Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers.
By H. Shigematsu, Li Lin, Takao Takahashi, M. Nomura, Makoto Suzuki, I. Wistuba, K. Fong, Hue Lee, S. Toyooka, N. Shimizu and 6 more. Journal of the National Cancer Institute, 2006
2,410 citations recorded by the source corpus.
Subfields: Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/c004dc240a05e96ec2f2088e8d259de054e6ab13
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In Oncology
- Adi F. Gazdar
- J. Engelman
- Jin-Yuan Shih
- P. Jänne
- Ping Wee
- William C. Hahn
- Zhixiang Wang
- Gregory Riely
In Pulmonary and Respiratory Medicine
Citations in the corpus
- AZD9291 in EGFR inhibitor-resistant non-small-cell lung cancer. (2015, neutral): “Any adverse event leading to drug discontinuation that was considered to be drug-related 2 (10) 0 1 (1) 3 (5) 1 (5) 7 (3)”
- Targeting the EGFR signaling pathway in cancer therapy (2012, background): “EGFR somatic mutations are inimitable and are a more common trait for a subset of NSCLC patients (women, East Asians, nonsmokers), although infrequent, it was also found in squamous cell carcinomas of the lung and other epithelial malignancies [114,115].”
- Mechanisms of Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non–Small Cell Lung Cancer (2008, background): “EGFR mutations are present more frequently in never-smokers, females, those with adenocarcinoma, and in patients of East Asian ethnicity (9).”
- An allosteric mechanism for activation of the kinase domain of epidermal growth factor receptor. (2006, background): “An adjacent leucine residue (Leu837) is mutated to glutamine in some lung cancer patients (Shigematsu et al., 2005).”
- Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “In the kinase domain, the most commonly seen EGFR point mutation is L858R, and makes up approximately 45% of mutations in the tyrosine kinase domain [81,82].”
- Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK. (2009, methodology): “based on clinical features commonly associated with EGFR mutation.(20,21) As a result, the cohort of screened patients was enriched for women, for never/light smokers, and for patients with adenocarcinomas or adenocarcinomas with bronchioloalveolar features (ie, BAC; Table 1).”
- Identification of a Novel Biomarker, SEMA5A, for Non–Small Cell Lung Carcinoma in Nonsmoking Women (2010, background): “Cancer Res 2008; :6913–21. ng DW, Leung EL, So KK, et al. The EML4-ALK fusion gene is olved in various histologic types of lung cancers from nonsmokers h wild-type EGFR and KRAS.”