[Paper-level Aggregated] PMCID: PMC5021039

Evidence Type(s): Predictive, Oncogenic, Functional

Justification: Predictive: The text discusses the effectiveness of targeted therapies based on specific EGFR mutations, indicating that the presence of these mutations can predict the response to treatments like gefitinib, erlotinib, and afatinib. Oncogenic: The mention of somatic mutations in the EGFR gene being present in lung adenocarcinomas suggests that these mutations contribute to the development of cancer. Functional: The text implies that certain mutations, such as G719X, E709K, S768I, and L861Q, have functional implications in terms of their sensitivity to specific EGFR-tyrosine kinase inhibitors, indicating their role in the biological activity of the receptor.

Gene→Variant (gene-first): EGFR(1956):E709K EGFR(1956):G719X EGFR(1956):L858R EGFR(1956):L861Q EGFR(1956):S768I

Genes: EGFR(1956)

Variants: E709K G719X L858R L861Q S768I

[Paragraph-level] PMCID: PMC5021039 Section: ABSTRACT PassageIndex: 1

Evidence Type(s): Predictive, Oncogenic

Justification: Predictive: The passage discusses the response rates of various EGFR mutations, including E709K, G719X, L858R, and L861Q, to targeted therapies such as gefitinib and erlotinib, indicating their correlation with treatment sensitivity. Oncogenic: The passage mentions that somatic mutations in the EGFR gene, including the variants listed, are present in lung adenocarcinomas and contribute to tumor development, which supports their classification as oncogenic.

Gene→Variant (gene-first): 1956:E709K 1956:G719X 1956:L858R 1956:L861Q 1956:S768I

Genes: 1956

Variants: E709K G719X L858R L861Q S768I