期刊
NATURE GENETICS
卷 42, 期 4, 页码 338-U95出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.542
关键词
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资金
- Fund for Scientific Research (FWO) Flanders [G.0198.08, G.0869.10N]
- GOA-UGent [12051203]
- IWT-Vlaanderen [060848]
- Children Cancer Fund Ghent
- Leukemia Research UK
- Stichting Kinderen Kankervrij [KiKa 2007-012]
- Belgian Program of Interuniversity Poles of Attraction
- Belgian Foundation against Cancer
- Austrian Ministry of Science and Research [GZ 200.136/1-VI/1/2005]
- US National Library of Medicine [1R01LM010140-01]
- ECOG tumor bank
- DCOG tumor bank
- Spain's Plan Nacional [BFU 2007-60990, PlanE2009-0110]
- Comunidad de Madrid [S-SAL0304-2006]
- Fundacion MM [RECAVA RD06/0014/1012]
- Fundacion Ramon Areces
- Alex's Lemonade Stand Foundation
- US Northeast Biodefense Center [U54-AI057158]
- US National Institutes of Health [R01CA120196, R01CA129382]
- Rally across America Foundation
- Swim across America Foundation
- Golfers against Cancer Foundation
- Leukemia and Lymphoma Society
- NATIONAL CANCER INSTITUTE [U24CA114737, R01CA129382, R01CA155743, R01CA120196] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U54AI057158] Funding Source: NIH RePORTER
- NATIONAL LIBRARY OF MEDICINE [R01LM010140] Funding Source: NIH RePORTER
Tumor suppressor genes on the X chromosome may skew the gender distribution of specific types of cancer(1,2). T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in males(3). In this study, we report the identification of inactivating mutations and deletions in the X-linked plant homeodomain finger 6 (PHF6) gene in 16% of pediatric and 38% of adult primary T-ALL samples. Notably, PHF6 mutations are almost exclusively found in T-ALL samples from male subjects. Mutational loss of PHF6 is importantly associated with leukemias driven by aberrant expression of the homeobox transcription factor oncogenes TLX1 and TLX3. Overall, these results identify PHF6 as a new X-linked tumor suppressor in T-ALL and point to a strong genetic interaction between PHF6 loss and aberrant expression of TLX transcription factors in the pathogenesis of this disease.
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