@article{89026577452141f78c8b8f69d1735ce0,
title = "RASA2 and NF1; two-negative regulators of Ras with complementary functions in melanoma",
abstract = "RASA2 has previously been shown to be a functional RasGAP in melanoma cells [1]. Mutation or loss of RASA2 promotes RAS activation in melanoma [1]. Our genetic analysis of RASA2 mutations identified that RASA2 and NRAS mutations are mutually exclusive (p = 0.002, Fisher{\textquoteright}s exact test), and that NF1 mutations [2, 3] significantly co-occur with RASA2 mutations (p = 0.000011, Fisher{\textquoteright}s exact test) in BRAF and NRAS wild-type melanomas, suggesting that loss of RASA2 and NF1 have complementary pro-tumorigenic functions (Fig. 1A).",
author = "Rand Arafeh and {Di Pizio}, Antonella and Elkahloun, {Abdel G.} and Orly Dym and Niv, {Masha Y.} and Yardena Samuels",
note = "We thank T. Wiesel for graphical assistance. This work was supported by the Intramural Research Program of the National Cancer Institute. Y.S. is supported by the Israel Science Foundation grant number 696/17. This project has received funding from the European Research Council (ERC) under the European Union{\textquoteright}s Horizon 2020 research and innovation Programme (grant agreement No 754282), the ERC (StG-335377), the Minerva Foundation Grant, the Henry Chanoch Krenter Institute for Biomedical Imaging and Genomics, the estate of Alice Schwarz-Gardos, the estate of John Hunter, the Knell Family, the Peter and Patricia Gruber Award, and the Hamburger Family. R.A. is supported by Clore foundation. A.D.P is a Lady Davis postdoctoral fellow.",
year = "2019",
month = mar,
day = "28",
doi = "10.1038/s41388-018-0578-4",
language = "الإنجليزيّة",
volume = "38",
pages = "2432--2434",
journal = "Oncogene",
issn = "0950-9232",
publisher = "Springer Nature",
number = "13",
}
