• Although epidermal growth factor receptor (EGFR) is often over-expressed in soft tissue sarcoma (STS), a phase II trial using an EGFR inhibitor gefitinib showed a low response rate. (oncotarget.com)
  • For patients with locally advanced or metastasized SCCs treatment with cetuximab, a monoclonal antibody against epidermal growth factor receptor (EGFR), has been proposed and so far, treatment of five DEB patients with cetuximab has been published. (biomedcentral.com)
  • Tyrosine kinase inhibitors (TKIs) against the human epidermal growth factor receptor (EGFR) are now standard treatment in the clinic for patients with advanced EGFR mutant non-small-cell lung cancer (NSCLC). (researchgate.net)
  • The deregulation of the epidermal growth factor receptor (EGFR) pathway plays a major role in the pathogenesis of prostate cancer (PCa). (udg.edu)
  • Zalutumumab (proposed trade name HuMax-EGFR) is a fully human IgG1 monoclonal antibody (mAb) directed towards the epidermal growth factor receptor (EGFR). (wikipedia.org)
  • Mutations in the kinase domain of the epidermal growth factor receptor (EGFR) are found in a subset of patients with lung cancer and correlate with response to EGFR tyrosine kinase inhibitors (TKI). (elsevierpure.com)
  • AXL dimerizes with and phosphorylates epidermal growth factor receptor (EGFR), resulting in activation of phospholipase Cγ (PLCγ)-protein kinase C (PKC), which, in turn, activates mTOR. (iucc.ac.il)
  • Breast cancer therapy has improved following the development of drugs with specific molecular targets, exemplified by inhibitors of human epidermal growth factor receptor-2 (HER2) or epidermal growth factor receptor (EGFR) such as trastuzumab and lapatinib. (jcancer.org)
  • Since 2011, several quinoline compounds have shown Epidermal Growth Factor Receptor (EGFR) inhibition 22 . (nature.com)
  • Therapeutic anticancer strategies that target and inactivate the epidermal growth factor receptor (EGFR) are under intense study in the clinic. (rcsb.org)
  • Thus, GAGs/PGs may modulate downstream signaling of key cellular mediators including insulin growth factor receptor (IGFR), epidermal growth factor receptor (EGFR), estrogen receptors (ERs), or Wnt members. (hindawi.com)
  • Injurious dust exposures in the agricultur al workplace involve the release of inflammatory mediators and activation of epidermal growth factor receptor (EGFR) in the respiratory epithelium. (cdc.gov)
  • Approximately 30-50% of colorectal tumors are known to have a mutated (abnormal) KRAS gene, indicating that up to 50% of patients with colorectal cancer (CRC) might respond to anti-epidermal growth factor receptor (EGFR) antibody therapy. (medscape.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)
  • CO-1686 is a novel, oral, targeted covalent (irreversible) inhibitor of the cancer-causing mutant forms of epidermal growth factor receptor (EGFR) currently being studied for the treatment of non-small cell lung cancer (NSCLC). (adooq.com)
  • BMS-690514 is a potent and selective inhibitor of epidermal growth factor receptor (EGFR), HER2, and HER4, as well as the VEGF receptor kinases. (adooq.com)
  • Erlotinib hydrochloride is a reversible tyrosine kinase inhibitor, which acts on the epidermal growth factor receptor (EGFR). (adooq.com)
  • BIBW2992 (Afatinib) is tyrosine kinase inhibitor (TKI) that irreversibly inhibits human epidermal growth factor receptor 2 (Her2) and epidermal growth factor receptor (EGFR) kinases. (adooq.com)
  • Epidermal growth factor receptor (EGFR) inhibitors are an increasingly important treatment option for metastasized cancer in patients. (skintherapyletter.com)
  • Current EGFR inhibitors are limited by off-target toxicity and intrinsic and acquired resistance. (onclive.com)
  • Moreover, the mechanism of action of AFM24 can surpass the obstacles of current EGFR inhibitors because of its independence to EGFR activity and resulting signaling pathway resistance. (onclive.com)
  • In contrast, EGFR ligand-induced CD44 expression was reduced by EGFR inhibitors, AG1478 and lapatinib, respectively. (iiarjournals.org)
  • However, only small incremental advancements have been made for the use of angiogenesis inhibitors in NSCLC and it remains elusive why the inhibition of VEGF-mediated neovascularization is not therapeutically efficacious. (luc.edu)
  • In this review, we summarize the available post-progression therapies including third-generation EGFR inhibitors and combination treatment strategies for treating patients with NSCLC harboring EGFR mutations and address the known mechanisms of resistance. (researchgate.net)
  • In the present study, we were interested in analyzing if this intrinsic resistance mechanism might contribute to the inefficacy of EGFR inhibitors in PCa. (udg.edu)
  • Cells were treated with three EGFR inhibitors (cetuximab, gefinitib and erlotinib) and the sensitivity to each treatment was assessed. (udg.edu)
  • Hsp90 inhibitors, such as 17-allylamino-17-demethoxygeldanamycin (17-AAG), induce the degradation of EGFR and other Hsp90 interacting proteins and may thus have utility in tumors dependent upon sensitive Hsp90 clients. (elsevierpure.com)
  • Combined treatment with PI3Kα and either EGFR, AXL, or PKC inhibitors reverts this resistance. (iucc.ac.il)
  • Both the similarities and differences in binding of these two antibodies have important implications for the development of inhibitors that could exploit this same mechanism of EGFR inhibition. (rcsb.org)
  • PF-06459988 was discovered as a novel, third generation irreversible inhibitor, which demonstrates (i) high potency and specificity to the T790M-containing double mutant EGFRs, (ii) minimal intrinsic chemical reactivity of the electrophilic warhead, (iii) greatly reduced proteome reactivity relative to earlier irreversible EGFR inhibitors, and (iv) minimal activity against WT EGFR. (rcsb.org)
  • Primary human bronchial epithelial (BEC) and BEAS-2B cells were treated with an aqueous extract of swine confinement facility dust (DE) in the presence of DHA and AREG or EGFR inhibitors. (cdc.gov)
  • Treatment is strict glucose control, angiotensin inhibition (using angiotensin-converting enzyme [ACE] inhibitors or angiotensin II receptor blockers [ARBs]), and control of blood pressure and lipids. (msdmanuals.com)
  • AFM24] may offer an alternative therapeutic option, particularly for patients with resistance to conventional EGFR-targeting agents," concluded the study authors. (onclive.com)
  • This study identified a new secondary resistance mechanism of gefitinib in STS, and developed new strategies to improve the effectiveness of EGFR inhibition particularly by blocking the STAT3 pathway. (oncotarget.com)
  • We demonstrated that seven STS cell lines of diverse histological origin showed resistance to gefitinib despite blockade of phosphorylated EGFR (pEGFR) and downstream signal transducers (pAKT and pERK) in PI3K/AKT and RAS/ERK pathways. (oncotarget.com)
  • One of the hallmarks of cancer is heterogeneity and I have previously demonstrated that tumor heterogeneity within NSCLC cells lines harboring EGFR kinase domain mutations gives rise to divergent resistance mechanisms in response to treatment. (luc.edu)
  • While NSCLC cells with acquired EGFR TKI resistance and EMT phenotype did not exhibit growth advantage in vitro, a 50% epithelial EGFR TKI sensitive and 50% mesenchymal EGFR TKI resistant admix provided significant growth advantage in vivo assessed by caliper measurement. (luc.edu)
  • I have discovered that epithelial EGFR TKI sensitive cells secrete a significant amount of VEGF-A and cells with acquired/transient EGFR TKI resistance with an EMT phenotype secrete substantial amount of EDN1. (luc.edu)
  • Informed by a literature search, I hypothesized that the presence of EDN1 in the tumor microenvironment contributes positively to EGFR TKI resistance, possibly through the vasoconstrictive property of EDN1. (luc.edu)
  • I observed that epithelial/mesenchymal admix tumors and ectopic overexpression of EDN1 in EGFR-mutated HCC827 cells conferred significantly more resistance to gefitinib in vivo. (luc.edu)
  • However, after a median duration of response of ~12 months, all patients develop tumor resistance, and in over half of these patients this is due to the emergence of the EGFR T790M resistance mutation. (researchgate.net)
  • 17-AAG alone delayed, but did not completely inhibit, the growth of H1650 and H1975 xenografts, two EGFR mutant models which show intermediate and high levels of gefitinib resistance. (elsevierpure.com)
  • These data suggest that Hsp90 inhibition in combination with chemotherapy may represent an effective treatment strategy for patients whose tumors express EGFR kinase domain mutations, including those with de novo and acquired resistance to EGFR TKIs. (elsevierpure.com)
  • Studying models of therapeutic resistance, we have observed that SCC cells that become refractory to PI3Kα inhibition maintain PI3K-independent activation of the mammalian target of rapamycin (mTOR). (iucc.ac.il)
  • non-canonical EGFR-Met interactions are implicated in resistance to anti-cancer drugs but have not been previously detected in drug-naïve cells. (nature.com)
  • It is unclear to what extent the lack of response in KRAS wild-type CRC is due to BRAF mutations, but data suggest that mutated BRAF confers resistance to anti-EGFR therapy given beyond first-line treatment. (medscape.com)
  • A reversible SRC-relayed COX2 inflammatory program drives resistance to BRAF and EGFR inhibition in BRAFV600E colorectal tumors. (ucsfhealth.org)
  • They have been associated with resistance to anti-EGFR drugs. (cancernetwork.com)
  • In this analysis, investigators evaluated the ability of AFM24 to elicit antibody-dependent cellular phagocytosis in solid tumor cell lines expressing EGFR wild-type or EGFR signaling pathway mutations. (onclive.com)
  • First-generation EGFR TKIs, binding competitively and reversibly to the ATP-binding site of the EGFR tyrosine kinase domain, have resulted in a significant improvement in outcome for NSCLC patients with activating EGFR mutations (L858R and Del19). (researchgate.net)
  • The second-generation EGFR/HER TKIs were developed to treat resistant disease, targeting not only T790M but EGFR-activating mutations and wild-type EGFR. (researchgate.net)
  • The third-generation EGFR TKIs selectively and irreversibly target EGFR T790M and activating EGFR mutations, showing promising efficacy in NSCLC resistant to the first- and second-generation EGFR TKIs. (researchgate.net)
  • Currently, the first-generation gefitinib and erlotinib and second-generation afatinib have been approved for first-line treatment of metastatic NSCLC with activating EGFR mutations. (researchgate.net)
  • We find that the EGFR mutations found most commonly in patients with lung adenocarcinoma who respond to EGFR TKIs are potently degraded by 17-AAG. (elsevierpure.com)
  • First generation EGFR TKIs (gefitinib, erlotinib) provide significant clinical benefit for NSCLC cancer patients with oncogenic EGFR mutations. (rcsb.org)
  • Tumour-associated activating mutations in EGFR can identify patients with NSCLC who are likely to have a good response to TKIs. (bmj.com)
  • A number of techniques have been employed for genotypic assessment of tumour-associated DNA to identify EGFR mutations, each of which has advantages and disadvantages. (bmj.com)
  • Angiogenesis in NSCLC has been identified as important therapeutic target in combination with EGFR TKIs. (luc.edu)
  • Among the third-generation EGFR TKIs, osimertinib is today the only drug approved by the Food and Drug Administration and the European Medicines Agency to treat metastatic EGFR T790M NSCLC patients who have progressed on or after EGFR TKI therapy. (researchgate.net)
  • I present experimental evidence that a subpopulation of NSCLC cells with EGFR TKI-induced EMT contributes toward the attenuation of the response to EGFR TKI therapy. (luc.edu)
  • This result led us to hypothesize that EDN1 may reduce MVD in EGFR-mutated NSCLC tumors leading to poor EGFR TKI penetrance in vivo. (luc.edu)
  • Taken together, I suggest that inhibition of the EDN1 signaling system may be an important component to a blood vascular-based approach to treatment of EGFR-mutation positive NSCLC. (luc.edu)
  • Although they exhibited promising anti-T790M activity in the laboratory, their clinical activity among T790M+ NSCLC was poor mainly because of dose-limiting toxicity due to simultaneous inhibition of wild-type EGFR. (researchgate.net)
  • 3 The development of molecular targeted therapies aimed at these molecular alterations has generated great optimism for the treatment of cancers such as NSCLC, and drugs targeting the EGFR tyrosine kinase domain are now available. (bmj.com)
  • AFM24 enhances macrophage-mediated antibody-dependent cellular phagocytosis of various EGFR-expressing tumor cell lines, irrespective of the EGFR signaling pathway," wrote lead study author Sheena Pinto, PhD, translational project leader at Affimed, and coauthors, in the poster. (onclive.com)
  • Therefore, we suggest that silibinin prevents the EGFR signaling pathway and may be used as an effective drug for the inhibition of metastasis of human breast cancer. (iiarjournals.org)
  • In this study, we investigated the effect of silibinin on EGFR signaling pathway and EGF ligand-induced CD44 expression in breast cancer cells. (iiarjournals.org)
  • We have further shown that knock-out of YAP sensitizes non-small cell lung cancer to EGFR inhibitor Erlotinib. (novartis.com)
  • Prior erlotinib, gefitinib or lapatinib therapy or prior exposure to any investigational EGFR or panErbB reversible or irreversible inhibitor or any prior panitumumab or investigational EGFR-directed monoclonal antibody. (yalemedicine.org)
  • We investigated the effects of TAK-285, a novel, investigational, dual EGFR/HER2 inhibitor that has been shown to penetrate the CNS and has comparable inhibitory efficacy to lapatinib which is a known Pgp substrate. (jcancer.org)
  • As reported in the Journal of Clinical Oncology by Maron et al, a retrospective study found that use of EGFR inhibitor therapy was associated with benefit in patients with unresectable or metastatic EGFR-amplified gastroesophageal adenocarcinoma. (ascopost.com)
  • As such, our goal was to develop a highly potent irreversible inhibitor with the largest selectivity ratio between the drug-resistant double mutants (L858R/T790M, Del/T790M) and WT EGFR. (rcsb.org)
  • In vivo, DHA treatment enhanced AREG production following DE exposure, whereas EGFR inhibitor-treated mice exhibited reduced AREG in their lung homogenates. (cdc.gov)
  • Canertinib (CI-1033) is an irreversible tyrosine-kinase inhibitor with activity against EGFR (IC50 0.8 nM), HER-2 (IC50 19 nM) and ErbB-4 (IC50 7 nM). (adooq.com)
  • Compound 56 is a cell-permeable, reversible, and ATP-competitive inhibitor of tyrosine kinase activity of EGFR. (adooq.com)
  • That is why it is important to add neprilysin inhibition to either an ACE-inhibitor or an ARB. (medscape.com)
  • EGFR inhibition rapidly induced enhanced gene expression of the EGF, betacellulin and neuregulin-1 ligands along with HER2, HER3 and HER4 receptors in the DU145 cells. (udg.edu)
  • In mouse and rat xenograft tumor models, TAK-285 showed antitumor activity against cancers that expressed HER2 or EGFR. (jcancer.org)
  • ErbB receptors comprise a family of four RTKs (EGFR/ErbB1, Her2/ErbB2, Her3/ErbB3 and Her4/ErbB4) with important roles in normal cell physiology and in cancer 1 . (nature.com)
  • Our research shows that HER2-targeted therapies, specifically dual anti-HER2 inhibition, is a promising strategy in patients with HER2-positive, RAS wild-type CRC. (cancernetwork.com)
  • The innate cell engager AFM24 showed greater efficacy in eliciting antibody-dependent cellular phagocytosis of EGFR wild-type and KRAS-mutant tumor cells compared with cetuximab. (onclive.com)
  • The innate cell engager ® (ICE) AFM24 showed greater efficacy in eliciting antibody-dependent cellular phagocytosis of EGFR wild-type and KRAS -mutant tumor cells compared with cetuximab (Erbitux), according to preclinical findings from a study presented in a poster during the 2021 SITC Annual Meeting . (onclive.com)
  • To do so, monocyte-differentiated macrophages from healthy donor peripheral blood mononuclear cells were co-cultured for 4 hours with CMFDA-labeled, wild-type EGFR-expressing or KRAS -mutant tumor cells in the presence of 10 µg/mL of AFM24 or cetuximab. (onclive.com)
  • Moreover, AFM24 was superior to cetuximab in eliciting phagocytosis in EGFR -positive cells in live cell imaging analysis over 24 hours. (onclive.com)
  • As the immunohistochemistry of the primary tumor from the right lower leg was positive for EGFR (Fig. 2 c), the patient received cetuximab with a loading dose of 400 mg/m 2 and afterwards 250 mg/m 2 weekly for about 6 months. (biomedcentral.com)
  • We compare this to our previous study of the cetuximab/EGFR interaction. (rcsb.org)
  • The only approved targeted therapy for HNSCC is the EGFR antibody Cetuximab. (kcl.ac.uk)
  • Given these findings, AFM24 is now being evaluated in a phase 1/2 trial (NCT04259450) in patients with advanced EGFR -positive solid tumors. (onclive.com)
  • I indirectly tested poor EGFR TKI penetrance by examining phosphorylated EGFR and found maintenance of the signal in admix and mesenchymal tumors. (luc.edu)
  • EGFR staining of 10 RDEB-related SCCs is positive in all tumors, although there is a notable variability among different tumors. (biomedcentral.com)
  • Studies of tumours at relapse have demonstrated expression of a T790M mutation in exon 20 of the EGFR TK domain in approximately 50% of cases. (bmj.com)
  • We also show that EGFR is frequently expressed in DEB-associated SCCs, although there were noticeable differences in the level of expression, which may influence responsiveness to EGFR-targeting therapies. (biomedcentral.com)
  • However, therapies targeting EGFR have demonstrated limited effectiveness in PCa. (udg.edu)
  • The academics believe these findings will have very important implications in the design of future clinical trials with ani-EGFR as well as other targeted therapies, suggesting the future use of these drugs needs to be considered in the context of the molecular makeup of the cancer. (kcl.ac.uk)
  • 17-AAG treatment, at its maximal tolerated dose, caused a significant delay in H3255 (L858R EGFR) xenograft growth but was less effective than the EGFR TKI gefitinib. (elsevierpure.com)
  • Multifunctional Nanopolymers for Blood-Brain Barrier Delivery and Inhibition of Glioblastoma Growth through EGFR/EGFRvIII, c-Myc, and PD-1. (cedars-sinai.edu)
  • Additional results showed that AFM24 increased antibody-dependent cellular phagocytosis of EGFR -positive tumor cells regardless of macrophage subtype. (onclive.com)
  • EGFR is over-expressed by many tumor cells. (wikipedia.org)
  • The Fab, or fragment antigen binding region of the antibody, binds to the antigen on the EGFr expressing tumor cells. (wikipedia.org)
  • Here we describe the mechanism of EGFR inhibition by an antibody drug IMC-11F8. (rcsb.org)
  • Patients with metastatic CRC who are being considered for anti-EGFR antibody therapy should be tested for the presence of a KRAS mutation prior to therapy. (medscape.com)
  • Furthermore, this synergistic effect can be attenuated by VEGFR2/EDNRA dual inhibition. (luc.edu)
  • Genetic ablation or pharmacological inhibition of tankyrase prominently suppresses YAP activity and YAP target gene expression. (novartis.com)
  • Surprisingly, ectopic overexpression of EDN1 in EGFR- mutated HCC827 cells resulted in significant growth retardation in vivo. (luc.edu)
  • A potential mechanism to overcome EGFR blockade in cancer cells is the autocrine activation of alternative receptors of the human EGFR (HER) family through the overexpression of the HER receptors and ligands. (udg.edu)
  • Amphiregulin (AREG), an EGFR ligand, mediates tissue repair and wound healing in the lung epithelium. (cdc.gov)
  • Receptor tyrosine kinases including EGFR, HER-2 and c-Met and non receptor tyrosine kinase including Jaks are selectively expressed in primary tissue and metastatic tumour of advanced ovarian cancer cells. (otago.ac.nz)
  • We present an overview of the various cutaneous side-effects associated with EGFR inhibition and discuss their respective therapeutic options. (skintherapyletter.com)
  • it remains unclear whether patients with KRAS wild-type CRC will definitely respond, although these individuals may be able to derive some benefit from anti-EGFR therapy. (medscape.com)
  • In addition, silibinin suppressed the EGF-induced phosphorylation of EGFR and extracellular signal-regulated kinase1/2 (ERK1/2), a downstream signaling molecule of EGFR. (iiarjournals.org)
  • In animal models, a single dose of 17-AAG was sufficient to induce degradation of mutant EGFR and inhibit downstream signaling. (elsevierpure.com)
  • TAK-285 was examined in a model of breast cancer brain metastasis using direct intracranial injection of BT-474-derived luciferase-expressing cells and showed greater inhibition of brain tumor growth compared to animals treated with lapatinib. (jcancer.org)
  • Across all dose levels, average steady-state plasma PF-04691502 concentrations approximated or exceeded the target concentration of 16.2 ng/mL required for ≥75 % tumor growth inhibition in preclinical models. (researchgate.net)
  • epidermal growth element receptor (EGFR) website II, the interface of EGFR dimerization, with high reactivity toward the prospective surface patch of EGFR website II. (healthyconnectionsinc.com)
  • We have applied this method to the development of proteins that bind epidermal growth element receptor (EGFR) website II. (healthyconnectionsinc.com)
  • In-vitro antiplasmodial efficacy of 4,7-dichloroquinoline revealed a significant growth inhibition of both sensitive strains of Plasmodium falciparum with IC 50 values of 6.7 nM (CQ-s) and 8.5 nM (CQ-r). (nature.com)
  • The purpose of this study was to assess the effect of gene alterations and tyrosine kinase inhibition (TKI) on median survival (MS) and cause of death (CoD) in patients with BM from lung adenocarcinoma (L-adeno). (healthpartners.com)
  • CONCLUSION: EGFR and ALK gene alterations are associated with delayed onset of BM and longer MS relative to patients without these alterations. (healthpartners.com)
  • No dose adjustment is needed in patients with mild renal impairment (eGFR between 60 and 90 mL/minute). (who.int)
  • CV012 trade name] should not be used in patients with severe renal impairment (eGFR less than 30 mL/minute, including patients with end-stage renal disease on haemodialysis) (see sections 4.4 and 5.2). (who.int)
  • An analysis of patients in the PARAMOUNT trial (designed to look at heart failure with preserved ejection fraction (HFpEF) showed that treatment with LCZ696 for 36 weeks led to slightly better eGFR than valsartan. (medscape.com)
  • These data indicate that EGFR/Src/HMG-CR is a new pathway mediating doxorubicin -induced cell death and that cholesterol control could be combined with doxorubicin treatment to enhance efficacy and thus reduce side effects. (bvsalud.org)
  • e Quantification of organoid survival, 4 days after inhibition of EGFR, MEK, ERK and/or induction of BRAFV600E, as in panel (b). (researchgate.net)
  • EGFR, which is also known as ErbB1 and HER1, is one of the most extensively analyzed proteins, and plays important roles in many cancers, including colorectal and lung malignancy [21]C[24]. (healthyconnectionsinc.com)
  • In a multivulva model of Caenorhabditis elegans expressing an active-EGFR mutant, doxorubicin decreased hyperplasia more efficiently in the absence than in the presence of cholesterol . (bvsalud.org)
  • Targeted Inhibition of EGFR and Glutaminase Induces Metabolic Crisis in EGFR Mutant Lung Cancer. (uclahealth.org)
  • The gene expression of the four EGFR/HER receptors and seven ligands of the HER family was analyzed by real-time PCR prior to and after each treatment. (udg.edu)
  • Interestingly, aux depletion causes a dramatic increase in EGFR signaling, with a strong accumulation of EGFR at the plasma membrane and an increased expression of EGFR ligands in response to tissue stress. (sdbonline.org)
  • Tested against a panel of 96 kinases, TAK-285 showed specificity for inhibition of HER family kinases. (jcancer.org)
  • Finally, blocking EGFR signaling completely suppresses the defects caused by aux depletion. (sdbonline.org)
  • Here, we also studied the effect of silibinin on EGFR ligand-induced CD44 expression, which is a hallmark of metastasis in various cancer cells. (iiarjournals.org)
  • Anti-cancer effect of doxorubicin is mediated by downregulation of HMG-Co A reductase via inhibition of EGFR/Src pathway. (bvsalud.org)
  • Here we exploit the multiplexing capabilities of Exchange-PAINT, a multiplexed variant of DNA-PAINT 14 , to image simultaneously five RTKs (EGFR, ErbB2, ErbB3, IGF-1R and Met) at endogenous levels of expression in BT20 cancer cells and to examine how receptor distribution changes following ligand stimulation. (nature.com)
  • This study investigated how AREG, DHA, and EGFR modulate lung repair processes following dust-induced injury. (cdc.gov)
  • Our findings may have clinical implications for optimising EGFR-targeted therapy in STS. (oncotarget.com)
  • The inhibition of neprilysin alone (in the form of candoxatril) was studied back in 1993 and reported in the journal Clinical Science . (medscape.com)
  • We report the X-ray crystal structure of the Fab fragment of IMC-11F8 (Fab11F8) in complex with the entire extracellular region and with isolated domain III of EGFR. (rcsb.org)
  • Interestingly, we observed that EGFR ligand-induced CD44 and matrix metalloproteinase-9 (MMP-9) expression was reduced by silibinin treatment in a dose-dependent manner. (iiarjournals.org)
  • The MS from first treatment for BM for EGFR and ALK-, EGFR+, ALK+ were 14, 23 (P (healthpartners.com)
  • b Quantification of the mean EGFR staining in tumor sections after normalization to keratin 14 staining in adjacent sections. (biomedcentral.com)
  • Specifically, it binds to the EGFR Domain III on the cell surface. (wikipedia.org)
  • AFM24 is a tetravalent ICE which can bind CD16A and EGFR, the latter of which is overexpressed in many solid cancers and can be associated with poor prognosis. (onclive.com)
  • Here, we stained 10 RDEB-gen sev-associated SCCs of different differentiation grades for EGFR expression. (biomedcentral.com)
  • Although the expression of wild-type EGFR was also down-regulated by 17-AAG, its degradation required higher concentrations of drug and a longer duration of drug exposure. (elsevierpure.com)
  • They also appear to have lower incidences of toxicity due to the limited inhibitory effect on wild-type EGFR. (researchgate.net)
  • This activity is mediated by YAP inhibition and not Wnt/β-catenin inhibition. (novartis.com)
  • disables inhibition of NF-kappa-B DNA-binding activity. (lu.se)
  • Inhibition of tankyrase or depletion of RNF146 stabilizes angiomotins. (novartis.com)
  • By using machine learning and subsequent biochemical validation we detect ligand-dependent, non-canonical interaction of EGFR and Met. (nature.com)
  • In all EGFR stained positive, although there was considerable heterogeneity in the staining intensity (Fig. 1 ). (biomedcentral.com)
  • Doxorubicin -induced HMG-CR downregulation was associated with inactivation of the EGFR-Src pathway. (bvsalud.org)
  • Another liability of the first generation drugs is severe adverse events driven by inhibition of WT EGFR. (rcsb.org)