DEK

Overview

DEK is a chromatin-associated oncoprotein involved in DNA repair, mRNA splicing, and chromatin organization. In cancer genomics, DEK has been reported as overexpressed or amplified in multiple tumor types. In the context of castration-resistant prostate cancer (CRPC), focal allelic imbalance of the DEK locus was identified as an alteration enriched in the neuroendocrine prostate cancer (CRPC-NE) subtype compared to adenocarcinoma histology.

Alterations observed in the corpus

  • Focal allelic imbalance at the DEK locus enriched in CRPC-NE vs. CRPC-Adeno (P = 0.04, binomial test) in a cohort of 114 metastatic biopsies from 81 patients with castration-resistant prostate cancer. PMID:26855148
  • DEK-NUP214 t(6;9) fusion identified in 15/1,540 (1%) AML patients in a large genomic classification cohort, representing a recurrent cytogenetic subgroup with distinct molecular features PMID:27276561
  • DEK — RNA fusion partner in a MAP3K8:DEK fusion detected in acral lentiginous melanoma (ALM); identified among 106 RNA fusions across 74% of 34 ALM patients PMID:28373299

Cancer types (linked)

  • PRAD (castration-resistant, neuroendocrine subtype): Focal allelic imbalance of DEK enriched in CRPC-NE (n=30 patients) vs. CRPC-Adeno (n=51 patients); P = 0.04, binomial test. Specific copy-number direction (gain vs. loss) not detailed as the primary finding. PMID:26855148

Co-occurrence and mutual exclusivity

  • Identified in the context of CRPC-NE, which is defined by concurrent RB1 loss + TP53 alteration (53.3% of CRPC-NE) and depletion of AR genomic alterations. DEK allelic imbalance was one of several focal events distinguishing CRPC-NE from CRPC-Adeno. PMID:26855148

Therapeutic relevance

  • No direct therapeutic implication established from this study. DEK allelic imbalance was reported as a genomic correlate of CRPC-NE; it was not a component of the 70-gene integrated NEPC classifier developed in the same study. PMID:26855148

Open questions

  • The functional role of DEK allelic imbalance in CRPC-NE — whether gain, loss, or structural rearrangement — was not characterized in this study. Whether DEK contributes causally to neuroendocrine transdifferentiation or is a secondary consequence of the divergent clonal evolution model proposed for CRPC-NE remains unknown. PMID:26855148

Sources

  • PMID:26855148 — Beltran et al. (2016), molecular characterization of 114 metastatic CRPC biopsies (nepc_wcm_2016), CRPC-NE vs. CRPC-Adeno integrated multi-omic profiling.

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