期刊
LEUKEMIA
卷 25, 期 1, 页码 130-134出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2010.247
关键词
PHF6; mutations; AML
资金
- Fund for Scientific Research (FWO) Flanders [G.0198.08, G.0869.10N]
- GOA-UGent [12051203]
- IWT-Vlaanderen [060848]
- Children Cancer Fund Ghent
- Belgian Program of Interuniversity Poles of Attraction
- Belgian Foundation Against Cancer
- ECOG tumor banks
- MSKCC tumor bank
- NCI
- National Institutes of Health [R01CA120196, R01CA129382]
- Rally Across America Foundation
- Swim Across America Foundation
- Golfers Against Cancer Foundation
- Howard Hughes Medical Institute
- NATIONAL CANCER INSTITUTE [R01CA149655, R01CA155743, R01CA120196, R01CA169784, R01CA129382] Funding Source: NIH RePORTER
Loss of function mutations and deletions encompassing the plant homeodomain finger 6 (PHF6) gene are present in about 20% of T-cell acute lymphoblastic leukemias (ALLs). Here, we report the identification of recurrent mutations in PHF6 in 10/353 adult acute myeloid leukemias (AMLs). Genetic lesions in PHF6 found in AMLs are frameshift and nonsense mutations distributed through the gene or point mutations involving the second plant homeodomain (PHD)-like domain of the protein. As in the case of T-ALL, where PHF6 alterations are found almost exclusively in males, mutations in PHF6 were seven times more prevalent in males than in females with AML. Overall, these results identify PHF6 as a tumor suppressor gene mutated in AML and extend the role of this X-linked tumor suppressor gene in the pathogenesis of hematologic tumors. Leukemia (2011) 25, 130-134; doi: 10.1038/leu.2010.247; published online 29 October 2010
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