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 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

doi:10.1038/ng.3427

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 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^*

^*Corresponding author for this work

Institute of Biochemistry, Food Science and Nutrition

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

91 Scopus citations

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 language	English
Pages (from-to)	1408-1410
Number of pages	3
Journal	Nature Genetics
Volume	47
Issue number	12
DOIs	https://doi.org/10.1038/ng.3427
State	Published - 1 Dec 2015

Bibliographical note

Publisher Copyright:
© 2015 Nature America, Inc. All rights reserved.

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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., ... Samuels, Y. (2015). Recurrent inactivating RASA2 mutations in melanoma. Nature Genetics, 47(12), 1408-1410. https://doi.org/10.1038/ng.3427

@article{4a37ff7cbbc74b2980ccff6bf4c767a6,

title = "Recurrent inactivating RASA2 mutations in melanoma",

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.",

author = "Rand Arafeh and Nouar Qutob and Rafi Emmanuel and Alona Keren-Paz and Jason Madore and Abdel Elkahloun and Wilmott, \{James S.\} and Gartner, \{Jared J.\} and \{Di Pizio\}, Antonella and Sabina Winograd-Katz and Sivasish Sindiri and Ron Rotkopf and Ken Dutton-Regester and Peter Johansson and Pritchard, \{Antonia L.\} and Nicola Waddell and Hill, \{Victoria K.\} and Lin, \{Jimmy C.\} and Yael Hevroni and Rosenberg, \{Steven A.\} and Javed Khan and Shifra Ben-Dor and Niv, \{Masha Y.\} and Igor Ulitsky and Mann, \{Graham J.\} and Scolyer, \{Richard A.\} and Hayward, \{Nicholas K.\} and Yardena Samuels",

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Arafeh, R, Qutob, N, Emmanuel, R, Keren-Paz, A, Madore, J, Elkahloun, A, Wilmott, JS, Gartner, JJ, Di Pizio, A, Winograd-Katz, S, Sindiri, S, Rotkopf, R, Dutton-Regester, K, Johansson, P, Pritchard, AL, Waddell, N, Hill, VK, Lin, JC, Hevroni, Y, Rosenberg, SA, Khan, J, Ben-Dor, S, Niv, MY, Ulitsky, I, Mann, GJ, Scolyer, RA, Hayward, NK & Samuels, Y 2015, 'Recurrent inactivating RASA2 mutations in melanoma', Nature Genetics, vol. 47, no. 12, pp. 1408-1410. https://doi.org/10.1038/ng.3427

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AU - Arafeh, Rand

AU - Qutob, Nouar

AU - Emmanuel, Rafi

AU - Keren-Paz, Alona

AU - Madore, Jason

AU - Elkahloun, Abdel

AU - Wilmott, James S.

AU - Gartner, Jared J.

AU - Di Pizio, Antonella

AU - Winograd-Katz, Sabina

AU - Sindiri, Sivasish

AU - Rotkopf, Ron

AU - Dutton-Regester, Ken

AU - Johansson, Peter

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AU - Waddell, Nicola

AU - Hill, Victoria K.

AU - Lin, Jimmy C.

AU - Hevroni, Yael

AU - Rosenberg, Steven A.

AU - Khan, Javed

AU - Ben-Dor, Shifra

AU - Niv, Masha Y.

AU - Ulitsky, Igor

AU - Mann, Graham J.

AU - Scolyer, Richard A.

AU - Hayward, Nicholas K.

AU - Samuels, Yardena

PY - 2015/12/1

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N2 - 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.

AB - 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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Recurrent inactivating RASA2 mutations in melanoma

Abstract

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