Epidermal growth factor receptor mutations in lung cancer

By Sreenath V. Sharma, D. Bell, J. Settleman, D. Haber. Nature Reviews. Cancer, 2007

3,159 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/e4a0a41af9424cc8629137a017f18a11c36f89d3

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In Molecular Biology

In Oncology

In Pulmonary and Respiratory Medicine

Citations in the corpus

Drug development of MET inhibitors: targeting oncogene addiction and expedience (2008, background): “Rational identification of responsive tumours Experience with EGFR tyrosine kinase inhibitors has demonstrated that they are only efficacious in a small subset of tumours, those that exhibit genetic alterations of the receptor itsel”
A gene expression signature associated with "K-Ras addiction" reveals regulators of EMT and tumor cell survival. (2009, background): “Clinically, this is seen in BCR-ABL-expressing chronic myelogenous leukemias and EGFR mutant non-small cell lung cancer (NSCLC) (Sharma et al., 2007).”
An overview of the c-MET signaling pathway (2011, background): “This phenomenon is known as ‘oncogene addiction’ and applies to all settings where cancer cells appear to be dependent on a single overactive oncogene for their proliferation and survival [Sharma et al. 2007; Sharma and Settleman, 2007].”
The crucial role of protein phosphorylation in cell signaling and its use as targeted therapy (Review) (2017, neutral): “Alteration of the phosphoproteome also affects gastrointestinal stromal tumors (GISTs) (98,99), lung cancer (73,100), hematologic malignancies (101,102), breast cancer (103,104), pancreatic cancer (105,106) and prostate cancer (103,107).”
Phase III study of afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations. (2013, background): “on epidermal growth factor receptor (EGFR) pathway signaling.(1) The addiction to EGFR signaling leaves the cancers uniquely susceptible to selective oral EGFR tyrosine kinase inhibitors (TKIs),(1) and patients with advanced EGFR-mutant non–smallcell lung cancer (NSCLC) may experience dramatic”
Metastasis: from dissemination to organ-specific colonization (2009, background): “Lung adenocarcinomas with epidermal growth factor receptor ( EGFR ) mutations respond to EGFR kinase inhibitors but frequently relapse owing to secondary EGFR mutations that confer resistanc”
Triple Negative Breast Cancer Cell Lines: One Tool in the Search for Better Treatment of Triple Negative Breast Cancer (2010, background): “, HER-2/Neu targeted therapies for HER-2/ Neu in breast cancers containing HER-2/Neu amplification or EGFR TKIs in lung cancer patients with activating EGFR mutations [71, 72]).”
Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer (2010, neutral): “gov/drugdictionary/?CdrID=453548">neratinib ; Wyeth), showed promising preclinical result”
EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer (2010, background): “Approximately 50–70% of cases of acquired drug resistance in non-small-cell lung cancer patients treated with EGFR inhibitors involve genetic changes including T790M ‘gatekeeper’ mutations in EGFR or amplification of the MET oncogene (Engelman et al., 2007; Sharma et al., 2007).”
Anoikis molecular pathways and its role in cancer progression. (2013, background): “Indeed, overexpression of EGF and ErbB2 receptors, a common feature of tumors, activatesMAPK signaling inducing Bimdegradation and blocking anoikis [201].”
WNT/TCF signaling through LEF1 and HOXB9 mediates lung adenocarcinoma metastasis (2009, background): “Prominent tumor-initiating events in lung adenocarcinoma include KRAS and EGFR mutations (Rodenhuis et al., 1988; Sharma et al., 2007).”
Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, positive): “This strategy has proven successful for the protein kinase oncogenes BCR-ABL (imatinib/Gleevec), EGFR (gefitinib/Iressa, erlotinib/Tarceva), and HER2 (trastuzumab/Herceptin) (Druker, 2002; Roberts and Der, 2007; Sharma et al., 2007), and efforts toward inhibition of BRAF, MDM2, and the lipid kinase ”