Skin Cutaneous Melanoma (Broad, Cell 2012)
Overview
The Broad melanoma dataset comprises 121 qualified melanoma tumor/normal pairs from 135 patients profiled by whole-exome sequencing. The study (Hodis et al., Cell 2012) focused on SKCM (cutaneous melanoma) with representation from multiple sample types (primary tumors, metastatic samples, short-term cultures from metastatic tissue). The cohort was used to discover six novel melanoma driver genes using the InVEx permutation statistical framework, which accounts for the high UV-induced somatic mutation background characteristic of melanoma.
Composition
- 121 qualified tumor/normal pairs from 135 melanoma patients
- Subtypes: 95 cutaneous, 5 acral, 2 mucosal, 1 uveal, 18 unknown primary
- Sample types: 15 primary tumors, 30 metastatic, 76 short-term cultures from metastatic tissue
- Validation extension sets: n=59, n=63, and n=175 additional melanoma samples (Sequenom genotyping)
- Cancer type: SKCM, MEL
Assays / panels (linked)
- whole-exome-seq — solution-phase hybrid capture; 103-fold mean target coverage
- affymetrix-snp6 — copy-number analysis with GISTIC
- gistic — applied to SNP 6.0 copy-number data
- sequenom-genotyping — validation genotyping in extension sets
Papers using this cohort
- PMID:22817889 — Hodis et al. Cell 2012 primary analysis
Notable findings derived from this cohort
- Median somatic mutation rate 14.4 coding mutations/Mb (highest of any tumor type at the time); 82.2% UV-signature C>T transitions PMID:22817889
- Six novel significantly mutated melanoma genes identified: PPP6C, RAC1, SNX31, TACC1, STK19, ARID2 PMID:22817889
- RAC1 P29S validated as gain-of-function, UV-induced driver at 3.9% prevalence across discovery + extension sets (14/355 patients) PMID:22817889
- 83% of samples had hotspot BRAF or NRAS mutations (mutually exclusive, p=3e-14); PTEN loss co-occurred with BRAF (44%) but rarely with NRAS (4%) PMID:22817889
- NF1 loss-of-function enriched in BRAF/NRAS-WT melanomas (25% vs 2%, p=5.8e-3) PMID:22817889
Sources
- PMID:22817889 — Hodis et al. Cell 2012
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