Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.11889/4174
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dc.contributor.authorQutob, Nouar-
dc.date.accessioned2017-01-30T09:17:32Z-
dc.date.available2017-01-30T09:17:32Z-
dc.date.issued2016-
dc.identifier.urihttp://hdl.handle.net/20.500.11889/4174-
dc.descriptionAuthors include:Rand Arafeh, Rafi Emmanuel, Alona Keren-Paz, Jason Madore, Abdel Elkahloun, James S. Wilmott, Jared J. Gartner, Antonella Di Pizio, Sabina Winograd-Katz, Sivasish Sindiri, Ron Rotkopf, Ken Dutton-Regester, Peter Johansson, Antonia Pritchard, Nicola Waddell, Victoria K. Hill, Jimmy C. Lin, Yael Hevroni, Steven A. Rosenberg, Javed Khan, Shifra Ben-Dor, Masha Y. Niv, Igor Ulitsky, Graham J Mann, Richard A. Scolyer, Nicholas K. Hayward, and Yardena Samuelsen_US
dc.description.abstractAnalysis of 501 melanoma exomes revealed 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 reveal RASA2 inactivation as a melanoma driver and highlight the importance of Ras GAPs in cancer.en_US
dc.language.isoen_USen_US
dc.subjectArrhythmiaen_US
dc.subjectCancer geneticsen_US
dc.subjectMelanoma - Genetic aspectsen_US
dc.titleRecurrent inactivating RASA2 mutations in melanomaen_US
dc.typeArticleen_US
newfileds.departmentScienceen_US
newfileds.item-access-typeopen_accessen_US
newfileds.thesis-prognoneen_US
newfileds.general-subjectnoneen_US
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