Desmoplastic Melanoma (DESM)
Overview
Desmoplastic melanoma (DESM) is a rare, deeply invasive cutaneous melanoma variant characterized by prominent stromal desmoplasia and spindled neoplastic melanocytes. It sits at OncoTree level 3 under MEL (Melanoma), tissue: Skin. Desmoplastic melanoma is genetically distinct from common-type cutaneous melanoma: it carries an exceptionally high mutation burden (median 62 mutations/Mb) driven by a UV-radiation C>T mutational signature, yet is conspicuously devoid of canonical BRAF V600E and NRAS Q61K/R drivers. MAPK/PI3K pathway activation is instead achieved through a diverse, non-mutually-exclusive set of alterations in NF1, CBL, ERBB2, MAP2K1, MAP3K1, EGFR, and others, affecting 73% of tumors. The high TMB positions DESM as a strong candidate for immune checkpoint blockade.
Cohorts in the corpus
- desm_broad_2015 — 62 desmoplastic melanomas: 20 fresh-frozen (discovery; 10 MSKCC, 10 Melanoma Institute Australia) with whole-genome + exome sequencing (13× and 89×), and 42 FFPE tumors (validation; UCSF) with targeted sequencing of 293 genes at 216× PMID:26343386.
Recurrent alterations
- TERT — promoter mutations in 85% (17/20) of evaluable samples; overall TERT activation (promoter + amplification) in 90% of tumors PMID:26343386.
- NFKBIE — novel recurrent promoter hotspot mutations in 14.5% of tumors (15/62); evidence for biallelic selection; not found in COSMIC or TCGA across any cancer type; proposed gain-of-function suppressing NFκB signaling PMID:26343386.
- CDKN2A — focal deletions in 11/62 cases; LOF mutations; p16 loss confirmed by IHC PMID:26343386.
- BRAF — V600E absent; kinase-impaired G466E/G469E/D594N substitutions in 3 tumors (paradoxically activate MAPK via CRAF) PMID:26343386.
- NRAS — canonical Q61K/R absent; atypical Q61H in 1 tumor PMID:26343386.
- NF1 — LOF mutations and focal deletions in 4 cases PMID:26343386.
- CBL — frequent truncating/damaging missense mutations with no synonymous mutations; supports tumor-suppressor role PMID:26343386.
- ERBB2 — recurrent S310F hotspot in 4/62 tumors PMID:26343386.
- EGFR — focal amplifications in 3 tumors; IHC-confirmed overexpression PMID:26343386.
- MAP2K1 — P124S/L hotspot in 2 tumors PMID:26343386.
- MAP3K1 — focal amplifications in 3 tumors; novel finding in melanoma PMID:26343386.
- PTPN11 — E76A/K hotspot in 2 tumors PMID:26343386.
- MET — focal amplifications in 2 tumors; IHC-confirmed PMID:26343386.
- RAC1 — P29S hotspot in 2 tumors PMID:26343386.
- TP53 — top LOF-burden candidate; IHC-confirmed protein-level alteration PMID:26343386.
- FBXW7 — truncating/WD-domain damaging mutations in 11% of tumors PMID:26343386.
- ARID2, ARID1A — inactivating SWI/SNF mutations; ARID1A IHC-confirmed PMID:26343386.
- RB1 — LOF mutations; IHC-confirmed protein loss PMID:26343386.
- Extreme mutation burden (median 62 mutations/Mb) with dominant UV-radiation C>T signature (88% of mutations); older patients (>55 years) had significantly more mutations (p=2×10⁻³) PMID:26343386.
Subtypes
- Pure and mixed desmoplastic subtypes are genetically similar based on the discovery/validation cohort analysis PMID:26343386.
- Tumors from sun-shielded sites had the lowest mutation burdens; one such tumor carried a germline CDKN2A mutation PMID:26343386.
Therapeutic landscape
- BRAF V600-directed inhibitors (vemurafenib, dabrafenib + trametinib) are not appropriate for desmoplastic melanoma due to absence of BRAF V600E and NRAS Q61K/R PMID:26343386.
- Targetable RTK/MAPK alterations identified in 73% of tumors; small-molecule inhibitors against MET, EGFR, ERBB2, IDH1, MAP2K1, PIK3CA, and CDK4 products represent potential therapeutic avenues PMID:26343386.
- Exceptionally high TMB (median 62 mutations/Mb) positions DESM as a strong candidate for immune checkpoint inhibitor therapy PMID:26343386.
Sources
- PMID:26343386 — Shain et al. (2015). Whole-genome, exome, and targeted sequencing of 62 desmoplastic melanomas; identified extreme mutation burden, UV signature, absence of BRAF V600E/NRAS canonical drivers, novel NFKBIE promoter hotspot, and diverse MAPK/PI3K activating alterations.
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