5 Matching Annotations
  1. Mar 2026
    1. A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS-mutant lung cancers

      [Paper-level Aggregated] PMCID: PMC10805385

      Evidence Type(s): Oncogenic

      Summary: Mutation: G12C | Summary: The G12C mutation in KRAS is associated with tumor development, as indicated by its presence in primary KRAS-mutant tumors and patient-derived xenograft models.

      Evidence Type: Oncogenic Mutation: G245V | Summary: The G245V mutation in TP53 is present in a KRAS-mutant tumor context, suggesting its contribution to tumor development and progression in the analyzed patient-derived xenograft models.

      Gene→Variant (gene-first): KRAS(3845):G12C TP53(7157):G245V

      Genes: KRAS(3845) TP53(7157)

      Variants: G12C G245V

    2. HOXC10 is overexpressed in 51% of primary KRAS-mutant tumors (Figure 3A; TCGA, >= 2SD over expression in normal lung), consistent with observations in cell lines (Figure 2B). By analyzing KRAS-mutant tumor/normal matched

      [Paragraph-level] PMCID: PMC10805385 Section: RESULTS PassageIndex: 17

      Evidence Type(s): Oncogenic

      Summary: Evidence Type: Oncogenic | Mutation: G12C | Summary: The G12C mutation in KRAS is associated with tumor development, as indicated by its presence in primary KRAS-mutant tumors and patient-derived xenograft models. Evidence Type: Oncogenic | Mutation: G245V | Summary: The G245V mutation in TP53 is present in a KRAS-mutant tumor context, suggesting its contribution to tumor development and progression in the analyzed patient-derived xenograft models.

      Gene→Variant (gene-first): 3845:G12C 7157:G245V

      Genes: 3845 7157

      Variants: G12C G245V

  2. Feb 2026
    1. A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS-mutant lung cancers

      [Paper-level Aggregated] PMCID: PMC10805385

      Evidence Type(s): Oncogenic, Predictive

      Justification: Oncogenic: The text indicates that HOXC10 is overexpressed in KRAS-mutant tumors, specifically mentioning the KRAS G12C variant, which is known to be associated with oncogenic activity in cancer. Predictive: The mention of robust HOXC10 expression in a patient-derived xenograft model with the KRAS G12C variant suggests that HOXC10 expression may predict response to treatment with MEK/BET inhibitors, indicating its potential as a predictive biomarker.

      Gene→Variant (gene-first): KRAS(3845):G12C TP53(7157):G245V

      Genes: KRAS(3845) TP53(7157)

      Variants: G12C G245V

    2. HOXC10 is overexpressed in 51% of primary KRAS-mutant tumors (Figure 3A; TCGA, >= 2SD over expression in normal lung), consistent with observations in cell lines (Figure 2B). By analyzing KRAS-mutant tumor/normal matched

      [Paragraph-level] PMCID: PMC10805385 Section: RESULTS PassageIndex: 17

      Evidence Type(s): Oncogenic, Predictive

      Justification: Oncogenic: The passage discusses the overexpression of HOXC10 in KRAS-mutant tumors, specifically mentioning the genotype KRAS G12C/TP53 G245V, indicating that these somatic variants contribute to tumor development or progression. Predictive: The passage mentions the efficacy of combined MEK/BET inhibitors causing tumor regression in KRAS-mutant patient-derived xenograft models, suggesting a correlation between the variants and response to therapy.

      Gene→Variant (gene-first): 3845:G12C 7157:G245V

      Genes: 3845 7157

      Variants: G12C G245V

    3. HOXC10 is overexpressed in 51% of primary KRAS-mutant tumors (Figure 3A; TCGA, >= 2SD over expression in normal lung), consistent with observations in cell lines (Figure 2B). By analyzing KRAS-mutant tumor/normal matched

      [Paragraph-level] PMCID: PMC10805385 Section: RESULTS PassageIndex: 17

      Evidence Type(s): Oncogenic, Predictive

      Justification: Oncogenic: The passage discusses the overexpression of HOXC10 in KRAS-mutant tumors, specifically mentioning the genotype KRAS G12C/TP53 G245V, indicating that these somatic variants contribute to tumor development or progression. Predictive: The passage mentions the efficacy of combined MEK/BET inhibitors causing tumor regression in KRAS-mutant patient-derived xenograft models, suggesting a correlation between the variants and response to therapy.

      Gene→Variant (gene-first): 3845:G12C 7157:G245V

      Genes: 3845 7157

      Variants: G12C G245V