERBB2, ERBB3 or ERBB4). Activation of downstream cytoplasmic signaling pathways occurs, leading to alterations in biological responses such as cellular proliferation, survival, motility, and adhesion. As EGFR is expressed in most developing and adult tissues, misregulation or dysfunction of EGFR activity severely impacts embryonic viability, tissue maintenance and multiple disease processes. Since EGFR was first proposed as a cancer drug target over twenty years ago, substantial research has defined a central role for aberrant ERBB signaling in cancer and led to the design of ...
TY - JOUR. T1 - Lapatinib plus capecitabine resolved human epidermal growth factor receptor 2-positive brain metastases. AU - Glück, Stefan. AU - Castrellon, Aurelio. PY - 2009/11/1. Y1 - 2009/11/1. N2 - Brain metastases affect 25%-30% of women with human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer and are associated with a high burden of disease and poor prognosis. A 55-year-old woman presented with HER2-positive, hormone receptor-positive, locally advanced infiltrating ductal carcinoma. She received 4 cycles of neoadjuvant docetaxel (75 mg/m2) plus trastuzumab (6 mg/kg) on a 21-day cycle, resulting in complete pathologic response at the time of surgery. Trastuzumab (6 mg/kg every 21 days) plus anastrozole (1 mg/d) was continued for 1 year. Two years later, the patient progressed with pulmonary nodules and a large pleural effusion. Computed tomography and positron emission tomography revealed multiple lesions in the liver and thoracic spine but no evidence of ...
TY - JOUR. T1 - Role for the Epidermal Growth Factor Receptor in Chemotherapy-Induced Alopecia. AU - Bichsel, Kyle J.. AU - Gogia, Navdeep. AU - Malouff, Timothy. AU - Pena, Zachary. AU - Forney, Eric. AU - Hammiller, Brianna. AU - Watson, Patrice. AU - Hansen, Laura A.. PY - 2013/7/19. Y1 - 2013/7/19. N2 - Treatment of cancer patients with chemotherapeutics like cyclophosphamide often causes alopecia as a result of premature and aberrant catagen. Because the epidermal growth factor receptor (EGFR) signals anagen hair follicles to enter catagen, we hypothesized that EGFR signaling may be involved in cyclophosphamide-induced alopecia. To test this hypothesis, skin-targeted Egfr mutant mice were generated by crossing floxed Egfr and Keratin 14 promoter-driven Cre recombinase mice. Cyclophosphamide treatment of control mice resulted in alopecia while Egfr mutant skin was resistant to cyclophosphamide-induced alopecia. Egfr mutant skin entered catagen normally, as indicated by dermal papilla ...
TY - JOUR. T1 - Expression and mutation analysis of epidermal growth factor receptor in head and neck squamous cell carcinoma. AU - Sheikh Ali, Mahmoud A L. AU - Gunduz, Mehmet. AU - Nagatsuka, Hitoshi. AU - Gunduz, Esra. AU - Cengiz, Beyhan. AU - Fukushima, Kunihiro. AU - Beder, Levent Bekir. AU - Demircan, Kadir. AU - Fujii, Masae. AU - Yamanaka, Noboru. AU - Shimizu, Kenji. AU - Grenman, Reidar. AU - Nagai, Noriyuki. PY - 2008. Y1 - 2008. N2 - The epidermal growth factor receptor (EGFR)-RAS-RAF-mitogen-activated protein kinase signaling cascade is an important pathway in cancer development and recent reports show that EGFR and its downstream signaling molecules are mutated in a number of cancers. We have analyzed 91 Japanese head and neck squamous cell carcinomas (HNSCC) and 12 HNSCC cell lines for mutations in EGFR, ErbB2, and K-ras. Exons encoding the hot-spot regions in the tyrosine kinase domain of both EGFR (exons 18, 19, and 21) and ErbB2 (exons 18-23), as well as exons 1 and 2 of K-ras ...
TY - JOUR. T1 - The benefits of achieving stable disease in advanced lung cancer. AU - Kelly, Karen. PY - 2003/7. Y1 - 2003/7. N2 - The cytostatic, molecular-targeted therapies becoming available for lung cancer and other human solid tumors are more likely to result in stable disease than to produce tumor regression. In the setting of advanced lung cancer, stable disease provides significant benefit to the patient. However, in the context of clinical trials, stable disease is vaguely defined, difficult to measure, and may represent a heterogeneous patient population. The inclusion of alternative trial end points such as symptom improvement and biologic activity may help to identify patients who have achieved clinically relevant stable disease. The epidermal growth factor receptor-tyrosine kinase inhibitor gefitinib (Iressa) has been shown to produce partial responses and stable disease in patients with advanced lung cancer who have previously received treatment with standard chemotherapies. In ...
TY - JOUR. T1 - Epidermal growth factor receptor, c-kit, and her2/neu immunostaining in advanced or recurrent thymic epithelial neoplasms staged according to the 2004 world health organization in patients treated with octreotide and prednisone. T2 - an eastern cooperative oncology group study. AU - Aisner, Seena C.. AU - Dahlberg, Suzanne. AU - Hameed, Meera R.. AU - Ettinger, David S.. AU - Schiller, Joan H.. AU - Johnson, David H.. AU - Aisner, Joseph. AU - Loehrer, Patrick J.. PY - 2010/6. Y1 - 2010/6. N2 - BACKGROUND:: Advanced or recurrent nonresectable thymic epithelial tumors show only a modest response to standard chemotherapy. A recent study using octreotide and prednisone in thymic tumors, Eastern Cooperative Oncology Group study E1C97, was conducted to verify the activity of octreotide for thymic tumors. The aim of this study was to determine whether epidermal growth factor receptor (EGFR) immunoreactivity correlated with outcomes and to identify new biologic markers for potential ...
TY - JOUR. T1 - Uncommon frame-shift exon 19 EGFR mutations are sensitive to EGFR tyrosine kinase inhibitors in non-small cell lung carcinoma. AU - Improta, Giuseppina. AU - Zupa, Angela. AU - Natalicchio, Maria Iole. AU - Sisinni, Lorenza. AU - Marinaccio, Anna. AU - Bozza, Giovanni. AU - Vita, Giulia. AU - Aieta, Michele. AU - Landriscina, Matteo. PY - 2018/1/31. Y1 - 2018/1/31. N2 - Exons 19-21 EGFR activating mutations are predictive biomarkers of response to EGFR tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC). However, uncommon exon 19 EGFR mutations, due to their low frequency, have an uncertain biological and clinical significance and very little is known about their TKI sensitivity. This study was designed to describe the TKI sensitivity of a small cohort of lung adenocarcinomas bearing uncommon exon 19 mutations and to evaluate in silico the correlation between frame-shift exon 19 mutations and EGFR sequence/structure modification. Among 1168 NSCLCs screened for ...
In the present study, we examined whether eosinophils induce MUC5AC mucin synthesis in airway epithelial cells. Our results showed that activated human eosinophils caused MUC5AC mucin synthesis in NCI-H292 cells. Similarly, the supernatant of activated eosinophils induced MUC5AC gene and protein synthesis in NCI-H292 cells, indicating that this effect of activated eosinophils was related to a secreted product.. Because EGFR activation is reported to cause mucin synthesis (13), we examined whether EGFR activation is required for activated eosinophil-induced mucin synthesis. Activated eosinophil supernatant induced EGFR phosphorylation in NCI-H292 cells, and selective inhibitors of EGFR tyrosine kinase blocked activated eosinophil-induced EGFR phosphorylation and MUC5AC synthesis completely; a selective PDGFR inhibitor (AG1295) and a negative control for tyrphostins (AG9) were without effect. These findings implicate EGFR tyrosine kinase phosphorylation in mucin synthesis induced by activated ...
TY - JOUR. T1 - Abnormal epithelial cell polarity and ectopic Epidermal Growth Factor Receptor (EGFR) expression induced in Emx2 KO Embryonic Gonads. AU - Kusaka, Masatomo. AU - Katoh-Fukui, Yuko. AU - Ogawa, Hidesato. AU - Miyabayashi, Kanako. AU - Baba, Takashi. AU - Shima, Yuichi. AU - Sugiyama, Noriyuki. AU - Sugimoto, Yukihiko. AU - Okuno, Yasushi. AU - Kodama, Ryuji. AU - Iizuka-Kogo, Akiko. AU - Senda, Takao. AU - Sasaoka, Toshikuni. AU - Kitamura, Kunio. AU - Aizawa, Shinichi. AU - Morohashi, Ken Ichirou. N1 - Copyright: Copyright 2011 Elsevier B.V., All rights reserved.. PY - 2010/12. Y1 - 2010/12. N2 - The gonadal primordium first emerges as a thickening of the embryonic coelomic epithelium, which has been thought to migrate mediodorsally to form the primitive gonad. However, the early gonadal development remains poorly understood. Mice lacking the paired-like homeobox gene Emx2 display gonadal dysgenesis. Interestingly, the knockout (KO) embryonic gonads develop an unusual surface ...
Abstract. A phase III clinical trial showed gemcitabine chemotherapy combined with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinib significantly improved overall survival in patients with advanced pancreatic cancer. Therefore, we studied whether addition of gemcitabine to erlotinib in cancer cells having intrinsic or acquired erlotinib resistance could restore chemosensitization in these cells. We studied the synergistic effect of erlotinib and gemcitabine in EGFR-overexpressing A-431 cells with acquired erlotinib resistance and in intrinsic erlotinib-resistant triple negative breast cancer (TNBC) BT-549, MDA-MB-231 and MDA-MB-468 cell lines. Erlotinib and gemcitabine were synergistic in both parental intrinsically erlotinib-sensitive A-431 cells (combination index = 0.69 at the effective dose [ED50]) and in two A-431 cell pools that had acquired erlotinib resistance (combination indices = 0.63 and 0.49 at ED50). The synergistic effect of erlotinib and gemcitabine on ...
2014 SCI Comparison of targeted next-generation sequencing with conventional sequencing for predicting the responsiveness to epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) therapy in never-smokers with lung adenocarcinoma: Lung cancer. 85(2):161~167 (3.737 ...
Phenotype data for mouse gene Eps15. Discover Eps15s significant phenotypes, expression, images, histopathology and more. Data for gene Eps15 is all freely available for download.
Signals from the epidermal growth factor receptor (EGFR) have typically been considered to provide catabolic activities in articular cartilage, and accordingly have been suggested to have a causal role in osteoarthritis progression. The aim of this study was to determine in vivo roles for endogenous EGFR signal activation in articular cartilage. Transgenic mice with conditional, limb-targeted deletion of the endogenous intracellular EGFR inhibitor Mig-6 were generated using CreLoxP (Mig-6-flox; Prx1Cre) recombination. Histology, histochemical staining and immunohistochemistry were used to confirm activation of EGFR signaling in the articular cartilage and joints, and to analyze phenotypic consequences of Mig-6 loss on articular cartilage morphology, proliferation, expression of progenitor cell markers, presence of chondrocyte hypertrophy and degradation of articular cartilage matrix. The articular cartilage of Mig-6-conditional knockout (Mig-6-cko) mice was dramatically and significantly thicker than
Oncotarget | https://doi.org/10.18632/oncotarget.12962 Xuejing Lin, Zhangxiao Peng, Xiaohui Fu, Chunying Liu, Yang Xu, Weidan Ji, Jianhui Fan, Lei Chen, Lin Fang, Yao Huang, Changqing Su
Duration of disease control, tumor growth rate, changes in overall tumor volume, and subjective symptoms are important predictors of the length of continued EGFR-TKI beyond RECIST PD [3,5,17]. CT or MRI scans, standard methods of assessment of RECIST criteria, can only be applied for evaluation of skeletal regions with identifiable soft tissue components [20]. The majority of skeletal metastasis regions are considered non-target areas, and PD is defined by new regions or unequivocal progression of preexisting skeletal metastasis [11,20]. Adjustment of RECIST PD in skeletal metastasis to previous classifications of progression patterns in EGFR-mutated NSCLC is difficult. Compared to previous studies, our study showed no differences in the duration of continued EGFR-TKI according to the presence of symptoms and changes or overall response of other extraskeletal or target regions [5,19]. Our data showed pain symptoms in 10 out of 12 patients in the group with disease progression of preexisting ...
Human Epidermal growth factor Receptor type 2 (HER2) is over expressed in 20.0-30.0% of breast cancers and is currently evaluated histopathologically. Immunohistochemistry and fluorescence in situ hybridization require invasive enucleation of the tumor tissue and may be affected by heterogeneity. Serum marker tests are more objective because of the uniformity of the study material. Serum HER2 levels are important for breast cancer care. However, the clinical utility of serum HER2 testing is unclear. We evaluated serum HER2 as a marker of therapeutic response in breast cancer.
The modest response of patients with head and neck squamous cell carcinoma (HNSCC) and non-small cell lung carcinoma (NSCLC) to epithelial growth factor receptor tyrosine kinase inhibitors such as gefitinib and erlotinib indicates the need for the development of biomarkers to predict response. We determined gefitinib sensitivity in a panel of HNSCC cell lines by a 5-day 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and confirmed these responses with analysis of downstream signaling by immunoblotting and cell cycle arrest. Basal gene expression profiles were then determined by microarray analysis and correlated with gefitinib response. These data were combined with previously reported NSCLC microarray results to generate a broader predictive index. Common markers of resistance between the two tumor types included genes associated with the epithelial to mesenchymal transition. We confirmed that increased protein expression of vimentin combined with the loss of E-cadherin, ...
The first-generation epidermal growth factor receptor tyrosine kinase inhibitors erlotinib and gefitinib have been incorporated into treatment paradigms for patients with advanced non-small cell lung cancer. These agents are particularly effective in a subset of patients whose tumors harbor activati …
Gefitinib, as the first epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) approved for the treatment of advanced non-small cell lung cancer (NSCLC), has been proved to significantly improve the progression-free survival (PFS) in the first-line setting but suffers from resistance 7-10 months after treatment initiation. Apatinib (YN968D1), a potent vascular endothelial growth factor receptor (VEGFR) 2-TKI, specifically binds to VEGFR2 and leads to anti-angiogenetic and anti-neoplastic effect. Concurrent inhibition of VEGFR and EGFR pathways represents a rational approach to improve treatment responses and delay the onset of treatment resistance in EGFR-mutant NSCLC. This ACTIVE study aims to assess the combination of apatinib and gefitinib as a new treatment approach for EGFR-mutant NSCLC as a first-line setting. This multicenter, randomized, double-blind, placebo-controlled phase III study (NCT02824458) has been designed to assess the efficacy and safety of apatinib or placebo
131214PRTartifical sequenceChemically synthesized 1Glu Leu Val Met Thr Gln Ser Pro Ser Ser Leu Ser Ala Ser Val Gly 1 5 10 15 Asp Arg Val Asn Ile Ala Cys Arg Ala Ser Gln Ser Ile Glu Thr Asn 20 25 30 Leu His Trp Tyr Gln Gln Lys Pro Gly Lys Ala Pro Arg Leu Leu Ile 35 40 45 Lys Tyr Thr Ser Arg Leu His Ser Gly Val Pro Ser Arg Phe Ser Gly 50 55 60 Ser Gly Ser Gly Thr Asp Phe Thr Leu Thr Ile Ser Ser Leu Gln Pro 65 70 75 80 Glu Asp Phe Ala Ile Tyr Tyr Cys Gln Gln Asn Asn Asn Trp Pro Thr 85 90 95 Thr Phe Gly Gly Gly Thr Lys Val Glu Ile Lys Arg Thr Val Ala Ala 100 105 110 Pro Ser Val Phe Ile Phe Pro Pro Ser Asp Glu Gln Leu Lys Ser Gly 115 120 125 Thr Ala Ser Val Val Cys Leu Leu Asn Asn Phe Tyr Pro Arg Glu Ala 130 135 140 Lys Val Gln Trp Lys Val Asp Asn Ala Leu Gln Ser Gly Asn Ser Gln 145 150 155 160 Glu Ser Val Thr Glu Gln Asp Ser Lys Asp Ser Thr Tyr Ser Leu Ser 165 170 175 Ser Thr Leu Thr Leu Ser Lys Ala Asp Tyr Glu Lys His Lys Val Tyr 180 185 190 Ala Cys Glu Val Thr His Gln Gly Leu Ser Ser Pro Val Thr ...
Gefitinib, a selective epidermal growth factor receptor tyrosine kinase inhibitor, is under clinical testing and use in cancer patients, including glioma. However, the molecular mechanisms involved in gefitinib-mediated anticancer effects against glioma remain largely uncharacterized. Gefitinib inhibits cell growth and induces apoptosis in human glioma cells. Gefitinib also induces death of H4 cells with characteristics of the intrinsic apoptotic pathway, including Bax mitochondrial translocation, mitochondrial outer membrane permeabilization, cytochrome c cytosolic release, and caspase-9/caspase-3 activation. The importance of Bax in mediating gefitinib-induced apoptosis was confirmed by the attenuation of apoptosis by Bax siRNA and Bax channel blocker. Gefitinib caused Bad dephosphorylation, particularly in serine-112, and increased its binding preference to Bcl-2 and Bcl-xL. The dephosphorylation of Bad in gefitinib-treated cells was accompanied by reduced intracellular cyclic AMP content and protein
Methods Thirty-eight MM specimens were submitted to EGFR mutation evaluation, and compared with the results of immunohistochemical staining and fluorescence in situ hybridization (FISH) analysis. DNA was extracted from paraffin blocks and PCR was performed to amplify exon regions 18-21 of the EGFR gene. Direct sequencing of the purified PCR products was performed. ...
TY - JOUR. T1 - STAP-2 protein promotes prostate cancer growth by enhancing epidermal growth factor receptor stabilization. AU - Kitai, Yuichi. AU - Iwakami, Masashi. AU - Saitoh, Kodai. AU - Togi, Sumihito. AU - Isayama, Serina. AU - Sekine, Yuichi. AU - Muromoto, Ryuta. AU - Kashiwakura, Jun Ichi. AU - Yoshimura, Akihiko. AU - Oritani, Kenji. AU - Matsuda, Tadashi. N1 - Funding Information: This study was supported in part by a grant-in-aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. The authors declare that they have no conflicts of interest with the contents of this article. Publisher Copyright: © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.. PY - 2017/11/24. Y1 - 2017/11/24. N2 - Signal-transducing adaptor family member-2 (STAP-2) is an adaptor protein that regulates various intracellular signaling pathways and promotes tumorigenesis in melanoma and breast cancer cells. However, the contribution of ...
Free Online Library: Potential Anticancer Mechanisms of a Novel EGFR/DNA-Targeting Combi-Molecule (JDF12) against DU145 Prostate Cancer Cells: An iTRAQ-Based Proteomic Analysis.(Research Article, epidermal growth factor receptor , Report) by BioMed Research International; Biotechnology industry High technology industry Apoptosis Care and treatment Cancer treatment Cellular signal transduction Epidermal growth factor receptors Gene expression Prostate cancer Drug therapy Genetic aspects Protein-protein interactions Proteins
Maini, Raj, Collison, David J., Maidment, Jill M., Davies, Peter D. and Wormstone, I. Michael (2002) Pterygial derived fibroblasts express functionally active histamine and epidermal growth factor receptors. Experimental Eye Research, 74 (2). pp. 237-244. ISSN 0014-4835 Full text not available from this repository. (Request a copy ...
Product Description Product Description Erlotinib hydrochloride For Treat Non-small Cell Lung Cancer 183319-69-9 Erlotinib hydrochloride---------Basic info Product Name Erlotinib hydrochloride CAS 183319-69-9 MF C22H24ClN3O4 MW 429.9 Chemical Properties Off-White Solid Usage Selective epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor. Antineoplastic Erlotinib HCl is an HER1/EGFR inhibitor with IC50 of 2 nM. Erlotinib HCl (OSI-744) is an…
Effectiveness of tyrosine kinase inhibitors on uncommon E709X epidermal growth factor receptor mutations in non-small-cell lung cancer Jenn-Yu Wu,1 Jin-Yuan Shih2 1Department of Internal Medicine, National Taiwan University Hospital Yun-Lin Branch, Yun-Lin, Taiwan; 2Department of Internal Medicine, National Taiwan University Hospital, and College of Medicine, National Taiwan University, Taipei, Taiwan Background: Clinical features of epidermal growth factor receptor (EGFR) mutations: L858R, deletions in exon 19, T790M, insertions in exon 20, G719X, and L861X in non-small-cell lung cancer (NSCLC) are well-known. The clinical significance of other uncommon EGFR mutations, such as E709X, is not well understood. This study aimed to improve the understanding of E709X, and the clinical response to tyrosine kinase inhibitors (TKIs) of NSCLC patients with such an uncommon mutation.Methods: Specimens from 3,146 patients were tested for EGFR mutations. We surveyed the clinical data and the effectiveness of TKI
Lung cancer is the leading cause of cancer-related mortality for both men and women in United States and is estimated to remain the most fatal cancer-related malignancy (1). Little improvement in the efficacy of chemotherapy has been made in the last 20 years, usually attributed to the overexpression and overactivity of EGFR in NSCLC (4, 29-31). However, the use of selective EGFR tyrosine kinase inhibitors (gefitinib) and monoclonal antibodies against EGFR toward the treatment of lung cancer has continuously failed (32, 33). Therefore, additional alternative therapies with low toxicity and increased efficacy should be explored. Although recent studies suggest that nonpsychoactive synthetic cannabinoids possess antitumor effects against various tumors, including breast cancer, not much is known about the effects of synthetic CB1/CB2 agonists on NSCLC growth and metastasis. In the present study, we analyzed the antitumorigenic and antimetastasis effects of CB1/CB2 agonists Win55,212-2 and CB2 ...
Objectives and Background To reveal the details system of miR-484 in myocardial ischemia-reperfusion (MI/R) damage. appearance of caspase-3/9 had been elevated in IR-C group. Weighed against the I/R Slc2a4 and IR-C groupings, the apoptotic index of myocardial cells in the ischemic area was reduced, the membrane potential was elevated, as well as the expression of caspase-3/9 was decreased in the miR group significantly. SMAD7 was the mark gene of miR-484. Conclusions MiR-484 protected myocardial cells from We/R damage by suppressing caspase-9 and caspase-3 appearance during cardiomyocyte apoptosis. MiR-484 decreased the appearance of IL-6, TNF-, and IL-1 in MI/R. MiR-484 might alleviate the decreasing of mitochondrial membrane potential in MI/R cells. Keywords: Apoptosis, Mitochondrial membrane potential, Caspase-3, Caspase-9 Launch Ischemia-reperfusion (I/R) damage is the injury caused when blood supply returns to the tissue after a period of ischemia. It is a Pyrazinamide complex process ...
Epidermal growth factor receptor (EGFR), member of the human epidermal growth factor receptor (HER) family, plays a critical role in regulating multiple cellular processes including proliferation, differentiation, cell migration and cell survival. Deregulation of the EGFR signaling has been found to be associated with the development of a variety of human malignancies including lung, breast, and ovarian cancers, making inhibition of EGFR the most promising molecular targeted therapy developed in the past decade against cancer. Human non small cell lung cancers (NSCLC) with activating mutations in the EGFR gene frequently experience significant tumor regression when treated with EGFR tyrosine kinase inhibitors (TKIs), although acquired resistance invariably develops. Resistance to TKI treatments has been associated to secondary mutations in the EGFR gene or to activation of additional bypass signaling pathways including the ones mediated by receptor tyrosine kinases, Fas receptor and NF-kB. In more than
The Human Epidermal Growth Factor Receptor (EGFR/HER1) can be activated by several ligands including Transforming Growth Factor alpha (TGF-α) and Epidermal Growth Factor (EGF). Following ligand binding, EGFR heterodimerizes with other HER family members, such as HER2 (human epidermal growth factor receptor-2). Previously, we showed that the EGFR is upregulated in trastuzumab resistant HER2 positive (HER2+) breast cancer cells. This study is aimed to determine the downstream effects on transcription following EGFR upregulation in HER2+ breast cancer cells. RNA-sequence and ChIP-sequence for H3K18ac and H3K27ac (Histone H3 lysine K18 and K27 acetylation) were conducted following an Epidermal Growth Factor (EGF) treatment time course in HER2+ breast cancer cells, SKBR3. The levels of several proteins of interest were confirmed by western blot analysis. The cellular localization of proteins of interest was examined using biochemically fractionated lysates followed by western blot analysis. Over the course
The identification of epidermal growth factor receptor (EGFR)-activating mutations and the subsequent development of EGFR tyrosine kinase inhibitors (TKIs) for advanced EGFR-mutant non-small cell lung cancer (NSCLC) represents a drastic change in treatment paradigms. Several randomised clinical trials have demonstrated that EGFR-TKI administration results in a superior response rate and longer progression-free survival than platinum-based chemotherapy for advanced EGFR-mutant NSCLC.1-3 However, patients who initially respond to EGFR-TKIs eventually acquire resistance.. The mechanisms of acquired EGFR-TKI resistance have been widely studied and several mechanisms have been identified. The most common mechanism of resistance to TKIs, observed in over 50% of patients, is a threonine-to-methionine substitution within the gatekeeper residue at amino acid position 790 (T790M) of the EGFR gene.4-7 EGFR-independent mechanisms include the MET proto-oncogene, receptor tyrosine kinase (MET) amplification ...
EGFR a receptor tyrosine kinase. This is a receptor for epidermal growth factor (EGF) and related growth factors including TGF-alpha, amphiregulin, betacellulin, heparin-binding EGF-like growth factor, GP30, and vaccinia virus growth factor. EGFR is involved in the control of cell growth and differentiation. It is a single-pass transmembrane tyrosine kinase. Ligand binding to this receptor results in receptor dimerization, autophosphorylation (in trans), activation of various downstream signaling molecules and lysosomal degradation. It can be phosphorylated and activated by Src. Activated EGFR binds the SH2 domain of phospholipase C-gamma (PLC-gamma), activating PLC-gamma-mediated downstream signaling. Phosphorylated EGFR binds Cbl, leading to its ubiquitination and degradation. Grb2 and SHC bind to phospho-EGFR and are involved in the activation of MAP kinase signaling pathways. Phosphorylation on Ser and Thr residues is thought to represent a mechanism for attenuation of EGFR kinase activity. ...
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are current treatments for advanced non-small cell lung cancer (NSCLC) harboring activating EGFR gene mutations. Although studies show an increased progression free survival (PFS) with use of EGFR TKIs in the first-line setting, most patients will develop resistance to therapy after the first about 10 months. Undoubtedly it is critical to choose an optimal clinical strategy for patients with EGFR sensitive mutation undergoing EGFR-TKI resistance. The second biopsy should be applied under condition permission to verify specific resistance mechanism. Here we discussed the mechanism of drug resistance and the choice of therapeutic regimen, also compared the superior and inferior of each treatment plan, which proposed a novel perspective for NSCLC target therapy.
Epidermal growth factor receptor[edit]. An example of RTKs that undergo autophosphorylation is the Epidermal Growth Factor ... 1: Activation of the Epidermal Growth Factor Receptor by autophosphorylation. Adapted from Pecorino (2008)[1] ... Insulin receptors[edit]. Another example is the binding of insulin to insulin receptors. Once released into the bloodstream ... This receptor is a protein with an (αβ)2 quaternary structure. The two large α-subunits are extracellular, while the smaller β- ...
... epidermal growth factor; EGFR, epidermal growth factor receptor; MoAbs, monoclonal antibodies; VEGF, vascular endothelial ... growth factor. The major challenge in the development of boron delivery agents has been the requirement for selective tumor ... Ono, Koji (28 March 2016). "An analysis of the structure of the compound biological effectiveness factor". Journal of Radiation ... In vivo growth suppression of experimental melanoma solid tumor". Cancer Letters. 150 (2): 177-82. doi:10.1016/S0304-3835(99) ...
Herbst RS (2004). "Review of epidermal growth factor receptor biology". International Journal of Radiation Oncology, Biology, ... Epidermal growth factor (EGF) Various enzymes; most notably: α-amylase (EC3.2.1.1), or ptyalin, secreted by the acinar cells of ... Researchers at the University of Florida at Gainesville have discovered a protein called nerve growth factor (NGF) in the ... It is the liquid medium in which chemicals are carried to taste receptor cells (mostly associated with lingual papillae). ...
Vertebrate hepatocyte growth factor-regulated tyrosine kinase substrate (HRS). Mammalian epidermal growth factor receptor ... Mammalian epidermal growth factor receptor substrate EPS15R. Drosophila melanogaster (Fruit fly) liquid facets (lqf), an epsin ... substrate 15 (EPS15), which is involved in cell growth regulation. ...
October 2003). "Aldosterone stimulates epidermal growth factor receptor expression". J. Biol. Chem. 278 (44): 43060-66. doi: ... and also by epidermal growth factor (EGF), which is a target of the signaling pathway activated by aldosterone Reduced ... Many of these remodelling effects seem to be mediated by transforming growth factor beta (TGF-beta), which is a common ... Binding to beta-1 receptors in the myocardium increases the heart rate and makes contractions more forceful in an attempt to ...
Herbst RS (2004). "Review of epidermal growth factor receptor biology". International Journal of Radiation Oncology, Biology, ... Effects of EGF Epidermal growth factor (EGF) results in cellular proliferation, differentiation, and survival. EGF is a low- ... Stomach as nutrition sensor The human stomach can "taste" sodium glutamate using glutamate receptors and this information is ... The stomach can also sense, independently of tongue and oral taste receptors, glucose, carbohydrates, proteins, and fats. This ...
... growth factor receptor antibodies which are inhibitors of epidermal growth factor binding and antagonists of epidermal growth ... Identification of high affinity receptors for epidermal growth factor by an anti-receptor monoclonal antibody. Proc Natl Acad ... "Targeting the epidermal growth factor receptor for cancer therapy". Journal of Clinical Oncology. Retrieved March 2, 2011. " ... "Epidermal growth factor receptor family and chemosensitization". Journal of the National Cancer Institute. Retrieved March 2, ...
... including epidermal growth factor receptor (EGFR; ERBB1), epidermal growth factor receptor 2 (HER2; ERBB2), vascular ... June 2007). "Inhibition of the T790M gatekeeper mutant of the epidermal growth factor receptor by EXEL-7647". Clinical Cancer ... June 2007). "Inhibition of the T790M gatekeeper mutant of the epidermal growth factor receptor by EXEL-7647". Clinical Cancer ... endothelial growth factor receptor (VEGFR), and ephrin B4 (EphB4). The drug activity was initially studied in non-small cell ...
... and interaction partners of epidermal growth factor receptor signaling after stimulation by epidermal growth factor using ... "Crystal structure of a truncated epidermal growth factor receptor extracellular domain bound to transforming growth factor α". ... "Crystal structure of a truncated epidermal growth factor receptor extracellular domain bound to transforming growth factor ... There are 11 growth factors that activate ErbB receptors. The ability ('+') or inability ('-') of each growth factor to ...
"Sprouty2 attenuates epidermal growth factor receptor ubiquitylation and endocytosis, and consequently enhances Ras/ERK ... "Ligand-induced ubiquitination of the epidermal growth factor receptor involves the interaction of the c-Cbl RING finger and ... "cbl-b inhibits epidermal growth factor receptor signaling". Oncogene. 18 (10): 1855-66. doi:10.1038/sj.onc.1202499. PMID ... "Identification of c-Cbl as a new ligase for insulin-like growth factor-I receptor with distinct roles from Mdm2 in receptor ...
Harari, P M (December 2004). "Epidermal growth factor receptor inhibition strategies in oncology". Endocrine-Related Cancer. 11 ... September 2006). "Assessment of epidermal growth factor receptor (EGFR) expression in primary colorectal carcinomas and their ... estrogens and progesterone receptor (ER & PR) staining are used both diagnostically (breast and gyn tumors) as well as ... The presence of hormone receptors can be used to determine if a tumor is potentially responsive to antihormonal therapy. One of ...
EPH receptor A2, ETV6, Epidermal growth factor receptor, Erythropoietin receptor, FRS2, Fas ligand, GAB1, GAB2, Glycoprotein ... The protein encoded by this gene binds receptors such as the epidermal growth factor receptor and contains one SH2 domain and ... Grb2 is best known for its ability to link the epidermal growth factor receptor tyrosine kinase to the activation of Ras and ... Liu YF, Deth RC, Devys D (March 1997). "SH3 domain-dependent association of huntingtin with epidermal growth factor receptor ...
2002). "Sprouty2 attenuates epidermal growth factor receptor ubiquitylation and endocytosis, and consequently enhances Ras/ERK ... 1999). "Cbl-b inhibits epidermal growth factor receptor signaling". Oncogene. 18 (10): 1855-66. doi:10.1038/sj.onc.1202499. ... CBLC has been shown to interact with FYN and Epidermal growth factor receptor. GRCh38: Ensembl release 89: ENSG00000142273 - ... 2002). "C-Cbl is involved in Met signaling in B cells and mediates hepatocyte growth factor-induced receptor ubiquitination". J ...
It binds to the epidermal growth factor receptor (EGFR). The US FDA approved necitumumab under the brand name Portrazza for use ...
CBLB has been shown to interact with: CRKL, Epidermal growth factor receptor, Grb2, NEDD4, PIK3R1, and SH3KBP1. GRCh38: Ensembl ... 2001). "Cbl-b-dependent coordinated degradation of the epidermal growth factor receptor signaling complex". J. Biol. Chem. 276 ... 1999). "cbl-b inhibits epidermal growth factor receptor signaling". Oncogene. 18 (10): 1855-66. doi:10.1038/sj.onc.1202499. ... "cbl-b inhibits epidermal growth factor receptor signaling". Oncogene. 18 (10): 1855-66. doi:10.1038/sj.onc.1202499. PMID ...
Inhibitors of Epidermal growth factor receptor (EGFR) *tyrosine kinase inhibitors (TKI's):[9] *erlotinib (Tarceva)[10][ ... Riely GJ, Politi KA, Miller VA, Pao W (December 2006). "Update on epidermal growth factor receptor mutations in non-small cell ... Shigematsu H, Gazdar AF (January 2006). "Somatic mutations of epidermal growth factor receptor signaling pathway in lung ... "Epidermal growth factor receptor mutations in small cell lung cancer". Clinical Cancer Research. 14 (19): 6092-6. doi:10.1158/ ...
"Heterogeneity of epidermal growth factor receptor signalling networks in glioblastoma". Nature Reviews Cancer. 15 (5): 302-310 ... "Oncogene Amplification in Growth Factor Signaling Pathways Renders Cancers Dependent on Membrane Lipid Remodeling". Cell ... "EGFR mutation-induced alternative splicing of Max contributes to growth of glycolytic tumors in brain cancer". Cell Metabolism ... including alterations in glucose and lipid metabolism that drive tumor growth, progression and drug resistance. These studies, ...
Argos is a secreted protein that is an inhibitor of the epidermal growth factor receptor (EGFR) pathway in Drosophila ... Klein DE, Nappi VM, Reeves GT, Shvartsman SY, Lemmon MA (August 2004). "Argos inhibits epidermal growth factor receptor ... Argos binds the epidermal growth factor domain of Spitz, preventing interaction between Spitz and EGFR. Argos does not directly ... receptor. EGFR inhibitor Freeman M, Klämbt C, Goodman CS, Rubin GM (June 1992). "The argos gene encodes a diffusible factor ...
Epidermal growth factor receptor kinase substrate 8 is an enzyme that in humans is encoded by the EPS8 gene. This gene encodes ... "Entrez Gene: EPS8 epidermal growth factor receptor pathway substrate 8". Offenhäuser N, Borgonovo A, Disanza A, Romano P, ... a substrate for the epidermal growth factor receptor kinase, enhances EGF-dependent mitogenic signals". EMBO J. 12 (10): 3799- ... Highly similar proteins in other organisms are involved in the transduction of signals from Ras to Rac and growth factor- ...
Epidermal growth factor receptor substrate 15 is a protein that in humans is encoded by the EPS15 gene. This gene encodes a ... "Entrez Gene: EPS15 epidermal growth factor receptor pathway substrate 15". "Salmonella infection data for Eps15". Wellcome ... "Parallel dimers and anti-parallel tetramers formed by epidermal growth factor receptor pathway substrate clone 15". J. Biol. ... The protein is present at clathrin-coated pits and is involved in receptor-mediated endocytosis of EGF. Notably, this gene is ...
Spitz is a protein in fruit flies which is the major activator of Epidermal Growth Factor Receptor (EGFR). Spitz is produced as ... Klein DE, Nappi VM, Reeves GT, Shvartsman SY, Lemmon MA (2004). "Argos inhibits epidermal growth factor receptor signalling by ... Shilo BZ (2003). "Signaling by the Drosophila epidermal growth factor receptor pathway during development". Experimental Cell ... There it associates with a cargo receptor called Star and is trafficked to the Golgi. In the Golgi, Spitz is cleaved by a ...
Epidermal growth factor receptor (EGFR) is constitutively bound to TLR9. It can be activated by CpG Oligodeoxynucleotides such ... Toll-like receptor 9 is a protein that in humans is encoded by the TLR9 gene. TLR9 has also been designated as CD289 (cluster ... TLR9 also controls the release of IgA and IFN-a in SLE, and loss of the receptor leads to higher levels of both molecules. In ... Omiya S, Omori Y, Taneike M, Protti A, Yamaguchi O, Akira S, Shah AM, Nishida K, Otsu K (December 2016). "Toll-like receptor 9 ...
Among the overexpressed targets are members of the epidermal growth factor receptor (EGFR) family, transmembrane proteins with ... "Epidermal growth factor receptor inhibition strategies in oncology". Endocrine-Related Cancer. 11 (4): 689-708. doi:10.1677/erc ... "Assessment of epidermal growth factor receptor (EGFR) expression in primary colorectal carcinomas and their related metastases ... Such hormone receptors can be detected by immunohistochemistry.[13] Imatinib, an intracellualar tyrosine kinase inhibitor, was ...
Epidermal growth factor receptor (EGFR) is another validated target in NSCLC. Additionally, the T790M "gatekeeper" mutation is ... Brigatinib acts as both an anaplastic lymphoma kinase (ALK) and epidermal growth factor receptor (EGFR) inhibitor. Brigatinib ...
Homologous desensitization also occurs with cytokine and other types of receptors, such as those of the epidermal growth factor ... "Desensitization by different strategies of epidermal growth factor receptor and ErbB4". Journal of Pharmacological Sciences. ... see Adrenergic receptorreceptors]. β-Blockade and direct inhibition of GRK2 restores β-adrenergic receptor signaling and has ... It commonly occurs with G protein-coupled receptors where it is mediated by the G protein-coupled receptor kinases (GRK) and ...
"Hrs interacts with sorting nexin 1 and regulates degradation of epidermal growth factor receptor". J. Biol. Chem. 276 (10): ... "Tyrosine phosphorylation mapping of the epidermal growth factor receptor signaling pathway". J. Biol. Chem. 277 (2): 1031-9. ... Hepatocyte growth factor-regulated tyrosine kinase substrate is an enzyme that in humans is encoded by the HGS gene. HGS (gene ... PDBe-KB provides an overview of all the structure information available in the PDB for Human Hepatocyte growth factor-regulated ...
"Time-resolved mass spectrometry of tyrosine phosphorylation sites in the epidermal growth factor receptor signaling network ... "Tyrosine phosphorylation mapping of the epidermal growth factor receptor signaling pathway". The Journal of Biological ... by mass spectrometry and its involvement in growth factor and cytokine receptor signaling pathways". The Journal of Biological ... HGS/HRS (hepatocyte growth factor-regulated tyrosine kinase substrate) has been found to bind and counteract the function of ...
"Tyrosine phosphorylation mapping of the epidermal growth factor receptor signaling pathway". The Journal of Biological ... by mass spectrometry and its involvement in growth factor and cytokine receptor signaling pathways". The Journal of Biological ... an adaptor protein involved in the downstream signaling of cytokine receptors, both of which contain a SH3 domain and the ...
"Signalling by the type 1 insulin-like growth factor receptor: interplay with the epidermal growth factor receptor". Growth ... "Epidermal growth factor induces rapid, reversible aggregation of the purified epidermal growth factor receptor". Biochemistry. ... The epidermal growth factor receptor is a member of the ErbB family of receptors, a subfamily of four closely related receptor ... "Bi-directional signaling between gastrointestinal peptide hormone receptors and epidermal growth factor receptor". Growth ...
Epidermal growth factor receptor (EGFR) inhibitor. Additional Keywords : COLORECTAL CANCER, Epidermal growth factor receptor ( ... Pharmacological Actions : Epidermal growth factor receptor (EGFR) inhibitor, NF-kappaB Inhibitor, Tumor Necrosis Factor (TNF) ... 59 Abstracts with Epidermal growth factor receptor (EGFR) inhibitor Research. Filter by Study Type. Animal Study. ... Pharmacological Actions : Epidermal growth factor receptor (EGFR) inhibitor. Additional Keywords : Chemotherapeutic Synergy: ...
Effective Inhibition of the Epidermal Growth Factor/Epidermal Growth Factor Receptor Binding by Anti-Epidermal Growth Factor ... Epidermal growth factor (EGF), transforming growth factor alpha (TGF-alpha), and amphiregulin are structurally and functionally ... Molecular cloning and expression of an additional epidermal growth factor receptor-related gene. G D Plowman, G S Whitney, M G ... Role of extracellular subdomains of p185c-neu and the epidermal growth factor receptor in ligand-independent association and ...
Somatic mutations of epidermal growth factor receptor signaling pathway in lung cancers.. Shigematsu H1, Gazdar AF. ... Somatic mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene in lung cancers have ... Epidemiological studies to identify possible carcinogenic factor(s) affecting different subpopulations are also of interest. In ... it is not the sole factor, and evidence is accumulating that EGFR gene amplification, other members of the EGFR family (HER2, ...
Epidermal growth factor receptor (EGFR) content was determined by a radioligand receptor assay in 140 primary laryngeal ... Prognostic significance of epidermal growth factor receptor in laryngeal squamous cell carcinoma.. Maurizi M1, Almadori G, ...
The author discusses three new studies in PLoS Medicine that shed light on the mechanisms involved in apoptosis triggered by EGFR kinase inhibitors.
Copy of Epidermal Growth Factor Receptor (EGFR). No description by Brendan Vonick. on 4 December 2012 ...
... growth factor receptors, or elements of growth factor signal-transduction pathways. Overexpression ... understanding of the mechanism of malignant transformation has come the knowledge that oncogene products are frequently growth ... Thefamily consists of epidermal growth factor receptor (EGFR), HER2, HER3, andHER4, and at least 10 ligands that bind and ... growth factor receptors, or elements of growth factor signal-transduction pathways. Overexpression ...
Epidermal growth factor receptor (EGFR), a tyrosine kinase receptor of the ErbB family, and the biological receptor of EGF and ... J. R. Grandis and D. J. Tweardy, "Elevated levels of transforming growth factor α and epidermal growth factor receptor ... "Asynchronous modulation of transforming growth factor α and epidermal growth factor receptor protein expression in progression ... Epidermal Growth Factor Receptor Protein: A Biological Marker for Oral Precancer and Cancer. Ashish Mahendra,1 Balasundari ...
Involved in the internalization of ligand-inducible receptors of the receptor tyrosine kinase (RTK) type, in particular EGFR. ... Involved in cell growth regulation. May be involved in the regulation of mitogenic signals and control of cell proliferation. ... Involved in endocytosis of integrin beta-1 (ITGB1) and transferrin receptor (TFR); internalization of ITGB1 as DAB2-dependent ...
Why do cancer cells become "addicted" to oncogenic epidermal growth factor receptor? PLoS Med. 2007 Oct;4(10):1620-2. doi: ...
... and its ligands have been long recognized as centrally involved in the growth and repair process of epithelia, as well as in ... The epidermal growth factor receptor (EGFR) and its ligands have been long recognized as centrally involved in the growth and ... Pastore S, Mascia F, Mariani V, Girolomoni G (2002) Epidermal growth factor receptor ligands and tumor necrosis factor-alpha ... Mendelsohn J, Baselga J (2006) Epidermal growth factor receptor targeting in cancer. Semin Oncol 33:369-385PubMedGoogle Scholar ...
One of the most common oncogenic drivers for this malignancy is the epidermal... ... Epidermal growth factor receptor variant III renders glioma cancer cells less differentiated by JAGGED1. ... One of the most common oncogenic drivers for this malignancy is the epidermal growth factor receptor variant III (EGFRvIII), ... Epidermal growth factor receptor and Ink4a/Arf: convergent mechanisms governing terminal differentiation and transformation ...
ERBB; ERBB1; Erb-B2 receptor tyrosine kinase 1; Erythroblastic leukemia viral (V-Erb-B) oncogene homolog (Avian); HER1; Proto- ... oncogene C-ErbB-1; Receptor tyrosine-protein kinase ErbB-1 The... ... Heparin-binding epidermal growth factor-like growth factor (HB- ... The epidermal growth factor receptor (EGFR, also known as ErbB1) is the first of four members of the ErbB lineage of receptor ... A mutation in the epidermal growth factor receptor in waved-2 mice has a profound effect on receptor biochemistry that results ...
Binding of epidermal growth factor (EGF) to its receptor leads to receptor dimerization, assembly of protein complexes, and ... Regulation of Epidermal Growth Factor Receptor Trafficking by Lysine Deacetylase HDAC6 Message Subject. (Your Name) has ... Regulation of Epidermal Growth Factor Receptor Trafficking by Lysine Deacetylase HDAC6. By Yonathan Lissanu Deribe, Philipp ... Regulation of Epidermal Growth Factor Receptor Trafficking by Lysine Deacetylase HDAC6. By Yonathan Lissanu Deribe, Philipp ...
epidermal growth factor receptor. News tagged with epidermal growth factor receptor. * Date 6 hours 12 hours 1 day 3 days all ... with epidermal growth factor receptor ... ...
Close, J. L., Liu, J., Gumuscu, B. and Reh, T. A. (2006), Epidermal growth factor receptor expression regulates proliferation ... Epidermal growth factor receptor expression regulates proliferation in the postnatal rat retina. ...
Recombinant immunotoxins are therapeutic molecules consisting of an antibody or receptor ligand joined to a protein cytotoxin, ... combining the specific targeting of a cancer-expressed receptor with the potent cell killing of cytotoxic enzymes. Over the ... Many epithelial cancers rely on enhanced expression of the epidermal growth factor receptor (EGFR) to drive proliferation and ... Many epithelial cancers rely on enhanced expression of the epidermal growth factor receptor (EGFR) to drive proliferation and ...
... patients with epidermal growth factor receptor (EGFR) mutations. Clinical samples were tested for EGFR mutations by peptide ... A Cox proportional hazards model indicated that negative EGFR mutation was a secondary prognostic factor (hazards ratio: 2.259 ... Gefitinib is an orally active epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that competes with ATP for the ... Pao W, Miller VA (2005) Epidermal growth factor receptor mutations, small-molecule kinase inhibitors, and non-small-cell lung ...
Detection of the extracellular domain of the epidermal growth factor receptor (EGFR ECD) in serum has been suggested as a ... Epidermal growth factor receptor-dependent mechanisms have been implicated in growth signal transduction pathways that ... Epidermal growth factor receptor-dependent mechanisms have been implicated in growth signal transduction pathways that ... Detection of the extracellular domain of the epidermal growth factor receptor (EGFR ECD) in serum has been suggested as a ...
... of the epidermal growth factor receptor (EGFr) in the serum of asbestosis patients was examined and the role of EGFr over ... The detection of increased amounts of the extracellular domain of the epidermal growth factor receptor in serum during ... of the epidermal growth factor receptor (EGFr) in the serum of asbestosis patients was examined and the role of EGFr over ...
... F. ... F. Meriggi and A. Zaniboni, "Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors for Elderly Patients with Advanced Non ...
Epidermal growth factor receptor su.... Epidermal growth factor receptor substrate 15-like 1 (Epidermal growth factor receptor ... Epidermal growth factor receptor substrate 15-like 1Imported. ,p>Information which has been imported from another database ... tr,A0A1D5RLS1,A0A1D5RLS1_MOUSE Epidermal growth factor receptor substrate 15-like 1 OS=Mus musculus OX=10090 GN=Eps15l1 PE=1 SV ... Epidermal growth factor receptor substrate 15-like 1. CRIGR. 915. Epidermal growth factor receptor pathway substrate 15 like 1 ...
Epidermal growth factor (EGF) receptor gene transcription. Requirement for Sp1 and an EGF receptor-specific factor KAGEYAMA R ... Expression of epidermal growth factor, transforming growth factor alpha and their receptor in gastro-oesophageal diseases ... Human epidermal growth factor receptor DNA sequence and aberrant expression of the amplified gene in A 431 epidermal carcinoma ... An immunohistological study of epidermal growth factor receptor and neu receptor expression in proliferative glomerulonephritis ...
Mutations of the Epidermal Growth Factor Receptor Gene in Lung Cancer. Takayuki Kosaka, Yasushi Yatabe, Hideki Endoh, Hiroyuki ... Mutations of the Epidermal Growth Factor Receptor Gene in Lung Cancer. Takayuki Kosaka, Yasushi Yatabe, Hideki Endoh, Hiroyuki ... frequently overexpresses receptors of the erbB family including the epidermal growth factor receptor (EGFR) encoded by erbB-1 ( ... Mutations of the Epidermal Growth Factor Receptor Gene in Lung Cancer Message Subject (Your Name) has forwarded a page to you ...
... epidermal growth factor receptor explanation free. What is epidermal growth factor receptor? Meaning of epidermal growth factor ... receptor medical term. What does epidermal growth factor receptor mean? ... Looking for online definition of epidermal growth factor receptor in the Medical Dictionary? ... epidermal growth factor receptor. Also found in: Acronyms, Wikipedia. epidermal growth factor receptor (EGFR), [MIM*131550] ...
Dyson NJ Insulin-like growth factor receptor I mediates resistance to anti-epidermal growth factor receptor therapy in primary ... association with epidermal growth factor receptor/transforming growth factor alpha expression in head and neck squamous ... Combined inhibition of epidermal growth factor receptor (EGFR) and JAK/Stat signaling results in superior growth inhibition in ... Mendelsohn J Growth inhibition of human tumor cells in athymic mice by anti-epidermal growth factor receptor monoclonal ...
Effects of Epidermal Growth Factor Receptor Inhibitor Therapy in the Skin of Cancer Patients. The safety and scientific ... Pilot Study of the Effects of Epidermal Growth Factor Receptor (EGFR) Inhibitors on the EGFR in Skin Lesions. ... Studying samples of tissue and blood in the laboratory from patients with cancer receiving epidermal growth factor receptor ( ... No severe underlying skin disorder (e.g., toxic epidermal necrolysis or severe dermatitis) that would preclude study treatment ...
Stereotactic Radiosurgery or Other Local Ablation Then Erlotinib in Epidermal Growth Factor Receptor (EGFR). The safety and ... Mutation Who Have Previously Progressed on an Epidermal Growth Factor Receptor-tyrosine Kinase Inhibitor (EGFR-TKI). ... of Stereotactic Radiosurgery or Other Local Ablation Followed by Erlotinib for Patients With Epidermal Growth Factor Receptor( ...
Angiogenesis is essential for tumor growth and metastases. Studies in breast carcinomas suggest that microvessel quantitation ... Tumor angiogenesis in node-negative breast carcinomas--relationship with epidermal growth factor receptor, estrogen receptor, ... carcinomas to evaluate angiogenesis as a prognostic marker and assess its relationship to epidermal growth factor receptor ( ... Angiogenesis is essential for tumor growth and metastases. Studies in breast carcinomas suggest that microvessel quantitation ...
  • The epidermal growth factor receptor is a member of the ErbB family of receptors, a subfamily of four closely related receptor tyrosine kinases: EGFR (ErbB-1), HER2/neu (ErbB-2), Her 3 (ErbB-3) and Her 4 (ErbB-4). (wikipedia.org)
  • Deficient signaling of the EGFR and other receptor tyrosine kinases in humans is associated with diseases such as Alzheimer's, while over-expression is associated with the development of a wide variety of tumors. (wikipedia.org)
  • Interruption of EGFR signalling, either by blocking EGFR binding sites on the extracellular domain of the receptor or by inhibiting intracellular tyrosine kinase activity, can prevent the growth of EGFR-expressing tumours and improve the patient's condition. (wikipedia.org)
  • Epidermal growth factor receptor (EGFR) is a transmembrane protein that is activated by binding of its specific ligands, including epidermal growth factor and transforming growth factor α (TGFα) ErbB2 has no known direct activating ligand, and may be in an activated state constitutively or become active upon heterodimerization with other family members such as EGFR. (wikipedia.org)
  • Upon activation by its growth factor ligands, EGFR undergoes a transition from an inactive monomeric form to an active homodimer. (wikipedia.org)
  • citation needed] In addition to forming homodimers after ligand binding, EGFR may pair with another member of the ErbB receptor family, such as ErbB2/Her2/neu, to create an activated heterodimer. (wikipedia.org)
  • The kinase domain of EGFR can also cross-phosphorylate tyrosine residues of other receptors it is aggregated with, and can itself be activated in that manner. (wikipedia.org)
  • Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein, which is expressed in normal human tissues. (mdpi.com)
  • EGFR signaling-dependent inhibition of glioblastoma growth by ginsenoside Rh2. (greenmedinfo.com)
  • Somatic mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene in lung cancers have generated enormous interest, because they predict for sensitivity to TK inhibitors (TKIs). (nih.gov)
  • While mutational status is of great importance in determining response to TKIs, it is not the sole factor, and evidence is accumulating that EGFR gene amplification, other members of the EGFR family (HER2, HER3) and genes downstream of EGFR signaling (KRAS, BRAF), may be involved in cancer pathogenesis and the response of TKIs. (nih.gov)
  • Ligands that activate the epidermal growth factor receptor (EGFR) are synthesized as membrane-anchored precursors that appear to be proteolytically released by members of the ADAM family of metalloproteases. (pnas.org)
  • These cells express both transforming growth factor α and amphiregulin and require autocrine signaling through the EGFR for proliferation and migration. (pnas.org)
  • Metalloprotease inhibitors also reduced growth of EGF-responsive tumorigenic cell lines and were synergistic with the inhibitory effects of antagonistic EGFR antibodies. (pnas.org)
  • The epidermal growth factor receptor (EGFR) plays an important role during development. (pnas.org)
  • A variety of ligands in addition to EGF have been shown to stimulate the EGFR, including transforming growth factor α (TGFα) ( 3 ), amphiregulin (AR) ( 4 ), heparin-binding EGF ( 5 ), and betacellulin ( 6 ). (pnas.org)
  • Disruption of the EGFR gene in mice indicates that epithelial cells are most profoundly affected by receptor loss ( 1 , 2 , 11 ). (pnas.org)
  • Although these data have been interpreted to indicate that proteolytic release of EGFR ligands is important in receptor function in vivo , this conclusion is contradicted by numerous in vitro studies that appear to show that membrane-anchored growth factors are biologically active in a juxtacrine fashion ( 12 - 14 ). (pnas.org)
  • Thefamily consists of epidermal growth factor receptor (EGFR), HER2, HER3, andHER4, and at least 10 ligands that bind and activate family members. (cancernetwork.com)
  • 3]Preclinical and clinical data support the involvement of the ligands'transforming growth factor-alpha and epidermal growth factor and EGFR in theformation and progression of human cancers. (cancernetwork.com)
  • EGFR expression levels in the premalignant lesion appear to be a sensitive factor in predicting the neoplastic potential of dysplastic tissues. (hindawi.com)
  • Epidermal growth factor receptor (EGFR), a tyrosine kinase receptor of the ErbB family, and the biological receptor of EGF and TGF- α are expressed or highly expressed in a variety of solid tumors, including oral cancers. (hindawi.com)
  • Epidermal growth factor receptor (EGFR, ErbB1, and HER1)-the first receptor tyrosine kinase, was discovered by Carpenter and coworkers at Vanderbilt University, USA, in 1978 [ 3 ]. (hindawi.com)
  • Involved in the internalization of ligand-inducible receptors of the receptor tyrosine kinase (RTK) type, in particular EGFR . (rcsb.org)
  • Therefore, we studied the effects of two AGE precursors, glyoxal (GO) and methylglyoxal (MGO), on the epidermal growth factor receptor (EGFR) signaling pathway in cultured cells. (diabetesjournals.org)
  • Our investigations were mainly focused on the epidermal growth factor receptor (EGFR) because high glucose concentrations lead to abnormal epidermal growth factor (EGF) signaling ( 14 ) and diabetes reduces EGFR autophosphorylation ( 15 - 17 ). (diabetesjournals.org)
  • The EGFR belongs to a large family of tyrosine kinase receptors and is involved in the regulation of multiple cellular processes, such as cell growth, motility, differentiation, survival, and death. (diabetesjournals.org)
  • The EGFR is a 170-kDa transmembrane receptor tyrosine kinase that is shared by several growth factors, including EGF, heparin-binding EGF, transforming growth factor-α, amphiregulin, neuroregulin, β-cellulin, and epiregulin ( 18 ). (diabetesjournals.org)
  • The epidermal growth factor receptor (EGFR) and its ligands have been long recognized as centrally involved in the growth and repair process of epithelia, as well as in carcinogenesis. (springer.com)
  • The epidermal growth factor receptor (EGFR, also known as ErbB1) is the first of four members of the ErbB lineage of receptor tyrosine kinases. (springer.com)
  • EGFR is one of the most well-studied cell surface receptor. (springer.com)
  • EGFR gene amplification in breast cancer: correlation with epidermal growth factor receptor mRNA and protein expression and HER-2 status and absence of EGFR-activating mutations. (springer.com)
  • Many epithelial cancers rely on enhanced expression of the epidermal growth factor receptor (EGFR) to drive proliferation and survival pathways. (mdpi.com)
  • This study was prospectively designed to evaluate a phase II study of gefitinib for non-small-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations. (nature.com)
  • A Cox proportional hazards model indicated that negative EGFR mutation was a secondary prognostic factor (hazards ratio: 2.259, P =0.036). (nature.com)
  • Detection of the extracellular domain of the epidermal growth factor receptor (EGFR ECD) in serum has been suggested as a potential biomarker for monitoring this effect in vivo. (cdc.gov)
  • The feasibility of using an enzyme linked immunosorbent assay (ELISA) to detect the extracellular domain (ECD) of the epidermal growth factor receptor (EGFr) in the serum of asbestosis patients was examined and the role of EGFr over expression in asbestos mediated carcinogenesis was evaluated. (cdc.gov)
  • Cetuximab (Erbitux, C225) is a chimeric, monoclonal antibody directed against the extra-cellular domain of the EGFR receptor which prevents ligand binding and receptor activation. (oncolink.org)
  • We showed that two protein tyrosine kinases, the epidermal growth factor receptor (EGFR) ErbB1 and Src, bound sequentially to dsRNA-activated TLR3 and phosphorylated the two tyrosine residues. (sciencemag.org)
  • Sensitizing mutations in epidermal growth factor receptor ( EGFR ) gene ( EGFR m + ), such as exon 19 deletions and exon 21 L858R point mutations, are the most important drivers in NSCLC patients. (dovepress.com)
  • Recently it has been reported that mutations in the tyrosine kinase domain of the epidermal growth factor receptor ( EGFR ) gene occur in a subset of patients with lung cancer showing a dramatic response to EGFR tyrosine kinase inhibitors. (aacrjournals.org)
  • Panitumumab is an investigational fully human monoclonal antibody that targets the epidermal growth factor receptor (EGFr), a protein that plays an important role in cancer cell signaling. (thefreedictionary.com)
  • ERBITUX is an IgG1 monoclonal antibody (IgG1 MAb) designed to inhibit the function of a molecular structure expressed on the surface of normal and tumor cells called the epidermal growth factor receptor (EGFR, HER1, c-ErbB-1). (thefreedictionary.com)
  • IMC-11F8, currently in Phase I testing in Europe, is a fully human, high-affinity antibody that blocks ligand-dependent activation of the epidermal growth factor receptor (EGFR). (thefreedictionary.com)
  • The targets of these studies included epidermal growth factor receptor (EGFR), vascular endothelial growth factor recptor-2 (VEGFR-2), insulin-like growth factor-1 receptor (IGF-1R), platelet-derived growth factor receptor alpha (PDGFRa), FMS-like tyrosine kinase 3 receptor (FLT3), and macrophage stimulating 1 receptor (RON), among others. (thefreedictionary.com)
  • Two types of epidermal growth factor receptor ( EGFR ) mutations in exon 19 and exon 21 (ex19del and L858R) are prevalent in lung cancer patients and sensitive to targeted EGFR inhibition. (dovepress.com)
  • In the present study, Rg3 treatment to A549 human lung adenocarcinoma led to cell death via not only apoptotic pathways but also the downregulation of epidermal growth factor receptor (EGFR). (sigmaaldrich.com)
  • A mechanism by which β2-adrenergic receptors (β2ARs) stimulate signaling is transactivation of the epidermal growth factor receptor (EGFR), a cardioprotective signaling pathway that requires the formation of a β2AR-EGFR complex and the activation of Src. (ahajournals.org)
  • Epidermal growth factor receptor (EGFR) plays a central role in the progression of several human malignancies. (urotoday.com)
  • Although EGFR is a membrane receptor, it undergoes nuclear translocation, where it has a distinct signalling pathway. (urotoday.com)
  • The transported receptor is active and stimulates the nuclear EGFR pathways. (urotoday.com)
  • RATIONALE: Studying samples of tissue and blood in the laboratory from patients with cancer receiving epidermal growth factor receptor ( EGFR ) inhibitors may help doctors understand the effects of EGFR inhibitor therapy in the skin. (clinicaltrials.gov)
  • The present study revealed that PQQ induces the activation (tyrosine autophosphorylation) of epidermal growth factor receptor (EGFR) and its downstream signaling in a ligand-independent manner, leading to increased cellular proliferation in an epithelial cell line A431. (sigmaaldrich.com)
  • The interaction of the activated epidermal growth factor (EGF) receptor (EGFR) with the Src homology 2 (SH2) domain of Grb2 (growth-factor-receptor-bound protein 2) initiates signalling through Ras and mitogen-activated protein kinase. (portlandpress.com)
  • Unexpectedly, experiments showed that microtubule destabilising agents inhibited phosphorylation and activation of the EGF-receptor, and that a tyrosine phosphatase inhibitor, sodium orthovanadate, could reverse the EGFR dephosphorylation. (diva-portal.org)
  • McEneaney V, Harvey BJ, Thomas W: Aldosterone rapidly activates protein kinase D via a mineralocorticoid receptor/EGFR trans-activation pathway in the M1 kidney CCD cell line. (hmdb.ca)
  • Xia W, Liu LH, Ho P, Spector NL: Truncated ErbB2 receptor (p95ErbB2) is regulated by heregulin through heterodimer formation with ErbB3 yet remains sensitive to the dual EGFR/ErbB2 kinase inhibitor GW572016. (hmdb.ca)
  • This study seeks to determine whether the addition of ABT-414 to concomitant radiotherapy and temozolomide (TMZ) followed by combination of ABT-414 with adjuvant TMZ prolongs overall survival (OS) among participants with newly diagnosed glioblastoma (GBM) with epidermal growth factor receptor (EGFR) amplification. (clinicaltrials.gov)
  • Here, we show that Mediator's dissociable cyclin dependent kinase 8 (CDK8) module (CKM), consisting of cdk-8 , cic-1 /Cyclin C , mdt-12 / dpy-22 , and mdt-13 / let-19 , is required to inhibit ectopic vulval cell fates downstream of the epidermal growth factor receptor (EGFR)-Ras-extracellular signal-regulated kinase (ERK) pathway. (genetics.org)
  • The effect of changing the ganglioside composition of Chinese hamster ovary K1 cells on the function of the epidermal growth factor receptor (EGFr) was examined by studying the signalling pathway generated after the binding of epidermal growth factor (EGF) both in cells depleted of glycosphingolipids by inhibiting glucosylceramide synthase activity and in cell lines expressing different gangliosides as the result of stable transfection of appropriate ganglioside glycosyltransferases. (biochemj.org)
  • We hypothesized that the GLP-1R could activate PI 3-kinase and promote β-cell proliferation through transactivation of the epidermal growth factor (EGF) receptor (EGFR), an event possibly linked to GPCRs via activation of c-Src and the production of putative endogenous EGF-like ligands. (diabetesjournals.org)
  • Epidermal growth factor receptor (EGFR) is an intriguing target in high-grade gliomas because it is frequently overexpressed due to amplification of the EGFR gene. (aacrjournals.org)
  • Gefitinib and erlotinib act as ATP mimetic agents, binding to the cytoplasmic ATP pocket domain and blocking receptor phosphorylations and, thereby, EGFR-mediated activation of downstream pathways. (aacrjournals.org)
  • Retrospective correlative analyses generated a plethora of putative predictive factors of activity of EGFR tyrosine kinase inhibitors. (aacrjournals.org)
  • Epidermal growth factor receptor (EGFR) amplification and overexpression, present in ∼50% of glioblastomas, are associated with a poor prognosis, especially when occurring in younger patients ( 5 , 6 ). (aacrjournals.org)
  • Frequently, in the context of gene amplification, the EGFR gene presents structural rearrangements and some mutations, the most common being EGFRvIII ( 9 , 10 ), characterized by the lack of a portion in the extracellular receptor domain. (aacrjournals.org)
  • Sequencing of the EGFR receptor identified mutations in the tyrosine kinase pocket that were associated with both tyrosine kinase inhibitor response and prolonged survival ( 20 - 22 ). (aacrjournals.org)
  • Because an epidermal growth factor receptor (EGFR) cascade induces MUC5AC mucin in airways, and because EGFR is up-regulated in asthmatic airways, we examined the effect of eosinophils on MUC5AC mucin production in NCI-H292 cells (a human airway epithelial cell line that produces mucins). (jimmunol.org)
  • Mucin production in airways is induced by an epidermal growth factor receptor (EGFR) 3 cascade ( 13 ). (jimmunol.org)
  • Specific activating mutations within the epidermal growth factor receptor ( EGFR ) identify a subset of non-small cell lung cancers with dramatic sensitivity to the specific tyrosine kinase inhibitors (TKI), gefitinib and erlotinib. (aacrjournals.org)
  • Somatic mutations in epidermal growth factor receptor ( EGFR ) seem to define a specific subset of non-small cell lung cancers (NSCLC), ∼10% of cases, which are most commonly adenocarcinomas and bronchoalveolar carcinomas arising in nonsmokers, with an increased prevalence in women and individuals of Asian ethnicity ( 1 - 4 ). (aacrjournals.org)
  • Most clinical studies have shown that NSCLC with rapid and dramatic responses to these tyrosine kinase inhibitors (TKI) harbor EGFR mutations, although long-term survival in TKI-treated patients may be affected by additional factors, including EGFR amplification, expression levels, and possibly other molecular markers ( 1 - 3 , 7 , 10 - 24 ). (aacrjournals.org)
  • This protocol describes the labeling of epidermal growth factor receptor (EGFR) on COS7 fibroblast cells, and subsequent correlative light- and electron microscopy of whole cells in hydrated state. (jove.com)
  • This protocol describes the labeling of epidermal growth factor receptor (EGFR) on COS7 fibroblast cells, and subsequent correlative fluorescence microscopy and environmental scanning electron microscopy (ESEM) of whole cells in hydrated state. (jove.com)
  • Fluorescent quantum dots (QDs) were coupled to EGFR via a two-step labeling protocol, providing an efficient and specific protein labeling, while avoiding label-induced clustering of the receptor. (jove.com)
  • To understand the dynamic operation of signaling cascades, we have developed a method enabling the simultaneous quantification of tyrosine phosphorylation of specific residues on dozens of key proteins in a time-resolved manner, downstream of epidermal growth factor receptor (EGFR) activation. (mcponline.org)
  • Cell signaling downstream of receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR), 1 comprises an interconnected network of pathways associated with various regulatory processes. (mcponline.org)
  • In the particular case of EGFR, ligand binding activates the receptor and dimerization results in autophosphorylation of selected tyrosine sites in the C-terminal region ( 1 ). (mcponline.org)
  • Indeed, because dysregulation of EGFR-activated pathways, often a consequence of receptor overexpression or mutation, has been shown to be correlated with many types of cancer, one promising step toward identifying mechanisms underlying tumorigenesis associated with aberrant EGFR signaling would be to generate a quantitative comparison of a broad variety of specific cellular signaling events downstream of this RTK under multiple biological cell states. (mcponline.org)
  • The epidermal growth factor receptor (EGFR) is a widely expressed Ag that is successfully targeted in tumor patients by mAbs or tyrosine kinase inhibitors. (jimmunol.org)
  • Molecular inhibition of epidermal growth factor receptor (EGFR/HER1) signaling is under active investigation as a promising cancer treatment strategy. (unboundmedicine.com)
  • We examined the potency of EGFR inhibition achieved by combining anti-EGFR monoclonal antibody and tyrosine kinase inhibitor, which target extracellular and intracellular domains of the receptor, respectively. (unboundmedicine.com)
  • Tumor overexpression of epidermal growth factor receptor (EGFR) correlates to therapeutic response in select patient populations. (rsc.org)
  • AbstractBackground.Postprogression repeat biopsies are critical in caring for patients with lung cancer with epidermal growth factor receptor (EGFR) mutations. (medworm.com)
  • A significant functional role for epidermal growth factor receptor (EGFR) in the suprachiasmatic nucleus is suggested by recent findings that epidermal growth factor receptor and its ligand transforming growth factor-α are highly expressed in the suprachiasmatic nucleus. (ovid.com)
  • It has also been reported that epidermal growth factor receptor (EGFR) is necessary for HCMV-mediated signaling and entry (X. Wang, S. M. Huong, M. L. Chiu, N. Raab-Traub, and E. E. Huang, Nature 424:456-461, 2003). (asm.org)
  • Integrins are known to signal synergistically with growth factor receptors, and this coordination was recently reported for EGFR and β3 integrins in the context of HCMV entry (X. Wang, D. Y. Huang, S. M. Huong, and E. S. Huang, Nat. (asm.org)
  • These results suggest that specific integrin heterodimers either act alone as the primary entry receptors or interact in conjunction with an additional receptor(s), other than EGFR, to facilitate virus entry. (asm.org)
  • Signaling through the epidermal growth factor receptor (EGFR) has been shown to result in NF-κB activation. (aacrjournals.org)
  • In 2009, molecular target therapy such as epidermal growth factor receptor (EGFR) inhibitors was recognized as a potential treatment for certain types of lung cancer [ 1 , 2 ]. (medsci.org)
  • Classic activating mutations in the form of deletions in exon 19 or a missense mutation L858R in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) predict dramatic responses to EGFR tyrosine kinase inhibitors such as gefitinib and erlotinib. (ovid.com)
  • The epidermal growth factor receptor (EGFR)/HER‑2 specific small molecule inhibitor, lapatinib (LAP), was used to select the drug resistant phenotype. (spandidos-publications.com)
  • Phosphorylation of tyrosine residues on the epidermal growth factor (EGF) receptor (EGFr) is an important early event in signal transduction, leading to cell replication for major human carcinomas. (aspetjournals.org)
  • Inhibition of EGFr phosphotyrosine in an ex vivo assay format effectively estimates the potency and degree of inhibition of EGFr-dependent human LICR-LON-HN5 head and neck carcinoma tumor growth. (aspetjournals.org)
  • We showed previously that LPA decreases epidermal growth factor receptor (EGFR) binding rapidly in BEAS-2B airway epithelial cells, and this decrease is sustained to at least 18 h. (aspetjournals.org)
  • Provided are anti-epidermal growth factor receptor (EGFR) antibodies, aglycosylated CDR-H2 anti-EGFR antibodies, and antigen binding fragments thereof. (patents.com)
  • Background Epidermal growth factor receptor (EGFR) gene mutation at the kinase domain and EGFR gene amplification are reported to be predictors of the response to EGFR tyrosine kinase inhibitors in lung cancer cases. (bmj.com)
  • To determine the expression of nucleostemin (NS), epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) mRNA in human esophageal squamous cell carcinoma (ESCC) tissues and their association in a human ESCC cell line. (ebscohost.com)
  • Background: EGFR is involved in the epidermal growth factors pathway that regulates cellular processes and is associated with the development of many types of cancer including colorectal cancer. (ebscohost.com)
  • To evaluate the clinical significance of mRNA expression of cytokeratin 19 (CK19), epidermal growth factor receptor (EGFR) and lung-specific X protein (LUNX), a total of 42 patients who were diagnosed with non-small cell lung cancer (NSCLC) by pathology were studied retrospectively. (ebscohost.com)
  • The requisite migration and proliferation of the fibroblasts is promoted by growth factors including those that activate the epidermal growth factor receptor (EGFR). (rupress.org)
  • We report here that IP-10 inhibited EGF- and heparin-binding EGF-like growth factor-induced Hs68 human dermal fibroblast motility in a dose-dependent manner (to 52% and 44%, respectively, at 50 ng/ml IP-10), whereas IP-10 had no effect on either basal or EGFR-mediated mitogenesis (96 ± 15% at 50 ng/ml). (rupress.org)
  • To define the molecular basis of this negative transmodulation of EGFR signaling, we found that IP-10 did not adversely impact receptor or immediate postreceptor signaling as determined by tyrosyl phosphorylation of EGFR and two major downstream effectors phospholipase C-γ and erk mitogen-activated protein kinases. (rupress.org)
  • All these attributes point to EGFR factors promoting wound healing. (rupress.org)
  • We analyzed the binding site(s) for Grb2 on the epidermal growth factor (EGF) receptor (EGFR), using cell lines overexpressing EGFRs containing various point and deletion mutations in the carboxy-terminal tail. (asm.org)
  • In the present paper, we summarize our recent study showing that integrin-dependent adhesion triggers ligand-independent EGFR (epidermal growth factor receptor) activation to transduce downstream signalling. (biochemsoctrans.org)
  • In this paper, we report the establishment of a system to specifically activate epidermal growth factor (EGF) receptor (EGFR) when it endocytoses into endosomes. (asm.org)
  • The epidermal growth factor receptor (EGFR) is activated by dimerization, but activation also generates higher-order multimers, whose nature and function are poorly understood. (berkeley.edu)
  • The aim of the present study was to investigate the mutation rate of the epidermal growth factor receptor (EGFR) in non-small cell lung cancer (NSCLC) patients and to apply logistic regression analysis to investigate the factors associated with EGFR gene mutation to provide data for the treatment of NSCLC. (ebscohost.com)
  • The discovery of epidermal growth factor receptor (EGFR) mutations in. (ebscohost.com)
  • Mutations in the epidermal growth factor receptor (EGFR) gene are commonly observed in non-small-cell lung cancer (NSCLC), particularly in tumors of adenocarcinoma (ADC) histology (NSCLC/ADC). (ebscohost.com)
  • Epidermal growth factor receptor (EGFR) mutations are the strongest response predictors to EGFR tyrosine kinase inhibitors (TKI) therapy, but knowledge of the EGFR mutation frequency on lung adenocarcinoma is still limited to retrospective studies. (ebscohost.com)
  • Purpose: Although epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have become key therapeutic agents for non-small cell lung cancer (NSCLC) patients with EGFR mutation, little is known about the efficacy of EGFR-TKIs according to different treatment timings. (ebscohost.com)
  • Epidermal growth factor (EGF) is a protein that stimulates cell growth and differentiation by binding to its receptor, EGFR. (wikipedia.org)
  • citation needed] Polypeptide growth factors include: EGF acts by binding with high affinity to epidermal growth factor receptor (EGFR) on the cell surface. (wikipedia.org)
  • Epidermal growth factor receptor inhibition strategies in pancreatic cancer: past, present and the future. (thefreedictionary.com)
  • A small molecule called PD 153035 inhibited the epidermal growth factor (EGF) receptor tyrosine kinase with a 5-pM inhibition constant. (sciencemag.org)
  • PD 153035 demonstrates an increase in potency over that of other tyrosine kinase inhibitors of four to five orders of magnitude for inhibition of isolated EGF receptor tyrosine kinase and three to four orders of magnitude for inhibition of cellular phosphorylation. (sciencemag.org)
  • Sakaguchi M, Kuroda Y, Hirose M: The antiproliferative effect of lidocaine on human tongue cancer cells with inhibition of the activity of epidermal growth factor receptor. (hmdb.ca)
  • The combination of cetuximab plus gefitinib or erlotinib enhanced growth inhibition over that observed with either agent alone. (unboundmedicine.com)
  • A, Under myelin‐associated inhibition, protein kinase C‐, Src‐Pyk2‐induced epidermal growth factor receptor‐extracellular‐regulated kinase signaling pathway was activated, resulting in TRIM32 inhibition and neuronal differentiation of neural stem cells inhibition. (medworm.com)
  • Go6976 and PP2 were used to inhibit PKC and Src‐Pyk2, respectively, which resulted in epidermal growth factor receptor phosphorylation inhibition indirectly. (medworm.com)
  • Epidermal growth factor receptor‐extracellular‐regulated kinase blockade can promote TRIM32 expression and antagonize myelin inhibition on neuronal differentiation of neural stem cells. (medworm.com)
  • Figure 1 Drug-dependent cell growth inhibition. (wjgnet.com)
  • Substantial growth inhibition of human tumor xenografts was achieved with p.o. doses of the compound (ED 50 = 10 mg/kg q.d. for 20 days). (aspetjournals.org)
  • When EGF receptor kinase inhibitor AG1478 was added, re-epithelialization was completely inhibited, while inhibition of re-epithelialization by MAP kinase kinase inhibitor PD08059 was mild. (arvojournals.org)
  • The biological effects of salivary EGF include healing of oral and gastroesophageal ulcers, inhibition of gastric acid secretion, stimulation of DNA synthesis as well as mucosal protection from intraluminal injurious factors such as gastric acid, bile acids, pepsin, and trypsin and to physical, chemical and bacterial agents. (wikipedia.org)
  • Bertics PJ, Weber W, Cochet C and Gill GN (1985) Regulation of the epidermal growth factor receptor by phosphorylation. (springer.com)
  • Bertics PJ and Gill GN (1985) Self-phosphorylation enhances the protein-tyrosine kinase activity of the epidermal growth factor receptor. (springer.com)
  • Unlike other TLRs, TLR3 requires phosphorylation of two specific tyrosine residues in its cytoplasmic domain to recruit the adaptor protein TRIF (Toll-interleukin-1 receptor domain-containing adaptor protein inducing interferon-β) and initiate the antiviral response. (sciencemag.org)
  • TLR3-mediated antiviral responses require phosphorylation of TLR3 by a growth factor receptor and a nonreceptor tyrosine kinase. (sciencemag.org)
  • Ligand binding to cell surface receptors initiates a cascade of signaling events regulated by dynamic phosphorylation events on a multitude of pathway proteins. (mcponline.org)
  • We also demonstrated that NO-mediated nitration of the EGF receptor caused a decrease in its phosphorylation, thus preventing regular proliferation signaling through the ERK/MAPK pathway. (frontiersin.org)
  • Ang II induces phosphorylation of the epidermal growth factor (EGF) receptor (EGF-R), which serves as a scaffold for various signaling molecules. (ahajournals.org)
  • Abstract -Angiotensin II (Ang II) is a vasoactive hormone with critical roles in vascular smooth muscle cell growth, an important feature of hypertension and atherosclerosis. (ahajournals.org)
  • Although the identities of all of the proteases involved have not been definitively established, recent data suggests that the release of TGFα involves TACE, a member of the ADAM family of metalloproteases, which originally was identified as being responsible for the release of tumor necrosis factor α ( 8 - 10 ). (pnas.org)
  • Moasser MM, Basso A, Averbuch SD, Rosen N: The tyrosine kinase inhibitor ZD1839 ("Iressa") inhibits HER2-driven signaling and suppresses the growth of HER2-overexpressing tumor cells. (hmdb.ca)
  • The present study will investigate the feasibility and clinical value of using circulating tumor DNA as selection for anti-epidermal growth factor receptor treatment for metastatic colorectal cancer. (centerwatch.com)
  • Following establishment of cetuximab-resistant cell lines, we observed that gefitinib or erlotinib retained the capacity to inhibit growth of lung and H&N tumor cells that were highly resistant to cetuximab. (unboundmedicine.com)
  • We analyzed pretreatment MR imaging scans from 147 consecutive patients with newly diagnosed glioblastoma and correlated MR imaging features with tumor epidermal growth factor receptor amplification status. (ajnr.org)
  • Integrating mechanistic studies with analyses of tumor tissue from patients treated in clinical trials, Mischel and colleagues discovered signaling, transcriptional, and metabolic co-dependencies that are downstream consequences of oncogene amplification, including alterations in glucose and lipid metabolism that drive tumor growth, progression and drug resistance. (wikipedia.org)
  • Overexpression of ASAP1 increased EGF receptor recycling, whereas ASAP1 containing mutated PxxxPR motif failed to promote this event. (diva-portal.org)
  • Somatic mutations of epidermal growth factor receptor signaling pathway in lung cancers. (nih.gov)
  • Dimerization of the receptor results in the autophosphorylation of tyrosine residues within the cytoplasmic domain of the receptors and initiates a variety of signaling pathways leading to cell proliferation and tumorigenesis. (hindawi.com)
  • Homo- or heterodimerization results in the autophosphorylation of tyrosine residues within the cytoplasmic domain of the receptors and initiates a variety of signaling pathways, principally the mitogen-activated protein kinase (MAPK), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), and protein kinase C (PKC) resulting in cell proliferation, survival, differentiation, angiogenesis, and invasion. (hindawi.com)
  • It was hypothesized that AGEs alter cell signaling by interfering with growth factor receptors. (diabetesjournals.org)
  • Because altered response to growth factor may be implicated in the pathogenesis of diabetic ulcers ( 12 ) and vascular diseases associated with diabetes ( 13 ), we hypothesized that GO and MGO may modify growth factor receptors and alter the subsequent signaling. (diabetesjournals.org)
  • Canguilhem B, Pradines A, Baudouin C, Boby C, Lajoie-Mazenc I, Charveron M, Favre G (2005) RhoB protects human keratinocytes from UVB-induced apoptosis through epidermal growth factor receptor signaling. (springer.com)
  • Spatial regulation of epidermal growth factor receptor signaling by endocytosis. (springer.com)
  • Grana TM, Sartor CI, Cox AD: Epidermal growth factor receptor autocrine signaling in RIE-1 cells transformed by the Ras oncogene enhances radiation resistance. (hmdb.ca)
  • Transcription factors and coregulators are important effectors of signaling pathway output, as they regulate downstream gene programs. (genetics.org)
  • However, the exact mechanism by which the GLP-1 receptor (GLP-1R), a member of the G protein-coupled receptor (GPCR) superfamily, activates the PI 3-kinase signaling pathway to promote β-cell growth remains unknown. (diabetesjournals.org)
  • Furthermore, the increased release of NO by activated iNOS +/+ microglial cells decreased the activation of the ERK/MAPK signaling pathway, which was concomitant with an enhanced nitration of the EGF receptor. (frontiersin.org)
  • Regarding the antiproliferative effect of NO, we found that NOC-18 caused the impairment of signaling through the ERK/MAPK pathway, which may be related to increased nitration of the EGF receptor in NSC. (frontiersin.org)
  • Proposed model depicting the epidermal growth factor receptor ‐extracellular‐regulated kinase‐TRIM32 signaling axis in the regulation of neuronal differentiation. (medworm.com)
  • These findings emphasize the importance of ROS in specific Ang II-stimulated growth-related signaling pathways and suggest that redox-sensitive EGF-R transactivation may be a potential target for antioxidant therapy in vascular disease. (ahajournals.org)
  • Portions of this work were published as part of a dissertation: Kassel KM (2007) Regulation of epidermal growth factor receptors and mitogenic signaling by lysophosphatidic acid and β 2 adrenergic receptors in airway cells. (aspetjournals.org)
  • NCAM exerts these functions by mediating cell-cell and cell-matrix adhesions and by activating intracellular signaling cascades, in which activation of the fibroblast growth factor receptor plays a prominent role. (springer.com)
  • Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers. (springer.com)
  • The mutations are clustered around the ATP-binding pocket of the receptor, and ∼80% consist of either a single missense mutation (L858R) or nested in-frame deletions (delE746-A750 and variants thereof). (aacrjournals.org)
  • The aim of the present study was to determine the prevalence of epidermal growth factor receptor mutations (EGFRmut) in the Gulf region (GR) and its correlation with demographic and clinical characteristics. (ebscohost.com)
  • Biswas R, Basu M, Sen-Majumdar A and Das M (1985) Intrapeptide autophosphorylation of the epidermal growth factor receptor: regulation of kinase catalytic function by receptor dimerization. (springer.com)
  • 3]Ligand-receptor binding results in receptor dimerization with the sameor different family member, autophosphorylation, kinase activation, and thegeneration of binding sites for downstream adaptor molecules and secondmessengers. (cancernetwork.com)
  • Both compounds prevented tyrosine autophosphorylation induced by epidermal growth factor (EGF) in a time- and dose-dependent manner as well as phospholipase Cγ1 recruitment and subsequent activation of extracellular signal-regulated kinases. (diabetesjournals.org)
  • Binding of the protein to a ligand induces receptor dimerisation and tyrosine autophosphorylation and leads to cell proliferation. (thefreedictionary.com)
  • PD 153035 rapidly suppressed autophosphorylation of the EGF receptor at low nanomolar concentrations in fibroblasts or in human epidermoid carcinoma cells and selectively blocked EGF-mediated cellular processes including mitogenesis, early gene expression, and oncogenic transformation. (sciencemag.org)
  • We found that metalloprotease inhibitors reduced cell proliferation in direct proportion to their effect on transforming growth factor α release. (pnas.org)
  • This month's installment of Clinical Trials Referral Resource is devoted to studies regarding epidermal growth factor receptor inhibitors. (cancernetwork.com)
  • Balagula Y, Garbe C, Myskowski PL, Hauschild A, Rapoport BL, Boers-Doets CB, Lacouture ME (2011) Clinical presentation and management of dermatological toxicities of epidermal growth factor receptor inhibitors. (springer.com)
  • Delbaldo C, Faivre S, Raymond E: [Epidermal growth factor inhibitors]. (hmdb.ca)
  • In recent years, small molecule inhibitors targeting tyrosine kinases, such as erlotinib (Tarceva) and gefitinib (Iressa), binding to the intracellular part of the receptor have been introduced in clinical practice. (aacrjournals.org)
  • HER1 in humans) is a transmembrane protein that is a receptor for members of the epidermal growth factor family (EGF family) of extracellular protein ligands. (wikipedia.org)
  • All four HER receptors comprise a cysteine-rich extracellular ligand binding site, a transmembrane lipophilic segment, and an intracellular domain with tyrosine kinase catalytic activity [ 2 ]. (hindawi.com)
  • Serum levels of the extracellular domain of the epidermal growth factor receptor in individuals exposed to arsenic in drinking water in Bangladesh. (cdc.gov)
  • The detection of increased amounts of the extracellular domain of the epidermal growth factor receptor in serum during carcinogenesis in asbestosis patients. (cdc.gov)
  • Nuclear transportation of exogenous epidermal growth factor receptor and androgen receptor via extracellular vesicles. (urotoday.com)
  • With the understanding of the mechanism of malignant transformation has come the knowledge that oncogene products are frequently growth factors, growth factor receptors, or elements of growth factor signal-transduction pathways. (cancernetwork.com)
  • Recent findings suggest that the cellular response to DNA damage ismarkedly impaired by deprivation of essential growth factors or by blockage ofgrowth-factor receptors, which suggests that these pathways contribute to theineffectiveness of chemotherapy and radiation. (cancernetwork.com)
  • They regulate cell growth, survival, and differentiation via multiple signal transduction pathways and participate in cellular proliferation and differentiation. (hindawi.com)
  • The HER2-HER3 heterodimer is the most potent stimulator of downstream pathways, particularly the PI3K/Akt, a master regulator of cell growth and survival. (hindawi.com)
  • Heparin-binding epidermal growth factor-like growth factor (HB-EGF) and proteolytic processing by a disintegrin and metalloproteinases (ADAM): a regulator of several pathways. (springer.com)
  • Epidermal growth factor receptor-dependent mechanisms have been implicated in growth signal transduction pathways that contribute to cancer development, including dermal carcinogenesis. (cdc.gov)
  • The results indicate that the interactions between estrogen, progesterone and epidermal growth factor receptor pathways may be considered relevant targets for the treatment of hormone-dependent breast cancers," she said. (thefreedictionary.com)
  • We propose that CIN85 functions as a scaffold molecule that binds to numerous endocytic accessory proteins, thus controlling distinct steps in trafficking of EGF receptors along the endocytic and recycling pathways. (diva-portal.org)
  • Polypeptide growth factors have been recognized as important determinants In the regulation of cellular proliferation and differentiation (for a review: Sporn and Roberts, 1988). (springer.com)
  • The proliferation and differentiation of cancer in the body are usually controlled by growth factors and their receptors on cancer cell surface. (hindawi.com)
  • Pyrroloquinoline quinone stimulates epithelial cell proliferation by activating epidermal growth factor receptor through redox cycling. (sigmaaldrich.com)
  • Finally, coculturing the prostatic cancer cell line LNCaP that lacks GLP-1 responsiveness with INS cells increased LNCaP cell proliferation in the presence of GLP-1, thus revealing that INS cells secrete a growth factor in response to GLP-1. (diabetesjournals.org)
  • We show that NO from inflammatory origin leads to a decreased function of the EGF receptor, which compromised proliferation of NSC. (frontiersin.org)
  • A, Glutamate stimulates neural stem/progenitor cell (NSPC) proliferation and enhances survival through AMPA receptor activation. (medworm.com)
  • Integrin signalling co-ordinates with signalling originating from growth factor receptors in the co-operative control of cell proliferation, survival and migration. (biochemsoctrans.org)
  • It is probable that at these sites integrins regulate adhesion and at the same time physically constrain and direct the response to soluble growth factors towards proliferation or survival stimuli. (biochemsoctrans.org)
  • We have previously reported that, in the in vitro corneal wound healing model using mouse corneal epithelial cell line, epidermal growth factor (EGF) promoted re-epithelialization of denuded area, and that the re-epithelialization did not depend on cell proliferation. (arvojournals.org)
  • Because family members can be activated by multiple ligands andligand-receptor expression determines homo/heterodimerization between receptorsas well as rate of receptor internalization and degradation, the efficiency anddiversity of signal transduction through these receptor complexes is remarkable.Activation of this family of growth-factor receptors influences cellproliferation, survival, motility, adhesion, invasion, and angiogenesis. (cancernetwork.com)
  • Targeted inactivation of the EGF and amphiregulin genes reveals distinct roles for EGF receptor ligands in mouse mammary gland development. (springer.com)
  • Activation of the receptor is important for the innate immune response in human skin. (wikipedia.org)
  • The binding of ligand to the receptor causes activation of its intrinsic tyrosine kinase activity and rapid internalization of the receptor-ligand complex into the cell. (harvard.edu)
  • The epidermal growth factor receptor (erbB1)is a dimeric membrane bound protein responsible for an array of downstream growth factor activation after ligand binding. (oncolink.org)
  • These findings imply that activation of the protein tyrosine kinase activity at the cell membrane is sufficient for the growth-enhancing effects of EGF. (sciencemag.org)
  • Cytokine receptor activation is dependent on ligand-induced receptor dimerization or oligomerization and subsequent activation of several intracellular proteins. (dissertations.se)
  • Activation of Janus kinases (Jaks) is probably the first intracellular event that occurs after receptor dimerization. (dissertations.se)
  • Activation of EGFRs by ligand also triggers rapid endocytosis of EGF-receptor complexes. (portlandpress.com)
  • Recent studies indicate that epidermal growth factor receptor activation induces behavioral and physiological effects, strengthening the notion that epidermal growth factor receptor can modulate suprachiasmatic nucleus neural function and behavior. (ovid.com)
  • A global transcriptional profiling study is performed to investigate the gene expression response to epidermal growth factor receptor activation in the suprachiasmatic nucleus. (ovid.com)
  • Tissue factor pathway inhibitor-2 (TFPI-2) is a Kunitz-type serine proteinase inhibitor that inhibits plasmin-dependent activation of several metalloproteinases. (ebscohost.com)
  • The defective barrier causes activation of keratinocytes and epidermal γδ T cells, which produce interleukin-1 family member 8 and S100A8/A9 proteins. (pubmedcentralcanada.ca)
  • Molecular basis for multimerization in the activation of the epidermal growth factor receptor. (berkeley.edu)
  • Flipped script for gefitinib: a reapproved tyrosine kinase inhibitor for first-line treatment of epidermal growth factor receptor mutation positive metastatic nonsmall cell lung cancer. (springer.com)
  • The inhibitor was specific for the EGF receptor tyrosine kinase and inhibited other purified tyrosine kinases only at micromolar or higher concentrations. (sciencemag.org)
  • Ciardiello F, Caputo R, Bianco R, Damiano V, Pomatico G, De Placido S, Bianco AR, Tortora G: Antitumor effect and potentiation of cytotoxic drugs activity in human cancer cells by ZD-1839 (Iressa), an epidermal growth factor receptor-selective tyrosine kinase inhibitor. (hmdb.ca)
  • In renal cell carcinoma (RCC) models, maximal cytotoxicity of the proteasome inhibitor bortezomib is dependent on efficient blockade of constitutive nuclear factor κB (NF-κB) activity. (aacrjournals.org)
  • Expression and methylation status of tissue factor pathway inhibitor-2 gene in non-small-cell lung cancer. (ebscohost.com)
  • Either EGF receptor kinase inhibitor AG1478 (2.5μM), MAP kinase kinase inhibitor PD08059 (20μM), PI3 kinase inhibitor LY294002 (50μM), or Wortmannin (5μM) was added to the culture and decrease of denuded area was evaluated. (arvojournals.org)
  • Antibodies for epidermal growth factor receptor 3 (her3). (google.com)
  • MX2014006735A - Antibodies for epidermal growth factor receptor 3 (her3). (google.com)
  • CIN85 associates with multiple effectors controlling intracellular trafficking of epidermal growth factor receptors. (diva-portal.org)
  • Identification of a mutant epidermal growth factor (EGF) receptor that does not undergo downregulation has provided a genetic probe to investigate the role of internalization in ligand-induced mitogenesis. (sciencemag.org)
  • Contact-inhibited cells expressing this internalization-defective receptor exhibited a normal mitogenic response at significantly lower ligand concentrations than did cells expressing wild-type receptors. (sciencemag.org)
  • The human epidermal growth factor receptor (HER) family of receptors plays a central role in the pathogenesis of several human cancers. (hindawi.com)
  • Simon N, FitzGerald D. Immunotoxin Therapies for the Treatment of Epidermal Growth Factor Receptor-Dependent Cancers. (mdpi.com)
  • Increased expression of the epidermal growth factor (EGF) receptors, HER1 and HER2 are related to poor prognosis in most cancers studied. (ebscohost.com)
  • Patterns of epidermal growth factor receptor mutation in non-small-cell lung cancers in the Gulf region. (ebscohost.com)
  • The prognostic significance of proliferating cell nuclear antigen, epidermal growth factor receptor , and mdr gene expression in colorectal cancer. (thefreedictionary.com)
  • We previously provided evidence that glucagon-like peptide 1 (GLP-1) induces pancreatic β-cell growth nonadditively with glucose in a phosphatidylinositol (PI) 3-kinase- and protein kinase C ζ-dependent manner. (diabetesjournals.org)
  • Finally, GLP-1 induces several immediate early response genes and proto-oncogenes in INS cells that are implicated in cell growth/apoptosis control, such as c- fos , c- jun , junD, and nur77 ( 15 , 16 ). (diabetesjournals.org)
  • Cetuximab: an epidermal growth factor receptor monoclonal antibody for the treatment of colorectal cancer. (thefreedictionary.com)
  • CIN85 is a multidomain adaptor protein involved in Cbl-mediated down-regulation of epidermal growth factor (EGF) receptors. (diva-portal.org)
  • The HER2 receptor is a 1255 amino acid, 185 kD transmembrane glycoprotein located at the long arm of human chromosome 17 (17q12) [ 6 ]. (hindawi.com)
  • A gene on chromosome 7p12 that encodes epidermal growth factor, a transmembrane glycoprotein of the protein kinase superfamily, which is a receptor for members of the epidermal growth factor family. (thefreedictionary.com)
  • Epidermal growth factor receptor gene amplification and expression in disseminated pediatric low-grade gliomas. (virtualtrials.com)
  • Epidermal Growth Factor Receptor Protein Expression and Gene Amplification in Normal, Hyperplastic, and Cancerous. (srce.hr)
  • The purpose of this study was to examine the potential usefulness of morphologic and diffusion MR imaging signs in the prediction of epidermal growth factor receptor gene amplification status in patients with glioblastoma. (ajnr.org)
  • Siriwardena, A.K. Epidermal Growth Factor Receptor in Pancreatic Cancer. (mdpi.com)
  • CBD can be used as a novel therapeutic option to inhibit growth and metastasis of highly aggressive breast cancer subtypes including TNBC. (greenmedinfo.com)
  • Why Do Cancer Cells Become "Addicted" to Oncogenic Epidermal Growth Factor Receptor? (plos.org)
  • The ErbB family of growth-factor receptors is well characterizedand has generated significant interest as a target for cancer therapeutics. (cancernetwork.com)
  • It is found at abnormally high levels on the surface of many types of cancer cells, so these cells may divide excessively in the presence of epidermal growth factor. (hindawi.com)
  • Busam KJ, Capodieci P, Motzer R, Kiehn T, Phelan D, Halpern AC (2001) Cutaneous side-effects in cancer patients treated with the antiepidermal growth factor receptor antibody C225. (springer.com)
  • EGF mutant receptor vIII as a molecular target in cancer therapy. (springer.com)
  • Recombinant immunotoxins are therapeutic molecules consisting of an antibody or receptor ligand joined to a protein cytotoxin, combining the specific targeting of a cancer-expressed receptor with the potent cell killing of cytotoxic enzymes. (mdpi.com)
  • Effect of Tat-645-662 on cell viability and colony growth of various human cancer and normal cell lines. (plos.org)
  • A combined approach of inhibiting both the hormones and the epidermal growth factor receptor may be beneficial for some women in treating hormone-dependent breast cancer. (thefreedictionary.com)
  • Epidermal growth factor receptor immunohistochemical reactivity in patients with American Joint Committee on Cancer Stage IV colon adenocarcinoma: implications for a standardized scoring system. (thefreedictionary.com)
  • This multicenter, randomized, adaptive Phase II/III study will evaluate the efficacy and safety of trastuzumab emtansine (T-DM1) compared to standard taxane (docetaxel or paclitaxel) treatment in participants with human epidermal growth factor receptor 2 (HER2)-positive advanced gastric cancer. (clinicaltrials.gov)
  • Purpose: We examined hospital use of the epidermal growth factor receptor assay in patients with lung cancer in the United States. (rti.org)
  • Conclusion: In 2010, only 12% of US acute-care hospitals ordered the epidermal growth factor receptor assay, suggesting that most patients with lung cancer did not have access to this test. (rti.org)
  • The management of human epidermal growth factor receptor 2 (HER2)-positive breast cancer has changed dramatically with the introduction and widespread use of HER2-targeted therapies. (hkmj.org)
  • Epidermal growth factor-related peptides and their receptors in human malignancies. (nih.gov)
  • Brogden NK, Mehalick L, Fischer CL, Wertz PW, Brogden KA (2012) The emerging role of peptides and lipids as antimicrobial epidermal barriers and modulators of local inflammation. (springer.com)
  • It is specific for EPIDERMAL GROWTH FACTOR and EGF related peptides including TRANSFORMING GROWTH FACTOR ALPHA, amphiregulin, and heparin-binding EGF-like growth factor. (harvard.edu)
  • CIN85 src homology 3 domains specifically bind to a proline-arginine (PxxxPR) motif in Cbl, and this association seems to be important for EGF receptor endocytosis. (diva-portal.org)
  • This stimulates ligand-induced dimerization, activating the intrinsic protein-tyrosine kinase activity of the receptor (see the second diagram). (wikipedia.org)
  • Human epidermal growth factor receptor 2 (HER2) is a member of the epidermal growth factor receptor family having tyrosine kinase activity. (hindawi.com)
  • HER2 is expressed in many tissues and its major role in these tissues is to facilitate excessive/uncontrolled cell growth and tumorigenesis [ 7 - 9 ]. (hindawi.com)
  • High incidence of amplification of the epidermal growth factor receptor gene in human squamous carcinoma cell lines. (nii.ac.jp)
  • Boonstra J, de Laat SW and Ponec M (1985b) Epidermal growth factor receptor expression related to differentiation capacity in normal and transformed keratinocytes. (springer.com)
  • Bulgaru AM, Mani S, Goel S, Perez-Soler R: Erlotinib (Tarceva): a promising drug targeting epidermal growth factor receptor tyrosine kinase. (hmdb.ca)
  • Here we report the cloning of another member of the human EGF receptor (HER) family of receptor tyrosine kinases, which we have named "HER3/ERRB3. (pnas.org)
  • These reagents will allow us to determine whether HER3 binds amphiregulin or other growth regulatory proteins and what role HER3 protein plays in the regulation of cell growth. (pnas.org)
  • Recently, a high expression of the two remaining receptors of the EGF system, HER3 and HER4 has been related to a favourable prognosis. (ebscohost.com)
  • Cell and molecular biology of epidermal growth factor receptor. (springer.com)
  • It has been suggested that the transcription factor nuclear factor κB (NF-κB) represents a principal molecular target of bortezomib ( 10 ). (aacrjournals.org)
  • Epidermal growth factor receptor amplification is a common molecular event in glioblastomas. (ajnr.org)
  • Epigallocatechin-3-gallate inhibits the growth and increases the apoptosis of human thyroid carcinoma cells. (greenmedinfo.com)
  • Abnormal polarization of EGF receptors and autocrine stimulation of cyst epithelial growth in human ADPKD. (springer.com)
  • Human epidermal growth factor receptor cDNA sequence and aberrant expression of the amplified gene in A431 epidermoid carcinoma cells. (springer.com)
  • Expression of the Drosophila homologue (DER) of the human epidermal growth factor (EGF) receptor has been studied during development by RNA blot hybridizations and in situ hybridizations. (biologists.org)
  • In human malignant mesothelioma biopsies, SV40 has been shown to bind and inactivate p53 and pRb, and to activate c-met, insulin growth factor (IGF)-I, and other oncogenes. (aacrjournals.org)
  • Human epidermal growth factor receptor‑2 (HER‑2) expression in the presence or absence of hormone receptors dictates HER‑2‑targeted therapy with or without endocrine therapy. (spandidos-publications.com)
  • The hybridoma antibody TL5, which precipitates the EGF receptor from the human epidermoid carcinoma cell line A431, has been shown to recognize the blood-group-A carbohydrate structure. (portlandpress.com)
  • For the majority of human carcinomas, growth factor receptors play an important role in tumorigenesis and progression to terminal disease states. (aspetjournals.org)
  • The invention relates to a novel antibody capable of binding specifically to the human c-Met receptor and/or capable of specifically inhibiting the tyrosine. (patents.com)
  • Recombinant human epidermal growth factor, sold under the brand name Heberprot-P, is used to treat diabetic foot ulcers. (wikipedia.org)
  • Novel roles of ginsenoside Rg3 in apoptosis through downregulation of epidermal growth factor receptor. (sigmaaldrich.com)
  • Toll-like receptors (TLRs) recognize specific microbial products and elicit innate immune signals to activate specific transcription factors that induce protective proteins, such as interferon. (sciencemag.org)
  • GLP-1 interaction with its specific high-affinity receptor (GLP-1R), a member of the G protein-coupled receptor (GPCR) superfamily, increases cAMP levels in several β-cell models to activate the protein kinase A signal transduction system ( 4 , 17 , 18 ). (diabetesjournals.org)
  • These co-operative effects might depend on integrin ability to activate growth factor receptors. (biochemsoctrans.org)
  • For the re-epithelialization of denuded area, PI3 kinase pathway is the main pathway of the downstream of EGF receptor. (arvojournals.org)
  • Downregulation of p57 accelerates the growth and invasion of hepatocellular carcinoma. (ebscohost.com)
  • The factor(s) that determine gefitinib sensitivity has long been an enigma. (aacrjournals.org)
  • B, Cetuximab and gefitinib can directly block epidermal growth factor receptor. (medworm.com)
  • Boonstra J, Mummery CL, Feyen A, de Hoog WJ, van der Saag PT and de Laat SW (1987) Epidermal growth factor expression during morphological differentiation of pheochromocytoma cells, induced by nerve growth factor or dibutyryl cyclic AMP. (springer.com)
  • A cell surface receptor involved in regulation of cell growth and differentiation. (harvard.edu)
  • GLP-1 increases the expression level of the β-cell-specific transcription factor pancreatic and duodenal homeobox gene-1 (PDX-1) ( 9 ), which is implicated in the regulation of the expression of insulin, GLUT2, and glucokinase genes and in β-cell differentiation ( 10 - 12 ). (diabetesjournals.org)
  • Also, we found that the mutant receptor EGFRvIII could be transported to the nucleus of other cells via EVs. (urotoday.com)
  • A mutation in the epidermal growth factor receptor in waved-2 mice has a profound effect on receptor biochemistry that results in impaired lactation. (springer.com)
  • Using cluster analysis, we observed coordinate upregulation of EGF, IL-6, macrophage inflammatory protein-1 beta and vascular endothelial growth factor. (diva-portal.org)
  • VEGFR, vascular endothelial growth factor receptor. (biochemsoctrans.org)
  • These secreted polypeptides all bind to the 170-kDa cell-surface EGF receptor, activating its intrinsic kinase activity. (pnas.org)
  • These findings suggest that amphiregulin may interact with a separate receptor in certain cell types. (pnas.org)
  • Those studies typically have used artificial systems in which the cell expressing the ligand is distinct from the cell expressing the receptor ( 12 - 14 ). (pnas.org)
  • Hyperactive receptor signalingpromotes deregulated cell growth and subsequent development of malignancy. (cancernetwork.com)
  • In India approximately 94% of oral malignancies are those of oral squamous cell carcinomas (OSCC) whose etiology is multifactorial with various intrinsic and extrinsic factors [ 2 ]. (hindawi.com)
  • The HER receptors exist as monomers on the cell surface. (hindawi.com)
  • Involved in cell growth regulation. (rcsb.org)
  • For instance, MGO inhibits mitochondrial respiration, membrane ATPases and glyceraldehyde-3-phosphate dehydrogenases ( 10 ), and DNA and protein synthesis, thereby inducing growth arrest and cell death ( 11 ). (diabetesjournals.org)
  • The ErbB family members are cell surface receptors that are expressed in most tissues throughout the body and form both homo- and heterodimers to generate signals. (springer.com)
  • Thus, these results reveal a connection between antiviral innate immunity and cell growth regulators. (sciencemag.org)
  • Research has shown that asbestos exposure generates reactive oxygen species and activates macrophages and other cell types to produce these compounds as well as cytokines and growth factors ( 5 ). (aacrjournals.org)
  • Virion interaction with HSPGs is easily dissociable with soluble heparin, but the virus quickly transitions to a second, more stable interaction with one or more different receptors that ultimately leads to pH-neutral fusion of the virion, presumably at the cell surface ( 5 ). (asm.org)
  • The ability of HCMV to enter a wide variety of cell types suggests that HCMV utilizes multiple receptors and/or a widely distributed cell surface receptor for entry. (asm.org)
  • Lysophosphatidic acid (LPA) and epidermal growth factor (EGF) are important mediators of lung cell function and lung diseases. (aspetjournals.org)
  • Increasing evidence suggests that integrins form physical complexes at the cell membrane with growth factor receptors, giving rise to signalling platforms at the adhesive sites. (biochemsoctrans.org)
  • Disulfide bond formation generates three structural loops that are essential for high-affinity binding between members of the EGF-family and their cell-surface receptors. (wikipedia.org)