KMT2D loss drives aggressive tumor phenotypes in cutaneous squamous cell carcinoma.
Cara Daucha, Sharon Shimb, Matthew Wyatt Colea c, Nijole C. Pollocka, Abigail J. Beera, Johnny R. Ramroopa, Victoria Kleed, Dawn C. Allaind, Reena Shakyae, Sue E. Knoblaughf, Jesse Kulewskyg, Amanda Ewart Tolanda d e
- aDepartment of Cancer Biology and Genetics, The Ohio State University College of Medicine Columbus, OH 43210, USA
- bCentral Michigan University College of Medicine Mount Pleasant, MI 48858, USA
- cDepartment of Radiation Oncology, The Ohio State University Columbus, OH 43210, USA
- dDepartment of Internal Medicine, Division of Human Genetics, The Ohio State University Columbus, OH 43210, USA
- eComprehensive Cancer Center, The Ohio State University Columbus, OH 43210, USA
- fDepartment of Veterinary Biosciences, The Ohio State University Columbus, OH 43210, USA
- gDepartment of Pathology, The Ohio State University Wexner Medical Center Columbus, OH 43210, USA
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Abstract
loss-of-function mutations may promote more aggressive and invasive behaviors in cSCC, suggesting that KMT2D-related pathways could be targets for cancer therapies. Future studies to determine the downstream genes and mechanism of phenotypic effect are needed.
TL;DRIt is suggested that K MT2D loss-of-function mutations may promote more aggressive and invasive behaviors in cSCC, suggesting that KMT2D-related pathways could be targets for cancer therapies. (Semantic Scholar)