RASA2 and NF1; two-negative regulators of Ras with complementary functions in melanoma

Rand Arafeh; Antonella Di Pizio; Abdel G. Elkahloun; Orly Dym; Masha Y. Niv; Yardena Samuels

doi:10.1038/s41388-018-0578-4

RASA2 and NF1; two-negative regulators of Ras with complementary functions in melanoma

Rand Arafeh, Antonella Di Pizio, Abdel G. Elkahloun, Orly Dym, Masha Y. Niv, Yardena Samuels

Weizmann Institute of Science, The Hebrew University of Jerusalem

Research output: Contribution to journal › Letter › peer-review

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’s exact test), and that NF1 mutations [2, 3] significantly co-occur with RASA2 mutations (p = 0.000011, Fisher’s exact test) in BRAF and NRAS wild-type melanomas, suggesting that loss of RASA2 and NF1 have complementary pro-tumorigenic functions (Fig. 1A).

Original language	English
Pages (from-to)	2432-2434
Number of pages	3
Journal	Oncogene
Volume	38
Issue number	13
Early online date	26 Nov 2018
DOIs	https://doi.org/10.1038/s41388-018-0578-4
State	Published - 28 Mar 2019

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

All Science Journal Classification (ASJC) codes

Molecular Biology
Genetics
Cancer Research

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10.1038/s41388-018-0578-4

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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.",

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doi = "10.1038/s41388-018-0578-4",

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AU - Arafeh, Rand

AU - Di Pizio, Antonella

AU - Elkahloun, Abdel G.

AU - Dym, Orly

AU - Niv, Masha Y.

AU - Samuels, Yardena

N1 - 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’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.

PY - 2019/3/28

Y1 - 2019/3/28

N2 - 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’s exact test), and that NF1 mutations [2, 3] significantly co-occur with RASA2 mutations (p = 0.000011, Fisher’s exact test) in BRAF and NRAS wild-type melanomas, suggesting that loss of RASA2 and NF1 have complementary pro-tumorigenic functions (Fig. 1A).

AB - 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’s exact test), and that NF1 mutations [2, 3] significantly co-occur with RASA2 mutations (p = 0.000011, Fisher’s exact test) in BRAF and NRAS wild-type melanomas, suggesting that loss of RASA2 and NF1 have complementary pro-tumorigenic functions (Fig. 1A).

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RASA2 and NF1; two-negative regulators of Ras with complementary functions in melanoma

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