Neuregulin-1
Neuregulins
Receptor, erbB-3
Receptor, Epidermal Growth Factor
Receptor, erbB-2
Epidermal Growth Factor
Genes, erbB
Oncogene Proteins v-erbB
Genes, erbB-2
Signal Transduction
Quinazolines
Phosphorylation
Mucin-4
Immune responses to all ErbB family receptors detectable in serum of cancer patients. (1/5700)
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. (2/5700)
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)An intramembrane modulator of the ErbB2 receptor tyrosine kinase that potentiates neuregulin signaling. (3/5700)
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)Immunohistochemical analysis of c-yes and c-erbB-2 oncogene products and p53 tumor suppressor protein in canine mammary tumors. (4/5700)
In order to evaluate the involvement of c-yes and c-erbB-2 oncogene products, and p53 tumor suppressor protein in canine mammary neoplastic lesions, sections of archived paraffin-embedded samples of 79 mammary tumors were analyzed immunohistochemically using antibodies against human c-yes p62 and c-erbB-2 products and p53. These 79 tumors were divided into 2 groups: 32 benign (2 adenosis, 7 simple adenomas, 14 complex adenomas, and 9 benign mixed mammary tumors) and 47 malignant tumors (26 simple adenocarcinomas, 7 complex adenocarcinomas, 5 solid carcinomas, 2 sclerosing carcinomas, 6 malignant mixed mammary tumors, and 1 malignant myoepithelioma). As a result of immunostaining, 40.6% (13/32) of the benign tumors and 21.3% (10/47) of the malignant tumors expressed the c-Yes oncogene product, ErbB-2 expression was detected in 50% (16/32) of the benign tumors and in 19.1% (9/47) of the malignant tumors. P53 expression was detected in 16% (4/25) of the benign tumors and in 30.6% (11/36) of the malignant tumors. Co-expression of c-Yes and ErbB-2, ErbB-2 and p53, and all 3 products was detected in 6, 1 and 7 tumors, respectively. (+info)Tyrosine kinase inhibitor emodin suppresses growth of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. (5/5700)
Overexpression of the HER-2/neu proto-oncogene, which encodes the tyrosine kinase receptor p185neu, has been observed in tumors from breast cancer patients. We demonstrated previously that emodin, a tyrosine kinase inhibitor, suppresses tyrosine kinase activity in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. We found that emodin significantly inhibited tumor growth and prolonged survival in mice bearing HER-2/neu-overexpressing human breast cancer cells. Furthermore, the combination of emodin and paclitaxel synergistically inhibited the anchorage-dependent and -independent growth of HER-2/neu-overexpressing breast cancer cells in vitro and synergistically inhibited tumor growth and prolonged survival in athymic mice bearing s.c. xenografts of human tumor cells expressing high levels of p185neu. Both immunohistochemical staining and Western blot analysis showed that emodin decreases tyrosine phosphorylation of HER-2/neu in tumor tissue. Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. The results may have important implications in chemotherapy for HER-2/neu-overexpressing breast tumors. (+info)Trimodality therapy in stage III non-small cell lung cancer: prediction of recurrence by assessment of p185neu. (6/5700)
In a trimodality treatment approach for stage III non-small cell lung cancer the prognostic impact of pretherapeutic p185neu assessment was evaluated. Fifty-four patients were admitted to chemotherapy followed by twice-daily radiation with concomittant low-dose chemotherapy and subsequent surgery. Immunohistochemical assessment of p185neu expression was performed in paraffin-embedded mediastinal lymph node metastases, by mediastinoscopy biopsy prior to therapy. Paraffin-embedded biopsies of mediastinal lymph node metastases were available in 33 cases. Seven out of eight patients with positive p185neu staining developed distant metastases, in contrast to seven out of 25 negative cases. Expression of p185neu in mediastinal lymph node metastases was a significant predictor for progression-free survival (p=0.047) and resulted mainly from significant differences in metastases-free survival (p185neu-positive versus p185neu-negative: median, 11 versus 19 months; 2- and 3-yr rates, 13% and 0% versus 40% and 32%; p=0.04). On the basis of these preliminary results it was concluded that further evaluation of p185neu expression in trials on neoadjuvant and adjuvant therapy is warranted. When the prognostic impact of p185neu in such trials with larger patient numbers is confirmed, this may contribute to the identification of stratification variables for future treatment approaches of non-small cell lung cancer. (+info)Inhibition of aberrant proliferation and induction of apoptosis in HER-2/neu oncogene transformed human mammary epithelial cells by N-(4-hydroxyphenyl)retinamide. (7/5700)
Epithelial cells from non-cancerous mammary tissue in response to exposure to chemical carcinogens or transfection with oncogenes exhibit hyperproliferation and hyperplasia prior to the development of cancer. Aberrant proliferation may, therefore, represent a modifiable early occurring preneoplastic event that is susceptible to chemoprevention of carcinogenesis. The synthetic retinoid N-(4-hydroxyphenyl)retinamide (HPR), has exhibited preventive efficacy in several in vitro and in vivo breast cancer models, and represents a promising chemopreventive compound for clinical trials. Clinically relevant biochemical and cellular mechanisms responsible for the chemopreventive effects of HPR, however, are not fully understood. Experiments were performed on preneoplastic human mammary epithelial 184-B5/HER cells derived from reduction mammoplasty and initiated for tumorigenic transformation by overexpression of HER-2/neu oncogene, to examine whether HPR inhibits aberrant proliferation of these cells and to identify the possible mechanism(s) responsible for the inhibitory effects of HPR. Continuous 7-day treatment with HPR produced a dose-dependent, reversible growth inhibition. Long-term (21 day) treatment of 184-B5/HER cells with HPR inhibited anchorage-dependent colony formation by approximately 80% (P < 0.01) relative to that observed in the solvent control. A 24 h treatment with cytostatic 400 nM HPR produced a 25% increase (P = 0.01) in G0/G1 phase, and a 36% decrease (P = 0.01) in S phase of the cell cycle. HPR treatment also induced a 10-fold increase (P = 0.02) in the sub-G0 (apoptotic) peak that was down-regulated in the presence of the antioxidant N-acetyl-L-cysteine. Treatment with HPR resulted in a 30% reduction of cellular immunoreactivity to tyrosine kinase, whereas immunoreactivity to p185HER remained essentially unaltered. HPR exposure resulted in time-dependent increase in cellular metabolism of the retinoid as evidenced by increased formation of the inert metabolite N-(4-methoxyphenyl)-retinamide (MPR) and progressive increase in apoptosis. Thus, HPR-induced inhibition of aberrant proliferation may be caused, in part, by its ability to inhibit HER-2/neu-mediated proliferative signal transduction, retard cell cycle progression and upregulate cellular apoptosis. (+info)Isolation and characterization of a new human breast cancer cell line, KPL-4, expressing the Erb B family receptors and interleukin-6. (8/5700)
A new human breast cancer cell line, KPL-4, was recently isolated from the malignant pleural effusion of a breast cancer patient with an inflammatory skin metastasis. This cell line can be cultured under serum-free conditions and is tumorigenic in female athymic nude mice. Flow cytometric analysis revealed the expression of Erb B-1, -2 and -3. Dot blot hybridization showed a 15-fold amplification of the erb B-2. Reverse transcription-polymerase chain reaction analysis showed a detectable level of mRNA expression of all the Erb B family receptors. In addition, all the receptors were autophosphorylated under a serum-supplemented condition. Unexpectedly, transplanted KPL-4 tumours induced cachexia of recipient mice. A high concentration of interleukin-6 (IL-6) was detected in both the culture medium and the serum of mice. The weight of tumours significantly correlated with the serum IL-6 level. The antiproliferative effect of a humanized anti-Erb B-2 monoclonal antibody, rhuMAbHER2, was investigated. This antibody significantly inhibited the growth of KPL-4 cells in vitro but modestly in vivo. Loss of mouse body weight was partly reversed by rhuMAbHER2. These findings suggest that KPL-4 cells may be useful in the development of new strategies against breast cancer overexpressing the Erb B family receptors and against IL-6-induced cachexia. (+info)Neuregulin-1 (NRG-1) is a growth factor that belongs to the neuregulin family and is involved in the development and function of the nervous system. It is a protein that is encoded by the NRG1 gene and is expressed in various tissues, including the brain. NRG-1 plays important roles in the regulation of neuronal survival, migration, differentiation, and synaptic plasticity. It acts as a ligand for the ErbB family of receptor tyrosine kinases, which are involved in intracellular signaling pathways that control various cellular processes. Abnormalities in NRG-1 signaling have been implicated in several neurological and psychiatric disorders, including schizophrenia, bipolar disorder, and Alzheimer's disease.
Neuregulins are a family of growth factors that play important roles in the development and maintenance of the nervous system. They bind to and activate receptors known as ErbB receptors, which are tyrosine kinase receptors. Neuregulins are involved in the regulation of various cellular processes, including proliferation, differentiation, migration, and survival.
There are several different forms of neuregulins, which are produced by alternative splicing of a single gene. These forms include heregulin, glial growth factor, and neu differentiation factor. Neuregulins are produced by various cell types in the nervous system, including neurons and glial cells. They are involved in the development and maintenance of the nervous system, including the formation of synapses, the regulation of myelination, and the survival of neurons.
Dysregulation of neuregulin signaling has been implicated in various neurological disorders, including schizophrenia, Alzheimer's disease, and epilepsy.
ErбB-3, also known as HER3 or EGFR3, is a type of receptor tyrosine kinase (RTK) that belongs to the ErbB family of receptors. It is a single-pass transmembrane protein composed of an extracellular ligand-binding domain, a transmembrane region, and an intracellular tyrosine kinase domain.
ErбB-3 plays a crucial role in regulating various cellular processes such as proliferation, differentiation, survival, and migration. However, unlike other ErbB receptors, ErbB-3 lacks intrinsic tyrosine kinase activity due to the presence of several mutations in its kinase domain. Therefore, it requires heterodimerization with other ErbB family members, such as ErbB2 or ErbB4, to become activated and initiate downstream signaling pathways.
The primary ligand for ErbB-3 is neuregulin 1 (NRG1), which binds to the extracellular domain of ErbB-3 and induces its dimerization with other ErbB receptors. This leads to the activation of several downstream signaling pathways, including the PI3K/Akt and MAPK pathways, which promote cell survival, proliferation, and migration.
Abnormal regulation of ErbB-3 has been implicated in various human cancers, such as breast, ovarian, lung, and colon cancer. Overexpression or mutations in ErbB-3 have been shown to contribute to tumor growth, progression, and resistance to therapy. Therefore, targeting ErbB-3 is an active area of research for the development of novel cancer therapies.
The Epidermal Growth Factor Receptor (EGFR) is a type of receptor found on the surface of many cells in the body, including those of the epidermis or outer layer of the skin. It is a transmembrane protein that has an extracellular ligand-binding domain and an intracellular tyrosine kinase domain.
EGFR plays a crucial role in various cellular processes such as proliferation, differentiation, migration, and survival. When EGF (Epidermal Growth Factor) or other ligands bind to the extracellular domain of EGFR, it causes the receptor to dimerize and activate its intrinsic tyrosine kinase activity. This leads to the autophosphorylation of specific tyrosine residues on the receptor, which in turn recruits and activates various downstream signaling molecules, resulting in a cascade of intracellular signaling events that ultimately regulate gene expression and cell behavior.
Abnormal activation of EGFR has been implicated in several human diseases, including cancer. Overexpression or mutation of EGFR can lead to uncontrolled cell growth and division, angiogenesis, and metastasis, making it an important target for cancer therapy.
"ErbB-2" is also known as "HER2" or "human epidermal growth factor receptor 2." It is a type of receptor tyrosine kinase (RTK) found on the surface of some cells. ErbB-2 does not bind to any known ligands, but it can form heterodimers with other ErbB family members, such as ErbB-3 and ErbB-4, which do have identified ligands. When a ligand binds to one of these receptors, it causes a conformational change that allows the ErbB-2 receptor to become activated through transphosphorylation. This activation triggers a signaling cascade that regulates cell growth, differentiation, and survival.
Overexpression or amplification of the ERBB2 gene, which encodes the ErbB-2 protein, is observed in approximately 20-30% of breast cancers and is associated with a more aggressive disease phenotype and poorer prognosis. Therefore, ErbB-2 has become an important target for cancer therapy, and several drugs that target this receptor have been developed, including trastuzumab (Herceptin), lapatinib (Tykerb), and pertuzumab (Perjeta).
Epidermal Growth Factor (EGF) is a small polypeptide that plays a significant role in various biological processes, including cell growth, proliferation, differentiation, and survival. It primarily binds to the Epidermal Growth Factor Receptor (EGFR) on the surface of target cells, leading to the activation of intracellular signaling pathways that regulate these functions.
EGF is naturally produced in various tissues, such as the skin, and is involved in wound healing, tissue regeneration, and maintaining the integrity of epithelial tissues. In addition to its physiological roles, EGF has been implicated in several pathological conditions, including cancer, where it can contribute to tumor growth and progression by promoting cell proliferation and survival.
As a result, EGF and its signaling pathways have become targets for therapeutic interventions in various diseases, particularly cancer. Inhibitors of EGFR or downstream signaling components are used in the treatment of several types of malignancies, such as non-small cell lung cancer, colorectal cancer, and head and neck cancer.
ERBB genes (also known as HER or human epidermal growth factor receptor) are a family of genes that encode for transmembrane receptor tyrosine kinases. These receptors play crucial roles in various cellular processes such as proliferation, differentiation, and survival. The ERBB gene family includes four members: EGFR (ERBB1), ERBB2 (HER2/neu), ERBB3 (HER3), and ERBB4 (HER4). Dysregulation of these genes has been implicated in several human cancers, making them attractive targets for cancer therapy.
The oncogene proteins v-erbB are derived from the erbB oncogene, which is a retroviral oncogene first discovered in avian erythroblastosis viruses (AEV). The erbB oncogene is homologous to the human epidermal growth factor receptor 2 (HER2/erbB-2) gene, which encodes a transmembrane tyrosine kinase receptor involved in cell proliferation and differentiation.
The v-erbB oncogene protein is a truncated and mutated version of the normal EGFR/erbB-1 receptor, which has lost its extracellular ligand-binding domain and gained constitutive tyrosine kinase activity. This results in uncontrolled cell growth and division, leading to the development of cancer.
The v-erbB oncogene protein has been extensively studied as a model system for understanding the molecular mechanisms of oncogenesis and has provided valuable insights into the regulation of cell growth and differentiation. Additionally, the study of v-erbB and other oncogenes has led to the development of targeted cancer therapies that inhibit the activity of these aberrant proteins and slow or stop the growth of cancer cells.
ERBB-2, also known as HER2/neu or HER2, is a gene that encodes for a tyrosine kinase receptor protein. This receptor is part of the EGFR/ERBB family and plays crucial roles in cell growth, differentiation, and survival. Amplification or overexpression of this gene has been found in various types of human cancers, including breast, ovarian, lung, and gastric cancers. In breast cancer, ERBB-2 overexpression is associated with aggressive tumor behavior and poorer prognosis. Therefore, ERBB-2 has become an important therapeutic target for cancer treatment, with various targeted therapies developed to inhibit its activity.
Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.
The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.
Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.
Breast neoplasms refer to abnormal growths in the breast tissue that can be benign or malignant. Benign breast neoplasms are non-cancerous tumors or growths, while malignant breast neoplasms are cancerous tumors that can invade surrounding tissues and spread to other parts of the body.
Breast neoplasms can arise from different types of cells in the breast, including milk ducts, milk sacs (lobules), or connective tissue. The most common type of breast cancer is ductal carcinoma, which starts in the milk ducts and can spread to other parts of the breast and nearby structures.
Breast neoplasms are usually detected through screening methods such as mammography, ultrasound, or MRI, or through self-examination or clinical examination. Treatment options for breast neoplasms depend on several factors, including the type and stage of the tumor, the patient's age and overall health, and personal preferences. Treatment may include surgery, radiation therapy, chemotherapy, hormone therapy, or targeted therapy.
A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.
Quinazolines are not a medical term per se, but they are a class of organic compounds that have been widely used in the development of various pharmaceutical drugs. Therefore, I will provide you with a chemical definition of quinazolines:
Quinazolines are heterocyclic aromatic organic compounds consisting of a benzene ring fused to a pyrazine ring. The structure can be represented as follows:
Quinazoline
They are often used as building blocks in the synthesis of various drugs, including those used for treating cancer, cardiovascular diseases, and microbial infections. Some examples of FDA-approved drugs containing a quinazoline core include the tyrosine kinase inhibitors gefitinib (Iressa) and erlotinib (Tarceva), which are used to treat non-small cell lung cancer, and the calcium channel blocker verapamil (Calan, Isoptin), which is used to treat hypertension and angina.
Phosphorylation is the process of adding a phosphate group (a molecule consisting of one phosphorus atom and four oxygen atoms) to a protein or other organic molecule, which is usually done by enzymes called kinases. This post-translational modification can change the function, localization, or activity of the target molecule, playing a crucial role in various cellular processes such as signal transduction, metabolism, and regulation of gene expression. Phosphorylation is reversible, and the removal of the phosphate group is facilitated by enzymes called phosphatases.
Mucin-4, also known as "Podocalyxin-like" or "PODXL," is a type of transmembrane mucin protein that is heavily glycosylated. It is primarily expressed on the surface of certain types of cells, including epithelial and endothelial cells.
Mucin-4 is a large molecule with a molecular weight ranging from 150 to 250 kDa, depending on its degree of glycosylation. It has a extracellular domain that contains several N-linked glycans and O-linked oligosaccharides, which give it a highly extended structure and contribute to its ability to form protective barriers on the cell surface.
Mucin-4 is involved in various biological processes, such as providing a barrier function, regulating cell adhesion, and modulating immune responses. It has been implicated in several diseases, including cancer, where it can promote tumor growth and metastasis by facilitating cell migration and invasion. In the kidney, Mucin-4 is expressed on the surface of podocytes, which are specialized epithelial cells that play a critical role in maintaining the filtration barrier in the glomerulus. Mutations in the MUC16 gene, which encodes Mucin-4, have been associated with nephrotic syndrome, a kidney disorder characterized by proteinuria and edema.
ErbB
PLXNB1
MMP16
Breast development
Epidermal growth factor receptor
TP53RK
DDX10
Neuregulin 2
HER2
Saliva testing
ERRFI1
PTGES3
List of MeSH codes (D12.776)
DNAJA3
Potato carboxypeptidase inhibitor
List of MeSH codes (D12.776.543)
Megakaryocyte-associated tyrosine kinase
Index of biochemistry articles
ERBB4
List of MeSH codes (D23)
Trastuzumab
ERBB3
GATA3
FOXA1
Epidermal growth factor
PA2G4
Retinoblastoma protein
Receptor tyrosine kinase
GRB7
V-erbA-related gene
Genetic polymorphisms in the EGFR (R521K) and estrogen receptor (T594T) genes, EGFR and ErbB-2 protein expression, and breast...
Protein RefSeq sequence for receptor tyrosine-protein kinase erbB-2 isoform a precursor [Homo sapiens]
ERBB receptors: from oncogene discovery to basic science to mechanism-based cancer therapeutics
Proteomic Approaches in Lung Cancer Biomarker Development
Expert consensus on the management of adverse events of ErbB family tyrosine kinase inhibitors in breast cancer] - PubMed
RCSB PDB - 1N8Z: Crystal structure of extracellular domain of human HER2 complexed with Herceptin Fab
Signalling pathways and mechanistic cues highlighted by transcriptomic analysis of primordial, primary, and secondary ovarian...
HSD17B1 | Cancer Genetics Web
Search Strategy Used to Create the PubMed Cancer Filter
ErbB - Wikipedia
Mouse ErbB2/Her2 Alexa Fluor® 700-conjugated Antibody FAB6744N-100UG: R&D Systems
Publication Detail
Biomarkers Search
c-erbB-2/HER-2/neu Antibody Staining Protocol for Immunohistochemistry
NIOSHTIC-2 Search Results - Full View
HER-2/neu Amplification in Benign Breast Disease and the Risk of Subsequent Breast Cancer | OncoLink
ErbB2 (HER-2) Polyclonal Antibody (PA5-16305)
Prognostic value of ERBB4 expression in patients with triple negative breast cancer | BMC Cancer | Full Text
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Mucin-4 | Harvard Catalyst Profiles | Harvard Catalyst
Study of Estrogen Receptor and Progesterone Receptor Expression in Breast Ductal ...
PTPN12 down-regulated by miR-146b-3p gene affects the malignant progression of laryngeal squamous cell carcinoma
EGF Positively Regulates the Proliferation and Migration, and Negatively Regulates the Myofibroblast Differentiation of...
HER2/ErbB2 (D8F12) XP® Rabbit mAb | Cell Signaling Technology
Medical Science Monitor | Association between polymorphisms of XRCC1, p53 and MDR1 genes, the expression of their protein...
Ottawa Hospital Research Institute
Salivary Abnormalities in Dentistry: Overview, Salivary Gland Anatomy, Salivation and Age
Mischel PS et al. (2002), Nerve growth factor signals via preexisting Trk... - Paper
Epidermal growth f24
- ERBB2 is a protein that is also known as HER2 (human epidermal growth factor receptor 2). (antibodyguide.com)
- It is a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases. (antibodyguide.com)
- Trastuzumab is a humanized monoclonal antibody that targets human epidermal growth factor receptor 2 (HER2)/neu, a receptor overexpressed in 30% of uterine serous carcinoma. (nih.gov)
- The ErbB family of proteins contains four receptor tyrosine kinases, structurally related to the epidermal growth factor receptor (EGFR), its first discovered member. (wikipedia.org)
- The ErbB protein family consists of 4 members ErbB-1, also named epidermal growth factor receptor (EGFR) ErbB-2, also named HER2 in humans and neu in rodents ErbB-3, also named HER3 ErbB-4, also named HER4 v-ErbBs are homologous to EGFR, but lack sequences within the ligand binding ectodomain. (wikipedia.org)
- Expression analyses of epidermal growth factor receptor and HER-2/neu: no advantage of prediction of recurrence or survival in breast cancer patients. (thieme-connect.de)
- The ErbB/HER family of receptor tyrosine kinases (RTKs) consists of four family members: the epidermal growth factor receptor (EGFR/ErbB1), HER2 (ErbB2/Neu), HER3 (ErbB3), and HER4 (ErbB4). (plos.org)
- The objective of this study was to determine the conversion rate of human epidermal growth factor receptor 2 (HER2), estrogen receptor (ER) and progesterone receptor (PR) between primary tumors and metastatic lesions in advanced breast cancer. (springer.com)
- The status of human epidermal growth factor receptor 2 (HER2) and the hormone receptors (HR), including estrogen receptor (ER) and progesterone receptor (PR), are the most relevant biomarkers for clinical practice, predicting response to anti-HER2 and endocrine therapies, respectively. (springer.com)
- c- erb B-2 (HER-2/ neu ) is a 185 kDa receptor tyrosine kinase belonging to the epidermal growth factor receptor family, which also includes EGFR (HER-1), c- erb B-3 (HER-3), and c- erb B-4 (HER-4). (ihcworld.com)
- MA5-14485 targets Epidermal Growth Factor Receptor in IHC (P) applications and shows reactivity with Human samples. (thermofisher.com)
- EGFR (Epidermal growth factor receptor, HER1, ErbB1) is encoded by the EGFR gene located on chromosome 7 in humans. (thermofisher.com)
- GW572016 (Lapatinib) is a tyrosine kinase inhibitor in clinical development for cancer that is a potent dual inhibitor of epidermal growth factor receptor (EGFR, ErbB-1) and ErbB-2. (rcsb.org)
- The status of the erbB-2 (human epidermal growth factor receptor 2/neu) proto-oncogene in canine osteosarcoma (OSA) has not been reported previously. (cdc.gov)
- Ligand binding to the four closely related members of this RTK family -epidermal growth factor receptor (EGFR, also known as ErbB-1 or HER1), ErbB-2 (HER2), ErbB-3 (HER3), and ErbB-4 (HER4)-induces the formation of receptor homo- and heterodimers and the activation of the intrinsic kinase domain, resulting in phosphorylation on specific tyrosine residues (pY) within the cytoplasmic tail. (genome.jp)
- Importance of epidermal growth factor receptor signaling in establishment of adenomas and maintenance of carcinomas during intestinal tumorigenesis. (nature.com)
- It selectively inhibits erbB1 (epidermal growth factor receptor), erbB2, erbB3, and erbB4 without blocking tyrosine kinase activity of many other receptors such as platelet-derived growth factor receptor, fibroblast growth factor receptor, and insulin receptor. (lclabs.com)
- With the addition of trastuzumab, a monoclonal antibody targeting the human epidermal growth factor receptor-2 (HER2), improvements in overall survival have been observed among patients with advanced HER2-positive disease. (carcinogenesis.com)
- One type of breast cancer is identified by the human epidermal growth factor receptor 2 (HER2) gene amplification. (carcinogenesis.com)
- The epidermal growth factor receptor (EGFR) tyrosine kinase (TK) plays an important role in the pathogenesis of NSCLC. (bmj.com)
- Alterations in receptor tyrosine kinases (TKs), such as the epidermal growth factor receptor (EGFR) and insulin-like growth factor receptor 1, include overexpression, amplification or mutations. (bmj.com)
- Novel therapeutic agents, in particular those that specifically target members of the human epidermal growth factor receptor (HER (ErbB1)) pathway, have shown encouraging therapeutic efficacy. (bmj.com)
- Receptor tyrosine-protein kinase erbB-2, also known as HER2/Neu (human epidermal growth factor receptor 2), is a member of the human epidermal growth factor receptor family. (meridianbioscience.com)
- Patients with breast cancer positive for human epidermal growth-factor receptor type 2 (HER2) are an important subgroup for consideration in the Asian context. (mcmaster.ca)
HER26
- The HER2 receptor does not bind to any known ligands, however, its dimerization arm is innately positioned in an open conformation. (plos.org)
- Being aware of the benefits that the correct systemic therapy provides to patients with advanced breast cancer, the Spanish Breast Cancer Research Group (GEICAM) performed a prospective, observational study to determine the conversion rate of receptor status (ER, PR and HER2) between the primary tumor and the recurrent lesion. (springer.com)
- Analizar las diferencias en la presentación de variables clínico-patológicas, de acuerdo con la expresión proteica de GRB7, en tumores HER2 positivos en mujeres colombianas con cáncer de mama invasivo, diagnosticado entre los años 2013 y 2015 en el Instituto Nacional de Cancerología E.S.E (INC). Métodos. (bvsalud.org)
- Se evaluó la expresión de los receptores hormonales (receptor de estrógeno (RE) y de progesterona (RP)), HER2, Ki67 y GRB7, mediante inmunohistoquímica (IHQ), y a partir de estos, se clasificaron los tumores en subtipos intrínsecos. (bvsalud.org)
- A single pathologist evaluated the protein expression of hormone receptors (estrogen (ER) and progesterone receptor (PR)), HER2, Ki67, and GRB7 by immunohistochemistry (IHC). (bvsalud.org)
- HER2 is a member of the cErbB family of receptor tyrosine kinases, and is responsible for HER2-mediated signal transduction in the cytoplasm. (carcinogenesis.com)
EGFR6
- EGFR belongs to the HER/ERbB family of proteins that includes three other receptor tyrosine kinases, ERbB2, ERbB3, ERbB4. (thermofisher.com)
- EGFR is a transmembrane receptor and binding of its cognate ligands such as EGF (Epidermal Growth Factor) and TGF alpha (Transforming Growth Factor alpha) to the extracellular domain leads to EGFR dimerization followed by autophosphorylation of the tyrosine residues in the cytoplasmic domain. (thermofisher.com)
- Phosphorylation of EGFR at certain residues is also mediated by Src-non-receptor kinase. (thermofisher.com)
- Upon receptor activation and signaling, EGFR is endocytosed and targeted for degradation or recycling. (thermofisher.com)
- Surprisingly, we found that GW572016 has a very slow off-rate from the purified intracellular domains of EGFR and ErbB-2 compared with OSI-774 and another EGFR selective inhibitor, ZD-1839 (Iressa). (rcsb.org)
- The ErbB-2 proto-oncogene, also called Neu, EGFR-2 or HER-2, is a member of the transmembrane receptor tyrosine kinase family, which also includes EGF receptor and EGFR-3 (HER-3 or ErbB-3). (activemotif.com)
Pathway5
- Here, we show that the dual inhibitor of ErbB receptors, lapatinib, enhances cytostatic and induces cytotoxic effects of GTC in two bladder cancer cell lines which differ with regard to expression levels of proteins taking part in the ErbB pathway. (edu.kz)
- The Shc- and/or Grb2-activated mitogen-activated protein kinase (MAPK) pathway is a common target downstream of all ErbB receptors. (genome.jp)
- As ErbB-family ligands and receptors are highly expressed within the stem-cell niche 7 , we hypothesize that strong endogenous regulators must control the pathway in the stem-cell compartment. (nature.com)
- Figure 4: Lrig1 controls endogenous signalling through the ErbB pathway. (nature.com)
- The degradative pathway of ErbB receptor tyrosine kinases stimulated by tyrosine kinase inhibitors appears to be chaperone mediated, and thus is similar to the pathways activated by the heat shock protein 90 (Hsp90) antagonist geldanamycin and by stress-induced mechanisms. (lclabs.com)
Proteins7
- In addition to plexins, various other proteins have been implicated either as receptors for semaphorins or as components of the semaphorin receptor complex ( Pasterkamp and Kolodkin, 2003 ). (rupress.org)
- This gene encodes a member of the receptor tyrosine kinase family of proteins and the product of the proto-oncogene MET. (creativebiolabs.net)
- The intracellular/cytoplasmic region of the ErbB receptor consists mainly of three subdomains: A juxtamembrane with approximately 40 residues, a kinase domain containing approximately 260 residues and a C-terminal domain of 220-350 amino acid residues that become activated via phosphorylation of its tyrosine residues that mediates interactions of other ErbB proteins and downstream signaling molecules. (wikipedia.org)
- The figure below shows the tridimensional structure of the ErbB family proteins, using the pdb files 1NQL (ErbB-1), 1S78 (ErbB-2), 1M6B (ErbB-3) and 2AHX (ErbB-4): The four members of the ErbB protein family are capable of forming homodimers, heterodimers, and possibly higher-order oligomers upon activation by a subset of potential growth factor ligands. (wikipedia.org)
- Notably, the ErbB1 and ErbB4 are the two most studied and intact among the family of ErbB proteins, Which forms functional intracellular tyrosine kinases. (wikipedia.org)
- SARS-CoV-2 has a single-stranded RNA genome encoding both structural and non-structural proteins. (news-medical.net)
- Several cytoplasmic docking proteins appear to be recruited by specific ErbB receptors and less exploited by others. (genome.jp)
Overexpression10
- 32 % of patients exhibited overexpression of HER-2/neu. (thieme-connect.de)
- Prospective studies correlating HER-2/neu overexpression with prognosis might provide additional data. (thieme-connect.de)
- c-erbB-2 protein overexpression in breast cancer is a risk factor in patients with involved and uninvolved lymph nodes. (thieme-connect.de)
- This family of RTKs has been highly implicated in the formation and progression of various cancers via aberrant overexpression, kinase activation, and mutation [1] , [2] . (plos.org)
- Amplification of the HER-2 gene with overexpression of the protein occurs in 20-30% of breast cancers, and tumor progression in mammary cancer is associated with elevated levels of tyrosine-phosphorylated neu and erbB-3. (ihcworld.com)
- Overexpression of the erbB-2 proto-oncogene in canine osteosarcoma cell lines and tumors. (cdc.gov)
- Given the importance of erbB-2 in human breast cancer, the finding of erbB-2 overexpression in canine OSA may be important in further understanding the pathogenesis and possible therapies of OSA. (cdc.gov)
- Although, ErbB-2 does not have any known high-affinity ligands, its kinase activity can be activated without ligand by either overexpression or heteroassociation with other members of the ErbB family. (activemotif.com)
- Amplification of the ErbB-2 gene and overexpression of its product has been detected in almost 40% of primary human breast tumors, which correlates with poor prognosis in node positive breast cancer. (activemotif.com)
- ErbB-2 overexpression is also observed in ovarian, gastric, salivary and non-small cell lung carcinomas. (activemotif.com)
Gene7
- Her-2/neu is an oncogene, which is a type of gene that can contribute to certain types of cancer. (medic8.com)
- Normal cells have two copies of the Her-2/neu gene and low levels of Her-2 protein are produced on the surface of the cells. (medic8.com)
- tumours that are associated with the Her-2/neu gene tend to be more aggressive and the outlook is generally not as positive. (medic8.com)
- The gene symbol, ErbB, is derived from the name of a viral oncogene to which these receptors are homologous: erythroblastic leukemia viral oncogene. (wikipedia.org)
- 5 Beckmann M W, Niederacher D, Schnurch H G, Bender H G. The erbB gene family: significance for tumor development, prognosis and new therapeutic modalities. (thieme-connect.de)
- 14 King C R, Kraus M H, Aaronson S A. Amplification of a novel v-erbB-related gene in a human mammary carcinoma. (thieme-connect.de)
- Gene expression profiling of ErbB receptor and ligand-dependent transcription. (rochester.edu)
Ligands2
- Classically, HER family members function from the cell surface, where binding to cognate ligands can induce receptor homo- or hetero-dimerization with other HER family receptors [3] . (plos.org)
- The ErbB family of receptor tyrosine kinases (RTKs) couples binding of extracellular growth factor ligands to intracellular signaling pathways regulating diverse biologic responses, including proliferation, differentiation, cell motility, and survival. (genome.jp)
Oncogene1
- Over-expression of the c-erbB-2 oncogene occurs in a proportion of human adenocarcinomas and in breast carcinoma is associated with poorer prognosis. (nih.gov)
Kinase9
- Here, we show that plexin-B family members stably associate with the receptor tyrosine kinase ErbB-2. (rupress.org)
- Binding of Sema4D to plexin-B1 stimulates the intrinsic tyrosine kinase activity of ErbB-2, resulting in the phosphorylation of both plexin-B1 and ErbB-2. (rupress.org)
- The ability ('+') or inability ('-') of each growth factor to activate each of the ErbB receptors is shown in the table below: The dimerization occurs after ligand bind to the extracellular domain of the ErbB monomers and monomer-monomer interaction establishes activating the activation loop in a kinase domain, that activates the further process of transphosphorylation of the specific tyrosine kinases in the kinase domain of ErbB's intracellular part. (wikipedia.org)
- For the activation of kinase domain in the ErbB dimer, asymmetric kinase domain dimer of the two monomers is required with the intact asymmetric (N-C lobe) interface at the site of adjoining monomers. (wikipedia.org)
- Activation of the tyrosine kinase domain leads to the activation of the whole range of downstream signaling pathways like PLCγ, ERK 1/2, p38 MAPK, PI3-K/Akt and more with the cell. (wikipedia.org)
- Brand TM, Iida M, Luthar N, Wleklinski MJ, Starr MM, Wheeler DL (2013) Mapping C-Terminal Transactivation Domains of the Nuclear HER Family Receptor Tyrosine Kinase HER3. (plos.org)
- This process leads to the activation of each receptors' tyrosine kinase and the subsequent phosphorylation of tyrosine residues located on their C-terminal tails. (plos.org)
- Canertinib (CI-1033, PD 183805) is a pan-erbB tyrosine kinase inhibitor. (lclabs.com)
- A cell surface protein-tyrosine kinase receptor that is overexpressed in a variety of ADENOCARCINOMAS. (bvsalud.org)
Estrogen receptor6
- Nodal positivity correlated with histological grade and tumour size, but not with estrogen receptor or c-erbB-2 status. (ispub.com)
- Results of estrogen receptor and c-erbB-2 status using immunohistochemistry were documented. (ispub.com)
- Chi square was used to test the association between ethnic group, tumour size (categorized as ≤2 cm, >2 cm and ≤5 cm, and >5 cm), histological grade, estrogen receptor (ER) status, c-erbB-2 status and lymph node metastases. (ispub.com)
- Cancer cells that have estrogen receptors are referred to as estrogen receptor-positive (ER-positive) cancers. (texasoncology.com)
- Furthermore, a new of drugs called estrogen-receptor antagonists work in a similar way as tamoxifen and have been shown to benefit some patients with breast cancer. (texasoncology.com)
- Like SERMs, estrogen receptor antagonists work by preventing estrogen from stimulating the growth of estrogen receptor-positive cells. (texasoncology.com)
Ubiquitylation and degradation2
- LRIG1 restricts growth factor signaling by enhancing receptor ubiquitylation and degradation. (nature.com)
- Drug-induced ubiquitylation and degradation of ErbB receptor tyrosine kinases: implications for cancer therapy. (lclabs.com)
Immunohistochemistry1
- Blinded determinations of receptor status on paired samples were performed by immunohistochemistry and fluorescence in situ hybridization at a central laboratory and compared with those performed locally. (springer.com)
Inhibitor3
- We evaluated the duration of the drug effect after washing away free compound and found that the rate of recovery of receptor phosphorylation in the tumor cells reflected the inhibitor off-rate from the purified intracellular domain. (rcsb.org)
- The differences in the off-rates of these drugs and the ability of GW572016 to inhibit ErbB-2 can be explained by the enzyme-inhibitor structures. (rcsb.org)
- Radiosensitization by pan ErbB inhibitor CI-1033 in vitro and in vivo. (lclabs.com)
Intracellular2
- Phosphorylated tyrosine residues recruit various intracellular adaptor and effector molecules that result in the propagation of growth promoting signal transduction cascades [1] , [2] . (plos.org)
- It not only inhibits tyrosine phosphorylation but also enhances ubiquitinylation and accelerates endocytosis and subsequent intracellular destruction of ErbB-2 molecules. (lclabs.com)
Tumor7
- Insufficient ErbB signaling in humans is associated with the development of neurodegenerative diseases, such as multiple sclerosis and Alzheimer's disease, while excessive ErbB signaling is associated with the development of a wide variety of types of solid tumor. (wikipedia.org)
- Excessive ErbB signaling is associated with the development of a wide variety of types of solid tumor. (wikipedia.org)
- Nuclear localized HER family receptor tyrosine kinases (RTKs) have been observed in primary tumor specimens and cancer cell lines for nearly two decades. (plos.org)
- Membrane-bound HER receptors activate numerous tumor promoting signaling cascades via this mechanism, including the PI3K/AKT, Ras/Raf/Mek/Erk, PLCγ/PKC, and signal transducer and activator of transcription (STAT) pathways [1] , [2] . (plos.org)
- In spite of the relevance of receptor status, the choice of systemic treatment for advanced disease is more often based on the biological characteristics of the primary tumor at the time of initial diagnosis than of the recurrent lesion at the time of relapse. (springer.com)
- Treatment of tumor cells with these inhibitors results in down-regulation of receptor tyrosine phosphorylation. (rcsb.org)
- The slow off-rate of GW572016 correlates with a prolonged down-regulation of receptor tyrosine phosphorylation in tumor cells. (rcsb.org)
Phosphorylation site1
- The total-ErbB-2 antibody supplied in the FACE ErbB-2 Kits recognizes ErbB-2 protein regardless of its phosphorylation site. (activemotif.com)
Antibodies2
- Sensitivity of HER-2/neu antibodies in archival tissue samples of invasive breast carcinomas. (thieme-connect.de)
- Each FACE ErbB-2 Kit provides 96 rxns each of 2 antibodies that enable you to monitor and compare the levels of both phosphorylated and total ErbB-2. (activemotif.com)
Activation7
- A dominant-negative form of ErbB-2 blocks Sema4D-induced RhoA activation as well as axonal growth cone collapse in primary hippocampal neurons. (rupress.org)
- Our data indicate that ErbB-2 is an important component of the plexin-B receptor system and that ErbB-2-mediated phosphorylation of plexin-B1 is critically involved in Sema4D-induced RhoA activation, which underlies cellular phenomena downstream of plexin-B1, including axonal growth cone collapse. (rupress.org)
- Binding of its ligand, hepatocyte growth factor, induces dimerization and activation of the receptor, which plays a role in cellular survival, embryogenesis, and cellular migration and invasion. (creativebiolabs.net)
- Activation of HER-2 is frequent in ductal carcinoma in situ suggesting that HER-2 signaling plays a critical role in the early stages of breast tumorigenesis. (ihcworld.com)
- Our findings reveal ErbB activation as a strong inductive signal for stem-cell proliferation. (nature.com)
- Figure 5: Lrig1 controls ErbB activation in vivo . (nature.com)
- Activation of the erbB-2 receptor occurs through heterodimer formation with a ligand-bound erbB receptor family member. (bvsalud.org)
Her32
- The current study aimed to map the putative transactivation domains (TADs) of the HER3 receptor. (plos.org)
- To understand how the B 1 and B 2 regions influenced the transcriptional functions of nuclear HER3, we performed cyclin D1 promoter-luciferase assays in which HER3 deleted of the B 1 and B 2 regions was severely hindered in regulating this promoter. (plos.org)
Pathways1
- Signaling effectors containing binding pockets for pY-containing peptides are recruited to activated receptors and induce the various signaling pathways. (genome.jp)
Tumours3
- all nine tumours were c-erbB-2 positive and in eight the in situ component was of comedo or solid type. (nih.gov)
- Given that receptor tyrosine kinases of the ErbB family are overexpressed in a high proportion of metastatic bladder tumours, approaches involving small-molecule inhibitors of ErbB receptors in combination with conventional cytostatic drugs are of potential interest. (edu.kz)
- The size of infiltrating ductal carcinoma (IDC) tumours at presentation is tabulated in table 1 and the histological grade of IDC, in table 2. (ispub.com)
Molecules1
- The specific tyrosine molecules mainly trans or auto-phosphorylated are at the site Y992, Y1045, Y1068, Y1148, Y1173 in the tail region of the ErbB monomer. (wikipedia.org)
Family6
- ErbB protein family signaling is important for development. (wikipedia.org)
- All four ErbB receptor family members are nearly same in the structure having single-chain of modular glycoproteins. (wikipedia.org)
- It is a complex process due to the domain specificity and nature of the members of ErbB family. (wikipedia.org)
- While the classical membrane-bound functions of HER family RTKs have been extensively studied, accumulating data suggest that these receptors can be found in the cell's nucleus where they can function as co-transcriptional activators [4] , [5] . (plos.org)
- The leucine-rich repeat protein LRIG1 is a negative regulator of ErbB family receptor tyrosine kinases. (nature.com)
- Essential erbB family phosphorylation in osteosarcoma as a target for CI-1033 inhibition. (lclabs.com)
Tumors1
- ErbB-1 and ErbB-2 are found in many human cancers, and their excessive signaling may be critical factors in the development and malignancy of these tumors. (wikipedia.org)
20221
- 32(2): 194-207, 2 de Agosto del 2022. (bvsalud.org)
Targets1
- Because of this, ErbB-2 is one of the major drug targets for breast cancer and other cancer treatments. (activemotif.com)
Neoplasms1
- This is a unique case due to the low frequency 2 , the atypical clinical history, but mainly the difficult histopathological differential diagnosis and immunohistochemical evaluation among these neoplasms. (bvsalud.org)
Monoclonal1
- Sections of formalin-fixed, paraffin-embedded tumour tissue from 22 patients with mammary and extramammary Paget's disease have been stained immunohistochemically using a monoclonal antibody (NCL-CB11) raised against a synthetic peptide from the C-terminal end of the predicted sequence of the c-erbB-2 protein product. (nih.gov)
Human2
- 2 Barnes D M, Lammie G A, Millis R R, Gullick W L, Allen D S, Altman D G. An immunohistochemical evaluation of c-erbB-2 expression in human breast carcinoma. (thieme-connect.de)
- The FACE ErbB-2 (Y877) Kit contains a phospho-ErbB-2 antibody that was raised in rabbit against a synthetic phospho-peptide corresponding to residues surrounding phosphorylated Tyr877 of human ErbB-2 and recognizes ErbB-2 only when phosphorylated at Tyr877. (activemotif.com)
Inhibitors1
- 2 , 3 , 4 Femara and Arimidex are nonsteroidal aromatase inhibitors that bind reversibly to aromatase. (texasoncology.com)
Node-positive breast cancer1
- HER-2/neu amplification predicts poor survival in node-positive breast cancer. (thieme-connect.de)
Carcinomas2
- About 5% of breast carcinomas are positive for phospho-c- erb B-2/HER-2/ neu oncoprotein. (ihcworld.com)
- 1, 2 Most studies of MUC1 expression in breast carcinomas have shown that increased membrane MUC1 mucin expression on the apical cell surface is associated with a better prognosis (reviewed in Rahn and colleagues 2 ), whereas circumferential staining in tumour cell cytoplasm is associated with a worse prognosis. (bmj.com)
Breast cancer4
- The disease is associated with high morbidity and mortality especially as we tend to see more advanced stages of breast cancer in our part of the world ( 2 , 3 ). (ispub.com)
- The histological type of breast cancer comprised 137 infiltrating ductal carcinoma (not otherwise specified), 4 invasive lobular carcinoma, 3 papillary, 2 mucinous, one each of medullary, tubular and inflammatory carcinoma, 27 ductal carcinoma in situ and 1 Non Hodgkin lymphoma. (ispub.com)
- The HER-2/neu onkogene may play a role in the prognosis and management of patients with breast cancer. (thieme-connect.de)
- With the technological advances, we are able to characterize molecular subtypes [2] , [3] of breast cancer which has facilitated the development of molecularly targeted therapeutics. (carcinogenesis.com)