[Paper-level Aggregated] PMCID: PMC4821611

Evidence Type(s): Oncogenic

Summary: Mutation: p.C1156Y | Summary: The mutation p.C1156Y contributes to tumor development or progression, as it is found in a significant percentage of RNA-seq reads in patient #1 and was detected in post-treatment tumor samples, particularly in the context of crizotinib resistance.

Evidence Type: Oncogenic Mutation: p.G1269A | Summary: The mutation p.G1269A is present in 100% of the RNA-seq reads in patient #3 and was also found in post-treatment tumor samples, indicating its role in tumor development or progression related to crizotinib resistance.

Gene→Variant (gene-first): ALK(238):p.C1156Y ALK(238):p.G1269A

Genes: ALK(238)

Variants: p.C1156Y p.G1269A

[Paper-level Aggregated] PMCID: PMC4821611

Evidence Type(s): Predictive

Summary: Mutation: p.C1156Y | Summary: The mutation p.C1156Y in the ALK gene has been reported to confer resistance against crizotinib, indicating a correlation with treatment response.

Evidence Type: Predictive Mutation: p.G1269A | Summary: No supporting paragraph-level outputs for this evidence type.

Gene→Variant (gene-first): ALK(238):p.C1156Y ALK(238):p.G1269A

Genes: ALK(238)

Variants: p.C1156Y p.G1269A

[Paragraph-level] PMCID: PMC4821611 Section: ABSTRACT PassageIndex: 1

Evidence Type(s): Oncogenic

Summary: Evidence Type: Oncogenic | Mutation: p.C1156Y | Summary: The ALK mutation p.C1156Y was detected in post-treatment tumor samples, indicating its contribution to tumor development or progression, particularly in the context of crizotinib resistance. Evidence Type: Oncogenic | Mutation: p.G1269A | Summary: The ALK mutation p.G1269A was also found in post-treatment tumor samples, suggesting its role in tumor development or progression related to crizotinib resistance.

Gene→Variant (gene-first): 238:p.C1156Y 238:p.G1269A

Genes: 238

Variants: p.C1156Y p.G1269A

[Paragraph-level] PMCID: PMC4821611 Section: RESULTS PassageIndex: 10

Evidence Type(s): Predictive, Oncogenic

Summary: Evidence Type: Predictive | Mutation: p.C1156Y | Summary: The mutation p.C1156Y in the ALK gene has been reported to confer resistance against crizotinib, indicating a correlation with treatment response. Evidence Type: Oncogenic | Mutation: p.C1156Y | Summary: The mutation p.C1156Y contributes to tumor development or progression as it is found in a significant percentage of RNA-seq reads in patient #1. Evidence Type: Oncogenic | Mutation: p.G1269A | Summary: The mutation p.G1269A is present in 100% of the RNA-seq reads in patient #3, indicating its role in tumor development or progression.

Gene→Variant (gene-first): 238:c.3467G>A 238:c.3806G>C 238:p.C1156Y 238:p.G1269A

Genes: 238

Variants: c.3467G>A c.3806G>C p.C1156Y p.G1269A

[Paper-level Aggregated] PMCID: PMC4821611

Evidence Type(s): Oncogenic, Predictive

Justification: Oncogenic: The presence of ALK mutations (p.C1156Y and p.G1269A) in post-treatment tumor samples indicates their role in conferring resistance to crizotinib, suggesting an oncogenic function in the context of non-small cell lung cancer. Predictive: The identification of specific ALK mutations associated with resistance to crizotinib suggests that these mutations can predict treatment outcomes in patients with ALK-positive non-small cell lung cancer.

Gene→Variant (gene-first): ALK(238):c.3467G>A ALK(238):c.3806G>C ALK(238):p.C1156Y ALK(238):p.G1269A

Genes: ALK(238)

Variants: c.3467G>A c.3806G>C p.C1156Y p.G1269A

[Paragraph-level] PMCID: PMC4821611 Section: ABSTRACT PassageIndex: 1

Evidence Type(s): Predictive, Oncogenic

Justification: Predictive: The passage discusses ALK mutations (p.C1156Y and p.G1269A) in the context of crizotinib resistance, indicating a correlation between these variants and resistance to the therapy. Oncogenic: The ALK mutations are described as being detected in post-treatment tumor samples, suggesting their contribution to tumor development or progression in the context of crizotinib resistance.

Gene→Variant (gene-first): 238:p.C1156Y 238:p.G1269A

Genes: 238

Variants: p.C1156Y p.G1269A

[Paragraph-level] PMCID: PMC4821611 Section: RESULTS PassageIndex: 10

Evidence Type(s): Predictive, Oncogenic

Justification: Predictive: The passage discusses mutations in the ALK gene, specifically p.C1156Y and p.G1269A, which have been reported to confer resistance against crizotinib, indicating a correlation with treatment response. Oncogenic: The presence of mutations in the ALK gene, such as p.C1156Y and p.G1269A, suggests that these somatic variants contribute to tumor development or progression, as they were identified in post-treatment tumor samples.

Gene→Variant (gene-first): 238:c.3467G>A 238:c.3806G>C 238:p.C1156Y 238:p.G1269A

Genes: 238

Variants: c.3467G>A c.3806G>C p.C1156Y p.G1269A

[Paragraph-level] PMCID: PMC4821611 Section: ABSTRACT PassageIndex: 1

Evidence Type(s): Predictive, Oncogenic

Justification: Predictive: The passage discusses ALK mutations (p.C1156Y and p.G1269A) in the context of crizotinib resistance, indicating a correlation between these variants and resistance to the therapy. Oncogenic: The ALK mutations are described as being detected in post-treatment tumor samples, suggesting their contribution to tumor development or progression in the context of crizotinib resistance.

Gene→Variant (gene-first): 238:p.C1156Y 238:p.G1269A

Genes: 238

Variants: p.C1156Y p.G1269A

[Paragraph-level] PMCID: PMC4821611 Section: RESULTS PassageIndex: 10

Evidence Type(s): Predictive, Oncogenic

Justification: Predictive: The passage discusses mutations in the ALK gene, specifically p.C1156Y and p.G1269A, which have been reported to confer resistance against crizotinib, indicating a correlation with treatment response. Oncogenic: The presence of mutations in the ALK gene, such as p.C1156Y and p.G1269A, suggests that these somatic variants contribute to tumor development or progression, as they were identified in post-treatment tumor samples.

Gene→Variant (gene-first): 238:c.3467G>A 238:c.3806G>C 238:p.C1156Y 238:p.G1269A

Genes: 238

Variants: c.3467G>A c.3806G>C p.C1156Y p.G1269A