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    1. EGFR blockade in GBM brain tumor stem cells synergizes with JAK2/STAT3 pathway inhibition to abrogate compensatory mechanisms in vitro and in vivo

      [Paper-level Aggregated] PMCID: PMC7086303

      Evidence Type(s): Oncogenic, Predictive

      Justification: Oncogenic: The G598V mutation in EGFR is described as an activating mutation that influences the sensitivity of BTSC cultures to afatinib, indicating its role in promoting tumor growth and response to treatment. Predictive: The presence of the G598V mutation is associated with increased sensitivity to afatinib, suggesting that it can predict the effectiveness of this treatment in BTSC cultures.

      Gene→Variant (gene-first): EGFR(1956):G598V

      Genes: EGFR(1956)

      Variants: G598V

    2. We first asked whether the EGFR inhibitor afatinib could reduce BTSC viability and sphere formation, using alamarBlue and neurosphere assays. Afatinib inhibited BTSC growth and sphere-forming capacity in a dose-dependent

      [Paragraph-level] PMCID: PMC7086303 Section: RESULTS PassageIndex: 3

      Evidence Type(s): Predictive, Oncogenic

      Justification: Predictive: The passage discusses how the G598V mutation influences the sensitivity of BTSC cultures to the EGFR inhibitor afatinib, indicating a correlation with treatment response. Oncogenic: The G598V mutation is described as an activating mutation in the context of EGFR, suggesting its role in tumor development or progression.

      Gene→Variant (gene-first): 1956:G598V

      Genes: 1956

      Variants: G598V