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Nat Genet. 2015 Dec;47(12):1408-10. doi: 10.1038/ng.3427. Epub 2015 Oct 26.

Recurrent inactivating RASA2 mutations in melanoma.

Author information

1
Molecular Cell Biology Department, Weizmann Institute of Science, Rehovot, Israel.
2
Melanoma Institute Australia, Sydney, New South Wales, Australia.
3
Discipline of Pathology, Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia.
4
National Human Genome Research Institute, US National Institutes of Health, Bethesda, Maryland, USA.
5
National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA.
6
Institute of Biochemistry, Food Science and Nutrition, Hebrew University, Rehovot, Israel.
7
Department of Biological Services, Weizmann Institute of Science, Rehovot, Israel.
8
QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia.
9
Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
10
Centre for Cancer Research, Westmead Millennium Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
11
Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia.

Abstract

Analysis of 501 melanoma exomes identified RASA2, encoding a RasGAP, as a tumor-suppressor gene mutated in 5% of melanomas. Recurrent loss-of-function mutations in RASA2 were found to increase RAS activation, melanoma cell growth and migration. RASA2 expression was lost in ≥30% of human melanomas and was associated with reduced patient survival. These findings identify RASA2 inactivation as a melanoma driver and highlight the importance of RasGAPs in cancer.

PMID:
26502337
PMCID:
PMC4954601
DOI:
10.1038/ng.3427
[Indexed for MEDLINE]
Free PMC Article

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