Rare mutations provide unique insight into oncogenic potential of STAT transcription factors
Lisa N. Heppler and David A. Frank
Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Address correspondence to: David A. Frank, Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, Massachusetts 02215, USA. Phone: 617.632.4714; Email: david_frank@dfci.harvard.edu.
Find articles by Heppler, L. in: JCI | PubMed | Google Scholar
Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Address correspondence to: David A. Frank, Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, Massachusetts 02215, USA. Phone: 617.632.4714; Email: david_frank@dfci.harvard.edu.
Find articles by Frank, D. in: JCI | PubMed | Google Scholar
First published December 4, 2017 - More info
J Clin Invest. 2018;128(1):113–115. https://doi.org/10.1172/JCI98619.
Copyright © 2018, American Society for Clinical Investigation
The inappropriate activation of transcription factors, including STATs, is known to promote tumor initiation and progression. The most common mechanisms of misregulation lead to constitutive activation of WT STATs. However, the recent discovery of rare STAT mutations in hematopoietic malignancies suggests that STAT mutants may be oncogenic. In this issue of the JCI, Pham et al. use a transgenic mouse model to demonstrate that STAT5BN642H is sufficient for the development of T cell neoplasia. This study, along with other studies of constitutively active STAT mutants, provides insight into the pathogenesis and treatment of STAT5-driven cancer.
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Copyright © 2018 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)