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A truncating mutation of HDAC2 in human cancers confers resistance to histone deacetylase inhibition.

Authors: Ropero, S  Fraga, MF  Ballestar, E  Hamelin, R  Yamamoto, H  Boix-Chornet, M  Caballero, R  Alaminos, M  Setien, F  Paz, MF  Herranz, M  Palacios, J  Arango, D  Orntoft, TF  Aaltonen, LA  Schwartz S, JR  Esteller, M 
Citation: Ropero S, etal., Nat Genet. 2006 May;38(5):566-9. Epub 2006 Apr 16.
Pubmed: (View Article at PubMed) PMID:16642021
DOI: Full-text: DOI:10.1038/ng1773

Disruption of histone acetylation patterns is a common feature of cancer cells, but very little is known about its genetic basis. We have identified truncating mutations in one of the primary human histone deacetylases, HDAC2, in sporadic carcinomas with microsatellite instability and in tumors arising in individuals with hereditary nonpolyposis colorectal cancer syndrome. The presence of the HDAC2 frameshift mutation causes a loss of HDAC2 protein expression and enzymatic activity and renders these cells more resistant to the usual antiproliferative and proapoptotic effects of histone deacetylase inhibitors. As such drugs may serve as therapeutic agents for cancer, our findings support the use of HDAC2 mutational status in future pharmacogenetic treatment of these individuals.


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RGD Object Information
RGD ID: 9590331
Created: 2014-11-25
Species: All species
Last Modified: 2014-11-25
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.