Sentences with phrase «in epidermal growth factor receptor»

Zhang, Y. and Wolf - Yadlin, A. and Ross, P. L. and Pappin, D. J. and Rush, J. and Lauffenburger, D. A. and White, F. M. (2005) Time - resolved mass spectrometry of tyrosine phosphorylation sites in the epidermal growth factor receptor signaling network reveals dynamic modules.

Approximately 10 - 15 % of Caucasian and 30 - 35 % of Asian patients with NSCLC have a mutation in the epidermal growth factor receptor (EGFR), which can be successfully targeted with EGFR inhibitors called tyrosine kinase inhibitors (TKI), such as erlotinib, gefitinib and afatinib.

The advent of therapies directed at tumors with mutations in epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), and B - Raf proto - oncogene (BRAF) genes over the past decade have dramatically changed outcomes, he says.

Between 10 and 30 percent of NSCLC cases are driven by mutations in the epidermal growth factor receptor (EGFR) gene.

Not exact matches

Here, we report that capsaicin has a cocarcinogenic effect on 12 - O - tetradecanoylphorbol -13-acetate (TPA)-- promoted skin carcinogenesis in vivo and is mediated through the epidermal growth factor receptor (EGFR), but not the transient receptor potential vanilloid subfamily member 1 (TRPV1).

High total and saturated fat intake were associated with greater risk of estrogen receptor - and progesterone receptor - positive (ER+PR +) breast cancer (BC), and human epidermal growth factor 2 receptor - negative (HER2 --RRB- disease, according to a new study published April 9 in the Journal of the National Cancer Institute.

Clinically important findings suggest that targeting the epidermal growth factor receptor (EGFR) and the fibroblast growth factor receptor (FGFR) cellular pathways may benefit thousands of patients with this disease, according to the study published today in the journal PLOS Genetics.

By using a range of tissue stains, they were able to assess levels of oestrogen receptor (ER), progesterone receptor (PR) and HER2 — human epidermal growth factor — in order to divide the samples into four subtypes.

«CRKII most likely regulates the stability of mutated epidermal growth factor receptors and drives cancer growth by promoting signaling, or communication, within cancer cells,» said Julia Petschnigg, lead author on the paper and a postdoctoral fellow at U of T. «We found that a combinatorial chemotherapy that inhibits those mutated receptors and CRKII could be beneficial in treating lung cancer.»

Multiplexed genetic screening for epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) gene rearrangements and subsequent biomarker - guided treatment is cost - effective compared with standard chemotherapy treatment without any molecular testing in the metastatic non-small cell lung cancer (NSCLC) setting in the United States.

Among patients with advanced non-small cell lung cancer without a mutation of a certain gene (EGFR), conventional chemotherapy, compared with treatment using epidermal growth factor receptor tyrosine kinase inhibitors, was associated with improvement in survival without progression of the cancer, but not with overall survival, according to a study in the April 9 issue of JAMA.

Patients with epidermal growth factor receptor (EGFR) expressing advanced squamous non-small-cell lung cancer benefit most from necitumumab added to gemcitabine and cisplatin chemotherapy, according to a subgroup analysis from the SQUIRE trial presented today at the European Lung Cancer Conference (ELCC) 2016 in Geneva, Switzerland.

Epidermal growth factor receptor (EGFR) mutations found in the circulating free tumor DNA (ctDNA) from the plasma of advanced non-small cell lung cancer (NSCLC) patients correlates well with the EGFR mutations from patient - matched tumor tissue DNA.

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are the preferred treatment option for patients with advanced non-small cell lung cancer (NSCLC) who have mutations in the EGFR gene.

Human epidermal growth factor receptor 2 (HER2) is upregulated in a subset of human breast cancers.

They found higher levels of JAK1 in resistant tumors, which caused increased expression of epidermal growth factor receptor (EGFR)-- a receptor tyrosine kinase that promotes cell proliferation.

Researchers at the San Diego Supercomputer Center (SDSC) and the Moores Cancer Center at the University of California, San Diego, have described for the first time the molecular mechanism of cancer development caused by well - known «resistance» mutations in the gene called epidermal growth factor receptor (EGFR).

The study, called «Molecular Determinants of Drug - Specific Sensitivity for Epidermal Growth Factor Receptor (EGFR) Exon 19 and 20 Mutants in Non-Small Cell Lung Cancer,» and published online in the journal Oncotarget, demonstrates how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patients.

Osimertinib binds tightly to a protein, epidermal growth factor receptor (EGFR), which is overexpressed in many tumours.

Epidermal growth factor receptor (EGFR) signal transduction plays a major role in growth, proliferation and differentiation of mammalian cells.

Josef Singer and Judith Fazekas, both lead authors of the study, discovered that a receptor frequently found on human tumor cells (epidermal growth factor receptor or EGFR) is nearly 100 percent identical with the EGF receptor in dogs.

Two studies are providing new insight into germline epidermal growth factor receptor (EGFR) T790M mutation in familial non-small cell lung cancer (NSCLC).

Alice Shaw recalls a signal moment in 2004 — just as she was finishing her oncology fellowship at MIT — when scientists discovered that mutations in a gene for epidermal growth factor receptor (EGFR) were the culprits in about 10 to 15 percent of lung cancer patients.

One of the key metabolic alterations that takes place during EMT is that of the epidermal growth factor receptor (EGFR) which is a pathway that regulates growth, survival, proliferation, and differentiation in mammalian cells.

The researchers, including scientists from pharmaceutical company AstraZeneca, report in an advanced online publication in Nature Medicine on May 4, that their findings indicate «an underappreciated genomic heterogeneity» in mechanisms of resistance to tyrosine kinase inhibitor (TKI) drugs that target the Epidermal Growth Factor Receptor (EGFR) mutation that drive some cases of non-small cell lung cancer (NSCLC).

microRNA - 7 inhibits the epidermal growth factor receptor and the Akt pathway and is down - regulated in glioblastoma

Changes in cell junctions induced by inhibition of epidermal growth factor receptor in oral squamous cell carcinoma cells.

An Open Label, Phase II Study of Neratinib in Patients with Solid Tumors with Somatic Human Epidermal Growth Factor Receptor (EGFR, HER2, HER3) Mutations or EGFR Gene Amplification

In addition to causing proteins to be secreted through general pathways from the cell and pathways involving metalloproteases, PMA specifically causes activation of an epidermal growth factor receptor (EGFR).

The epidermal growth factor receptor responsive miR - 125a represses mesenchymal morphology in ovarian cancer cells.

Drugs that target specificity proteins downregulate epidermal growth factor receptor in bladder cancer cells.

Aberrant epithelial morphology and persistent epidermal growth factor receptor signaling in a mouse model of renal carcinoma.

Dual targeting of the epidermal growth factor receptor using the combination of cetuximab and erlotinib: preclinical evaluation and results of the phase II DUX study in chemotherapy - refractory, advanced colorectal cancer.

DENVER — Leptomeningeal metastases (LM), a devastating complication and predictor of poor survival in lung cancer patients, was found to be more prevalent in non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations.

Mucosal melanomas with mutations in CDK4 may respond to palbociclib or ribociclib, which have demonstrated activity in advanced hormone receptor — positive, human epidermal growth factor receptor 2 — negative breast cancer.

A major challenge for assessing driver mutations, such as epidermal growth factor receptor (EGFR) mutations, in advanced disease is the scarcity of suitable biopsy tissue for molecular testing.

The most commonly mutated oncogene in NSCLC is the epidermal growth factor receptor (EGFR).

His graduate work at Yale University involved making lots of mutations in the transmembrane region of the epidermal growth factor receptor (EGFR) and collecting data on which mutations affected dimerization.

Along the same lines, in non-small cell lung cancer (NSCLC), acquired resistance to Gefitinib / Erlotinib kinase inhibitors has also been associated with a secondary mutation of the gatekeeper Thr790 residue of the epidermal growth factor receptor (EGFR).

Current studies focus mainly on two receptor systems - the mast cell surface receptor, FcεRI, and the receptor for epidermal growth factor that operate in immunological and cell proliferation responses.

The epidermal growth factor receptor (EGFR) pathway is a complex signaling cascade that is involved in the development and progression of cancer.

Epidermal growth factor receptor, also called EGFR, is a biomarker found in certain patients with lung cancer.

In addition to RIPK2 binding as part of this computer - based (initial) screening, we selected compounds that inhibited epidermal growth factor receptor (IC50 values > 1000 nM; weak inhibitory activity) along with weak binding interactions in the EGFR and c - ABL binding sites, two common off - targets for previously identified RIPK2 inhibitorIn addition to RIPK2 binding as part of this computer - based (initial) screening, we selected compounds that inhibited epidermal growth factor receptor (IC50 values > 1000 nM; weak inhibitory activity) along with weak binding interactions in the EGFR and c - ABL binding sites, two common off - targets for previously identified RIPK2 inhibitorin the EGFR and c - ABL binding sites, two common off - targets for previously identified RIPK2 inhibitors.

These results, also presented at the 2015 European Cancer Congress (ECC2015, abstract # 5BA) today, which involve the group of 1,626 patients with a Recurrence Score between 0 and 10, demonstrated that 99.3 percent of node - negative, estrogen receptor (ER)- positive, human epidermal growth factor receptor 2 (HER2)- negative patients who met accepted guidelines for recommending chemotherapy in addition to hormonal therapy, had no distant recurrence at five years after treatment with hormonal therapy alone.

Many women are «triple negative» No one yet knows precisely why, but African - American women are roughly twice as likely as white women to have triple - negative breast cancer — so called because tumor cells in this particularly aggressive form of the disease test negative for estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER - 2).

In vivo, breast cancer growth is regulated by estrogens and peptide growth factors, such as epidermal growth factor (EGF), the receptor of which has intrinsic PTK activity.

In highly proliferative lesions with increased Ki67, estrogen receptor was negative, but human epidermal growth factor receptor 2 was usually positive with a distribution that was similar to that reported for human intraepithelial lesions (7).