13 Matching Annotations
  1. Mar 2026
    1. RET fusions as primary oncogenic drivers and secondary acquired resistance to EGFR tyrosine kinase inhibitors in patients with non-small-cell lung cancer

      [Paper-level Aggregated] PMCID: PMC9441062

      Evidence Type(s): Oncogenic

      Summary: Mutation: G719C | Summary: The G719C mutation is part of a double-mutant patient cohort, indicating its contribution to tumor development in the context of acquired RET fusions.

      Evidence Type: Oncogenic Mutation: L858R | Summary: The L858R mutation is identified in a significant proportion of patients, suggesting its role in tumor development in NSCLC.

      Evidence Type: Oncogenic Mutation: S768I | Summary: The S768I mutation is included in a double-mutant patient cohort, indicating its contribution to tumor development in the context of acquired RET fusions.

      Gene→Variant (gene-first): EGFR(1956):G719C EGFR(1956):L858R EGFR(1956):S768I

      Genes: EGFR(1956)

      Variants: G719C L858R S768I

    2. RET fusions as primary oncogenic drivers and secondary acquired resistance to EGFR tyrosine kinase inhibitors in patients with non-small-cell lung cancer

      [Paper-level Aggregated] PMCID: PMC9441062

      Evidence Type(s): Prognostic

      Summary: Mutation: L858R | Summary: The L858R mutation is associated with prognosis in NSCLC patients, as indicated by the analysis of progression-free survival (PFS) among patients with this mutation compared to wild-type counterparts.

      Gene→Variant (gene-first): EGFR(1956):L858R

      Genes: EGFR(1956)

      Variants: L858R

    3. RET fusions as primary oncogenic drivers and secondary acquired resistance to EGFR tyrosine kinase inhibitors in patients with non-small-cell lung cancer

      [Paper-level Aggregated] PMCID: PMC9441062

      Evidence Type(s): Predictive

      Summary: Mutation: T790M | Summary: The T790M mutation is associated with resistance to EGFR-TKIs, indicating its role in treatment response.

      Evidence Type: Predictive Mutation: C797S/G | Summary: The C797S/G mutation is identified as a resistance mechanism to EGFR-TKIs, suggesting its relevance in therapy response.

      Evidence Type: Predictive Mutation: L718V/Q | Summary: The L718V/Q mutation is noted as a potential resistance mechanism to EGFR-TKIs, highlighting its impact on treatment sensitivity.

      Gene→Variant (gene-first): EGFR(1956):T790M EGFR(1956):C797S/G EGFR(1956):L718V/Q

      Genes: EGFR(1956)

      Variants: T790M C797S/G L718V/Q

    4. To characterize the AR mechanism through RET fusions in EGFR-mutated NSCLC patients and their survival outcomes, we compared the PFS among patients treated with different EGFR-TKI regimens. However, no significant differ

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 15

      Evidence Type(s): Prognostic

      Summary: Evidence Type: Prognostic | Mutation: L858R | Summary: The L858R mutation is associated with prognosis in NSCLC patients, as indicated by the analysis of progression-free survival (PFS) among patients with this mutation compared to wild-type counterparts.

      Gene→Variant (gene-first): 1956:L858R

      Genes: 1956

      Variants: L858R

    5. Despite their rarity, it is clear from previous studies that RTK fusions, such as RET rearrangements, are actionable resistance mechanisms to EGFR-TKIs. We aim to increase awareness of this emerging paradigm by comprehen

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 14

      Evidence Type(s): Predictive

      Summary: Evidence Type: Predictive | Mutation: T790M | Summary: The T790M mutation is associated with resistance to EGFR-TKIs, indicating its role in treatment response. Evidence Type: Predictive | Mutation: C797S/G | Summary: The C797S/G mutation is identified as a resistance mechanism to EGFR-TKIs, suggesting its relevance in therapy response. Evidence Type: Predictive | Mutation: L718V/Q | Summary: The L718V/Q mutation is noted as a potential resistance mechanism to EGFR-TKIs, highlighting its impact on treatment sensitivity.

      Gene→Variant (gene-first): 1956:C797S/G 1956:L718V/Q 1956:T790M

      Genes: 1956

      Variants: C797S/G L718V/Q T790M

    6. In the baseline cohort, 58.9% of patients were under 60 years (58.9% vs. 41.1%, P < 0.001), and the proportion of females was significantly higher than males (55.3% vs. 44.7%, P = 0.038, Table 1). Of the 71 patients with

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 4

      Evidence Type(s): Oncogenic

      Summary: Evidence Type: Oncogenic | Mutation: G719C | Summary: The G719C mutation is part of a double-mutant patient cohort, indicating its contribution to tumor development in the context of acquired RET fusions. Evidence Type: Oncogenic | Mutation: L858R | Summary: The L858R mutation is identified in a significant proportion of patients, suggesting its role in tumor development in NSCLC. Evidence Type: Oncogenic | Mutation: S768I | Summary: The S768I mutation is included in a double-mutant patient cohort, indicating its contribution to tumor development in the context of acquired RET fusions.

      Gene→Variant (gene-first): 1956:G719C 1956:L858R 1956:S768I

      Genes: 1956

      Variants: G719C L858R S768I

  2. Feb 2026
    1. RET fusions as primary oncogenic drivers and secondary acquired resistance to EGFR tyrosine kinase inhibitors in patients with non-small-cell lung cancer

      [Paper-level Aggregated] PMCID: PMC9441062

      Evidence Type(s): Oncogenic, Predictive, Prognostic

      Justification: Oncogenic: The presence of EGFR mutations, including L858R and G719C/S768I, is associated with oncogenic activity in NSCLC, as they are known to drive tumorigenesis. Predictive: The identified second-site EGFR mutations, such as T790M and C797S/G, are recognized as predictive markers for resistance to EGFR-TKIs, indicating their role in treatment response. Prognostic: The study reports that certain genetic alterations, including bypass pathway mutations and co-mutations of TP53 and RB1, are associated with significantly shorter progression-free survival (PFS) in patients treated with EGFR-TKIs, highlighting their prognostic significance.

      Gene→Variant (gene-first): EGFR(1956):C797S/G EGFR(1956):L718V/Q EGFR(1956):T790M EGFR(1956):G719C EGFR(1956):L858R EGFR(1956):S768I

      Genes: EGFR(1956)

      Variants: C797S/G L718V/Q T790M G719C L858R S768I

    2. To characterize the AR mechanism through RET fusions in EGFR-mutated NSCLC patients and their survival outcomes, we compared the PFS among patients treated with different EGFR-TKI regimens. However, no significant differ

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 15

      Evidence Type(s): Diagnostic, Prognostic

      Justification: Diagnostic: The passage mentions that patients with L858R mutations were included in a refined cohort, indicating that this variant is used to classify or define a specific group of patients with EGFR mutations in NSCLC. Prognostic: The passage discusses the progression-free survival (PFS) of patients with specific mutations, including L858R, suggesting that this variant correlates with disease outcome independent of therapy.

      Gene→Variant (gene-first): 1956:L858R

      Genes: 1956

      Variants: L858R

    3. Despite their rarity, it is clear from previous studies that RTK fusions, such as RET rearrangements, are actionable resistance mechanisms to EGFR-TKIs. We aim to increase awareness of this emerging paradigm by comprehen

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 14

      Evidence Type(s): Predictive, Oncogenic

      Justification: Predictive: The passage discusses how the variants T790M, C797S/G, and L718V/Q are associated with resistance mechanisms to EGFR-TKIs, indicating their role in treatment response. Oncogenic: The variants mentioned are described as second-site mutations that contribute to resistance in the context of tumor development and progression in NSCLC.

      Gene→Variant (gene-first): 1956:C797S/G 1956:L718V/Q 1956:T790M

      Genes: 1956

      Variants: C797S/G L718V/Q T790M

    4. In the baseline cohort, 58.9% of patients were under 60 years (58.9% vs. 41.1%, P < 0.001), and the proportion of females was significantly higher than males (55.3% vs. 44.7%, P = 0.038, Table 1). Of the 71 patients with

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 4

      Evidence Type(s): Diagnostic, Oncogenic

      Justification: Diagnostic: The passage states that all 71 patients harbored baseline EGFR mutations, including specific variants, indicating their role in defining the patient cohort and confirming the presence of a disease subtype (NSCLC). Oncogenic: The mention of EGFR mutations, including G719C, L858R, and S768I, suggests that these somatic variants contribute to tumor development or progression in the context of non-small cell lung cancer (NSCLC).

      Gene→Variant (gene-first): 1956:G719C 1956:L858R 1956:S768I

      Genes: 1956

      Variants: G719C L858R S768I

    5. To characterize the AR mechanism through RET fusions in EGFR-mutated NSCLC patients and their survival outcomes, we compared the PFS among patients treated with different EGFR-TKI regimens. However, no significant differ

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 15

      Evidence Type(s): Diagnostic, Prognostic

      Justification: Diagnostic: The passage mentions that patients with L858R mutations were included in a refined cohort, indicating that this variant is used to classify or define a specific group of patients with EGFR mutations in NSCLC. Prognostic: The passage discusses the progression-free survival (PFS) of patients with specific mutations, including L858R, suggesting that this variant correlates with disease outcome independent of therapy.

      Gene→Variant (gene-first): 1956:L858R

      Genes: 1956

      Variants: L858R

    6. Despite their rarity, it is clear from previous studies that RTK fusions, such as RET rearrangements, are actionable resistance mechanisms to EGFR-TKIs. We aim to increase awareness of this emerging paradigm by comprehen

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 14

      Evidence Type(s): Predictive, Oncogenic

      Justification: Predictive: The passage discusses how the variants T790M, C797S/G, and L718V/Q are associated with resistance mechanisms to EGFR-TKIs, indicating their role in treatment response. Oncogenic: The variants mentioned are described as second-site mutations that contribute to resistance in the context of tumor development and progression in NSCLC.

      Gene→Variant (gene-first): 1956:C797S/G 1956:L718V/Q 1956:T790M

      Genes: 1956

      Variants: C797S/G L718V/Q T790M

    7. In the baseline cohort, 58.9% of patients were under 60 years (58.9% vs. 41.1%, P < 0.001), and the proportion of females was significantly higher than males (55.3% vs. 44.7%, P = 0.038, Table 1). Of the 71 patients with

      [Paragraph-level] PMCID: PMC9441062 Section: RESULTS PassageIndex: 4

      Evidence Type(s): Diagnostic, Oncogenic

      Justification: Diagnostic: The passage states that all 71 patients harbored baseline EGFR mutations, including specific variants, indicating their role in defining the patient cohort and confirming the presence of a disease subtype (NSCLC). Oncogenic: The mention of EGFR mutations, including G719C, L858R, and S768I, suggests that these somatic variants contribute to tumor development or progression in the context of non-small cell lung cancer (NSCLC).

      Gene→Variant (gene-first): 1956:G719C 1956:L858R 1956:S768I

      Genes: 1956

      Variants: G719C L858R S768I