CASP8
Overview
CASP8 (Caspase-8) is a key initiator caspase in the extrinsic apoptosis pathway, activated by death receptor signaling (e.g., FAS/FASL, TRAIL). Somatic mutations in CASP8 impair apoptotic signaling, conferring a survival advantage to tumor cells. CASP8 is among the significantly mutated genes identified in head and neck squamous cell carcinoma (HNSCC) by large-scale whole-exome sequencing.
Alterations observed in the corpus
- CASP8 mutated in 8% of HNSCC tumors by whole-exome sequencing of 74 tumor-normal pairs; identified by MutSig analysis as a significantly mutated gene associated with apoptosis suppression (Broad Institute cohort, hnsc_broad) PMID:21798893
- CASP8 mutations identified in breast cancer WES of 100 tumors, implicating apoptotic pathway disruption in breast tumorigenesis PMID:22722201
- Mutated in 10% (4/40) of oral squamous cell carcinoma (OSCC); nonsense/splice/frameshift mutations consistent with loss-of-function; defines a molecular subtype with fewer CNAs and co-occurring HRAS mutations; CASP8 loss promotes aggressive xenograft phenotype PMID:23619168
- Mutated in 23.1% of cSCC (differentiation-related); significant driver in cutaneous squamous cell carcinoma PMID:25303977
- Clustered missense and inactivating mutations in 9% of HNSCC (279-tumor TCGA cohort; 92% of mutations in oral cavity); anti-correlated with 11q13 amplification; co-mutated with HRAS in M-class oral-cavity subset PMID:25631445
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Cancer types (linked)
- HNSC: CASP8 somatic mutation rate of 8% in whole-exome sequencing cohort (n=74 tumor-normal pairs); functional consequence is suppression of extrinsic apoptosis pathway PMID:21798893
Co-occurrence and mutual exclusivity
- CASP8 mutations co-occur in the context of broad HNSCC mutational landscape alongside TP53, CDKN2A, NOTCH1, and PIK3CA alterations PMID:21798893
- DDX3X mutations also classified as apoptosis-related in the same cohort PMID:21798893
Therapeutic relevance
- CASP8 inactivation may contribute to resistance to apoptosis-inducing therapies including TRAIL-based agents; no specific therapeutic strategies targeting CASP8-mutant HNSCC reported in this study.
Open questions
- Specific mutation types in CASP8 (missense, truncating, splice) were not detailed in this study; functional consequences of individual mutations remain uncharacterized.
Sources
- PMID:21798893 — The Mutational Landscape of Head and Neck Squamous Cell Carcinoma (Stransky et al., Science 2011)
This page was processed by crosslinker on 2026-05-14. - PMID:22722201
This page was processed by crosslinker on 2026-05-14. - PMID:23619168
This page was processed by crosslinker on 2026-05-14. - PMID:25303977
This page was processed by crosslinker on 2026-05-14. - PMID:25631445
This page was processed by crosslinker on 2026-05-14. - PMID:28988769
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