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Gene of the month: DDIT3
  1. Julio A Diaz-Perez1,
  2. Darcy A Kerr2
  1. 1 Department of Pathology, Virginia Commonwealth University, Richmond, Virginia, USA
  2. 2 Department of Pathology and Laboratory Medicine, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, USA
  1. Correspondence to Dr Darcy A Kerr, Pathology and Laboratory Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, NH 03756, USA; Darcy.A.Kerr{at}


DNA damage-inducible transcript 3 (DDIT3) gene, mapped to the human chromosome 12q13.3, encodes a protein that belongs to the CCAAT/enhancer-binding protein family of transcription factors. DDIT3 is involved in the proliferative control that responds to endoplasmic reticulum stress in normal conditions, dimerising other transcription factors with basic leucine zipper (bZIP) structural motifs. DDIT3 plays a significant role during cell differentiation, especially adipogenesis, arresting the maturation of adipoblasts. In disease, FUS/EWSR1::DDIT3 fusion is the pathogenic event that drives the development of myxoid liposarcoma. The amplification of DDIT3 in other adipocytic neoplasms mediates the presence of adipoblast-like elements. Another fusion, GLI1::DDIT3, has rarely been documented in other tumours. This paper reviews the structure and function of DDIT3, its role in disease—particularly cancer—and its use and pitfalls in diagnostic testing, including immunohistochemistry as a tissue-based marker.

  • antibodies, monoclonal
  • immunohistochemistry
  • pathology, molecular
  • sarcoma
  • soft tissue neoplasms

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  • Handling editor Vikram Deshpande.

  • Twitter @darcykerrMD

  • Contributors JAD-P and DAK contributed to the conception, literature review, writing and editing of this manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.