Germline ETV6 Mutations Confer Susceptibility to Acute Lymphoblastic Leukemia and Thrombocytopenia

Sabine Topka(Kettering University), Joseph Vijai(Memorial Sloan Kettering Cancer Center), Michael F. Walsh, Lauren Jacobs(Memorial Sloan Kettering Cancer Center), Ann Maria(Memorial Sloan Kettering Cancer Center), Danylo Villano(Memorial Sloan Kettering Cancer Center), Pragna Gaddam(Memorial Sloan Kettering Cancer Center), Gang Wu, Rose B. McGee, Emily A. Quinn, Hiroto Inaba, Christine Hartford, Ching‐Hon Pui, Alberto S. Pappo, Michael N. Edmonson, Michael Y. Zhang(University of Washington), Polina Stepensky(Hadassah Medical Center), Peter G. Steinherz(Memorial Sloan Kettering Cancer Center), Kasmintan A. Schrader(University of British Columbia), Anne Lincoln(Memorial Sloan Kettering Cancer Center), James B. Bussel(Cornell University), Steve M. Lipkin(Cornell University), Yehuda Goldgur(Kettering University), M Harit(Hebrew University of Jerusalem), Zsofia K. Stadler(Memorial Sloan Kettering Cancer Center), Charles G. Mullighan, Michael Weintraub(Hadassah Medical Center), Akiko Shimamura(University of Washington), Jinghui Zhang, James R. Downing, Kim E. Nichols, Kenneth Offit(Memorial Sloan Kettering Cancer Center)
PLoS Genetics
June 23, 2015
Cited by 156Open Access
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Abstract

Somatic mutations affecting ETV6 often occur in acute lymphoblastic leukemia (ALL), the most common childhood malignancy. The genetic factors that predispose to ALL remain poorly understood. Here we identify a novel germline ETV6 p. L349P mutation in a kindred affected by thrombocytopenia and ALL. A second ETV6 p. N385fs mutation was identified in an unrelated kindred characterized by thrombocytopenia, ALL and secondary myelodysplasia/acute myeloid leukemia. Leukemic cells from the proband in the second kindred showed deletion of wild type ETV6 with retention of the ETV6 p. N385fs. Enforced expression of the ETV6 mutants revealed normal transcript and protein levels, but impaired nuclear localization. Accordingly, these mutants exhibited significantly reduced ability to regulate the transcription of ETV6 target genes. Our findings highlight a novel role for ETV6 in leukemia predisposition.


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