15 Matching Annotations
  1. Mar 2026
    1. Phase I, Open-Label, Dose-Escalation/Dose-Expansion Study of Lifirafenib (BGB-283), an RAF Family Kinase Inhibitor, in Patients With Solid Tumors

      [Paper-level Aggregated] PMCID: PMC7325368

      Evidence Type(s): Oncogenic

      Summary: Mutation: B-RAFV600E | Summary: The B-RAFV600E mutation contributes to tumor development and progression in various cancers, including melanoma and thyroid cancer, as indicated by its presence in these cancer types and the observed treatment responses in patients.

      Evidence Type: Oncogenic Mutation: G13D | Summary: The K-RAS G13D mutation contributes to tumor development or progression, as it is part of the K-RAS mutations observed in patients with endometrial cancer and NSCLC.

      Gene→Variant (gene-first): BRAF(673):B-RAFV600E KRAS(3845):G13D

      Genes: BRAF(673) KRAS(3845)

      Variants: B-RAFV600E G13D

    2. Phase I, Open-Label, Dose-Escalation/Dose-Expansion Study of Lifirafenib (BGB-283), an RAF Family Kinase Inhibitor, in Patients With Solid Tumors

      [Paper-level Aggregated] PMCID: PMC7325368

      Evidence Type(s): Predictive

      Summary: Mutation: B-RAFV600E | Summary: The B-RAFV600E mutation is associated with responses to therapy, including partial responses (PR) and stable disease (SD) in clinical studies. It is also linked to treatment sensitivity in patients with B-RAF-mutated solid tumors, including melanoma, thyroid cancer, and low-grade serous ovarian cancer.

      Evidence Type: Predictive Mutation: G13D | Summary: The K-RAS G13D mutation is associated with treatment response, as patients with K-RAS mutations, including G13D, had confirmed responses and stable disease (SD) in the context of therapy.

      Gene→Variant (gene-first): BRAF(673):B-RAFV600E KRAS(3845):G13D

      Genes: BRAF(673) KRAS(3845)

      Variants: B-RAFV600E G13D

    3. The maximum tolerated dose was established as 40 mg/d; dose-limiting toxicities included reversible thrombocytopenia and nonhematologic toxicity. Across the entire study, the most common grade >= 3 treatment-emergent adv

      [Paragraph-level] PMCID: PMC7325368 Section: ABSTRACT PassageIndex: 6

      Evidence Type(s): Predictive, Oncogenic

      Summary: Evidence Type: Predictive | Mutation: B-RAFV600E | Summary: The B-RAFV600E mutation is associated with treatment responses in patients with melanoma, thyroid cancer, and low-grade serous ovarian cancer, indicating its predictive value for therapy outcomes. Evidence Type: Oncogenic | Mutation: B-RAFV600E | Summary: The B-RAFV600E mutation is implicated in tumor development and progression in various cancers, including melanoma and thyroid cancer, supporting its classification as an oncogenic variant.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E

    4. Lifirafenib is an investigational, reversible inhibitor of B-RAFV600E, wild-type A-RAF, B-RAF, C-RAF, and EGFR. This first-in-human, phase I, dose-escalation/dose-expansion study evaluated the safety, tolerability, and e

      [Paragraph-level] PMCID: PMC7325368 Section: ABSTRACT PassageIndex: 2

      Evidence Type(s): Predictive, Oncogenic

      Summary: Evidence Type: Predictive | Mutation: B-RAFV600E | Summary: The B-RAFV600E mutation is associated with the response to the investigational therapy lifirafenib, indicating its predictive value for treatment sensitivity in patients with B-RAF-mutated solid tumors. Evidence Type: Oncogenic | Mutation: B-RAFV600E | Summary: The B-RAFV600E mutation contributes to tumor development or progression, as it is mentioned in the context of solid tumors with B-RAF mutations.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E

    5. Across the entire study, 2 patients with K-RAS mutations (endometrial cancer [20 mg/d] and codon 12-mutated NSCLC [30 mg/d], n = 1 each) had confirmed responses, which resulted in an ORR of 3.4%; 32 patients (54.2%) with

      [Paragraph-level] PMCID: PMC7325368 Section: RESULTS PassageIndex: 11

      Evidence Type(s): Predictive, Oncogenic

      Summary: Evidence Type: Predictive | Mutation: G13D | Summary: The K-RAS G13D mutation is associated with treatment response, as patients with K-RAS mutations, including G13D, had confirmed responses and stable disease (SD) in the context of therapy. Evidence Type: Oncogenic | Mutation: G13D | Summary: The K-RAS G13D mutation contributes to tumor development or progression, as it is part of the K-RAS mutations observed in patients with endometrial cancer and NSCLC.

      Gene→Variant (gene-first): 3845:G13D

      Genes: 3845

      Variants: G13D

    6. Patients with B-RAF and K-RAS mutations from both phases had responses (Table 3). Among patients with B-RAF mutations, 8 (15.1%) of 53 achieved PR, including 1 patient with melanoma who received prior RAF inhibitor thera

      [Paragraph-level] PMCID: PMC7325368 Section: RESULTS PassageIndex: 10

      Evidence Type(s): Predictive, Oncogenic

      Summary: Evidence Type: Predictive | Mutation: B-RAFV600E | Summary: The B-RAFV600E mutation is associated with responses to therapy, as evidenced by patients achieving partial responses (PR) and stable disease (SD) in clinical studies. Evidence Type: Oncogenic | Mutation: B-RAFV600E | Summary: The B-RAFV600E mutation contributes to tumor development and progression, as indicated by its presence in various cancer types and the observed treatment responses in patients.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E

  2. Feb 2026
    1. Phase I, Open-Label, Dose-Escalation/Dose-Expansion Study of Lifirafenib (BGB-283), an RAF Family Kinase Inhibitor, in Patients With Solid Tumors

      [Paper-level Aggregated] PMCID: PMC7325368

      Evidence Type(s): Oncogenic, Predictive, Prognostic

      Justification: Oncogenic: The presence of B-RAFV600E and K-RAS mutations is associated with specific responses to treatment, indicating their role in tumorigenesis and cancer progression. Predictive: The study evaluates the efficacy of lifirafenib, a B-RAFV600E inhibitor, suggesting that the presence of this mutation can predict response to the treatment. Prognostic: The outcomes of patients with B-RAF and K-RAS mutations, including response rates and duration of response, provide prognostic information regarding their disease course and treatment efficacy.

      Gene→Variant (gene-first): BRAF(673):B-RAFV600E KRAS(3845):G13D

      Genes: BRAF(673) KRAS(3845)

      Variants: B-RAFV600E G13D

    2. The maximum tolerated dose was established as 40 mg/d; dose-limiting toxicities included reversible thrombocytopenia and nonhematologic toxicity. Across the entire study, the most common grade >= 3 treatment-emergent adv

      [Paragraph-level] PMCID: PMC7325368 Section: ABSTRACT PassageIndex: 6

      Evidence Type(s): Predictive, Diagnostic

      Justification: Predictive: The passage discusses the response of patients with B-RAFV600E mutations to therapy, indicating a correlation between the variant and treatment outcomes in various cancers. Diagnostic: The mention of B-RAFV600E in the context of specific cancer types suggests its use as a biomarker to classify or define these diseases.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E

    3. Lifirafenib is an investigational, reversible inhibitor of B-RAFV600E, wild-type A-RAF, B-RAF, C-RAF, and EGFR. This first-in-human, phase I, dose-escalation/dose-expansion study evaluated the safety, tolerability, and e

      [Paragraph-level] PMCID: PMC7325368 Section: ABSTRACT PassageIndex: 2

      Evidence Type(s): Predictive, Oncogenic

      Justification: Predictive: The passage discusses lifirafenib as an inhibitor specifically targeting B-RAFV600E, indicating a correlation with response to therapy in patients with B-RAF-mutated tumors. Oncogenic: The mention of B-RAFV600E in the context of mutated solid tumors suggests that this somatic variant contributes to tumor development or progression.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E

    4. Across the entire study, 2 patients with K-RAS mutations (endometrial cancer [20 mg/d] and codon 12-mutated NSCLC [30 mg/d], n = 1 each) had confirmed responses, which resulted in an ORR of 3.4%; 32 patients (54.2%) with

      [Paragraph-level] PMCID: PMC7325368 Section: RESULTS PassageIndex: 11

      Evidence Type(s): Predictive, Diagnostic, Oncogenic

      Justification: Predictive: The passage discusses the confirmed responses and stable disease (SD) in patients with K-RAS mutations, including G13D, indicating a correlation with treatment response. Diagnostic: The mention of K-RAS mutations, including G13D, in the context of specific cancer types (endometrial cancer and NSCLC) suggests its role in classifying or defining these diseases. Oncogenic: The reference to K-RAS mutations, including G13D, contributing to tumor development in specific cancer types supports the classification of this variant as oncogenic.

      Gene→Variant (gene-first): 3845:G13D

      Genes: 3845

      Variants: G13D

    5. Patients with B-RAF and K-RAS mutations from both phases had responses (Table 3). Among patients with B-RAF mutations, 8 (15.1%) of 53 achieved PR, including 1 patient with melanoma who received prior RAF inhibitor thera

      [Paragraph-level] PMCID: PMC7325368 Section: RESULTS PassageIndex: 10

      Evidence Type(s): Predictive, Oncogenic

      Justification: Predictive: The passage discusses the responses of patients with B-RAF mutations to therapy, indicating a correlation between the B-RAFV600E variant and treatment response, which is characteristic of predictive evidence. Oncogenic: The B-RAFV600E variant is mentioned in the context of patients with B-RAF-mutated tumors, suggesting its role in tumor development or progression, which aligns with oncogenic evidence.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E

    6. The maximum tolerated dose was established as 40 mg/d; dose-limiting toxicities included reversible thrombocytopenia and nonhematologic toxicity. Across the entire study, the most common grade >= 3 treatment-emergent adv

      [Paragraph-level] PMCID: PMC7325368 Section: ABSTRACT PassageIndex: 6

      Evidence Type(s): Predictive, Diagnostic

      Justification: Predictive: The passage discusses the response of patients with B-RAFV600E mutations to therapy, indicating a correlation between the variant and treatment outcomes in various cancers. Diagnostic: The mention of B-RAFV600E in the context of specific cancer types suggests its use as a biomarker to classify or define these diseases.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E

    7. Lifirafenib is an investigational, reversible inhibitor of B-RAFV600E, wild-type A-RAF, B-RAF, C-RAF, and EGFR. This first-in-human, phase I, dose-escalation/dose-expansion study evaluated the safety, tolerability, and e

      [Paragraph-level] PMCID: PMC7325368 Section: ABSTRACT PassageIndex: 2

      Evidence Type(s): Predictive, Oncogenic

      Justification: Predictive: The passage discusses lifirafenib as an inhibitor specifically targeting B-RAFV600E, indicating a correlation with response to therapy in patients with B-RAF-mutated tumors. Oncogenic: The mention of B-RAFV600E in the context of mutated solid tumors suggests that this somatic variant contributes to tumor development or progression.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E

    8. Across the entire study, 2 patients with K-RAS mutations (endometrial cancer [20 mg/d] and codon 12-mutated NSCLC [30 mg/d], n = 1 each) had confirmed responses, which resulted in an ORR of 3.4%; 32 patients (54.2%) with

      [Paragraph-level] PMCID: PMC7325368 Section: RESULTS PassageIndex: 11

      Evidence Type(s): Predictive, Diagnostic, Oncogenic

      Justification: Predictive: The passage discusses the confirmed responses and stable disease (SD) in patients with K-RAS mutations, including G13D, indicating a correlation with treatment response. Diagnostic: The mention of K-RAS mutations, including G13D, in the context of specific cancer types (endometrial cancer and NSCLC) suggests its role in classifying or defining these diseases. Oncogenic: The reference to K-RAS mutations, including G13D, contributing to tumor development in specific cancer types supports the classification of this variant as oncogenic.

      Gene→Variant (gene-first): 3845:G13D

      Genes: 3845

      Variants: G13D

    9. Patients with B-RAF and K-RAS mutations from both phases had responses (Table 3). Among patients with B-RAF mutations, 8 (15.1%) of 53 achieved PR, including 1 patient with melanoma who received prior RAF inhibitor thera

      [Paragraph-level] PMCID: PMC7325368 Section: RESULTS PassageIndex: 10

      Evidence Type(s): Predictive, Oncogenic

      Justification: Predictive: The passage discusses the responses of patients with B-RAF mutations to therapy, indicating a correlation between the B-RAFV600E variant and treatment response, which is characteristic of predictive evidence. Oncogenic: The B-RAFV600E variant is mentioned in the context of patients with B-RAF-mutated tumors, suggesting its role in tumor development or progression, which aligns with oncogenic evidence.

      Gene→Variant (gene-first): 673:B-RAFV600E

      Genes: 673

      Variants: B-RAFV600E