DDIT3
Overview
DDIT3 (DNA Damage Inducible Transcript 3), also known as CHOP or GADD153, encodes a transcription factor that is a key inhibitor of adipocyte differentiation. In cancer genomics, DDIT3 is most prominent in dedifferentiated liposarcoma (DDLPS), where it is recurrently amplified as part of the 12q13-15 amplicon and a broader set of adipocyte-differentiation-inhibitor amplifications. Its amplification is thought to block terminal adipogenic differentiation, contributing to the dedifferentiated phenotype.
Alterations observed in the corpus
- Amplification of DDIT3 (32%) is part of a cluster of adipocyte-differentiation-inhibitor focal amplifications in DDLPS, alongside JUN (42%), PTPRQ (46%), YAP1 (16%), and CEBPA (24%); JUN amplification defines the poor-prognosis K1 DDLPS cluster PMID:29100075.
Cancer types (linked)
- DDLS (Dedifferentiated Liposarcoma): DDIT3 amplification in 32% of DDLPS as part of the adipocyte-differentiation-inhibitor amplification cluster on chromosome 12q; co-occurring with JUN (42%) and PTPRQ (46%) amplifications PMID:29100075.
Co-occurrence and mutual exclusivity
Therapeutic relevance
- DDIT3 amplification is part of the DDLPS-defining amplicon; JUN amplification (which co-occurs) is proposed as a tractable therapeutic target as JUN inhibitors mature PMID:29100075.
Open questions
- The functional consequence of DDIT3 amplification relative to JUN amplification in driving DDLPS poor prognosis remains to be dissected.
Sources
This page was processed by crosslinker on 2026-05-15.