Cited by 107Melanoma and MAPK PathwaysProtein Kinase Regulation and GTPase SignalingProtein Tyrosine Phosphatases

Recurrent inactivating RASA2 mutations in melanoma

Open access
Arafeh, Rand, Qutob, Nouar, Emmanuel, Rafi, Keren-Paz, Alona, Madore, Jason, Elkahloun, Abdel, Wilmott, James S, Gartner, Jared J +20 more·2015·Nature Genetics

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.

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Crossref · 10.1038/ng.3427

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  • RASA2 is a GTPase-activating protein that boosts GTP hydrolysis by wild-type RAS.

    “RASA2, a GTPase-activating protein that stimulates the GTPase activity of wild-type RAS (Arafeh et al., 2015), has not been studied in the context of primary T cells and the immune system, but our findings suggest it may be a modulator of T cell proliferation, activation, and anti-tumor immunity.”

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1 of the 25 references couldn’t be matched to a known paper.

Research works printed but not linked: 3

  1. [13]Rodriguez-Viciana P Oses-Prieto J Burlingame A Fried M McCormick F Mol Cell 2006 22 217 30 16630891
  2. [20]Wei X Nat Genet 2011 43 442 6 21499247 PMC3161250
  3. [21]Dutton-Regester K Oncotarget 2014 5 2912 7 24913145 PMC4102779

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Authors
Arafeh, R., Qutob, N., Emmanuel, R., Keren-Paz, A., Madore, J., Elkahloun, A., Wilmott, J. S., Gartner, J. J., Di Pizio, A., Winograd-Katz, S., Sindiri, S., Rotkopf, R., Dutton-Regester, K., Johansson, P., Pritchard, A. L., Waddell, N., Hill, V. K., Lin, J. C., Hevroni, Y., Rosenberg, S. A., Khan, J., Ben-Dor, S., Niv, M. Y., Ulitsky, I., Mann, G. J., Scolyer, R. A., Hayward, N. K., & Samuels, Y.
Affiliations
  • Weizmann Institute of Science (IL)
  • The University of Sydney (AU)
  • National Institutes of Health (US)
  • QIMR Berghofer Medical Research Institute (AU)
  • Hebrew University of Jerusalem (IL)
Corresponding author
Samuels, Yardena
Venue
Nature Genetics
Published
2015-10-26
Volume
47
Issue
12
Pages
1408-1410
ISSN
  • 1061-4036 (ISSN-L)
  • 1546-1718
OpenAlex
W2181106088
Cited by
107
References
25
Citations by year
2026: 3 · 2025: 5 · 2024: 10 · 2023: 9 · 2022: 7 · 2021: 9 · 2020: 9 · 2019: 11 · 2018: 14 · 2017: 19 · 2016: 10
FWCI
6.22
Type
journal article
Language
en
Open access
Locations
  • Nature Genetics (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Israel Science Foundation
  • National Institutes of Health
  • National Health and Medical Research Council
  • National Medical Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
Keywords
melanoma, Ras GTPase-activating protein, tumor suppressor, Ras activation, loss-of-function mutations, patient survival, exome sequencing
MeSH terms
Humans, Melanoma, Mutation, Prognosis, Skin Neoplasms, Biomarkers, Tumor, Survival Rate, ras GTPase-Activating Proteins, High-Throughput Nucleotide Sequencing, Exome

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