Recurrent inactivating RASA2 mutations in melanoma

  • Rand Arafeh
  • , Nouar Qutob
  • , 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 A. Johansson
  • , Antonia L. 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, Yardena Samuels

Research output: Contribution to journalArticlepeer-review

89 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)1408-1410
Number of pages3
JournalNature Genetics
Volume47
Issue number12
Early online date26 Oct 2015
DOIs
Publication statusPublished - Dec 2015

Keywords

  • 3ref2021

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