Please use this identifier to cite or link to this item:
http://hdl.handle.net/20.500.11889/4174
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Qutob, Nouar | - |
dc.date.accessioned | 2017-01-30T09:17:32Z | - |
dc.date.available | 2017-01-30T09:17:32Z | - |
dc.date.issued | 2016 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11889/4174 | - |
dc.description | Authors 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 Samuels | en_US |
dc.description.abstract | Analysis 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.iso | en_US | en_US |
dc.subject | Arrhythmia | en_US |
dc.subject | Cancer genetics | en_US |
dc.subject | Melanoma - Genetic aspects | en_US |
dc.title | Recurrent inactivating RASA2 mutations in melanoma | en_US |
dc.type | Article | en_US |
newfileds.department | Science | en_US |
newfileds.item-access-type | open_access | en_US |
newfileds.thesis-prog | none | en_US |
newfileds.general-subject | none | en_US |
item.fulltext | With Fulltext | - |
item.languageiso639-1 | other | - |
item.grantfulltext | open | - |
Appears in Collections: | Fulltext Publications |
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emss-65345.pdf | 666.06 kB | Adobe PDF | View/Open |
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