Clonal evolution mechanisms in NT5C2 mutant-relapsed acute lymphoblastic leukaemia

Gannie Tzoneva, Chelsea L. Dieck, Koichi Oshima, Alberto Ambesi-Impiombato, Marta Sánchez-Martín, Chioma J. Madubata, Hossein Khiabanian, Jiangyan Yu, Esme Waanders, Ilaria Iacobucci, Maria Luisa Sulis, Motohiro Kato, Katsuyoshi Koh, Maddalena Paganin, Giuseppe Basso, Julie M. Gastier-Foster, Mignon L. Loh, Renate Kirschner-Schwabe, Charles G. Mullighan, Raul Rabadan and Adolfo A. Ferrando ()
Additional contact information
Gannie Tzoneva: Institute for Cancer Genetics, Columbia University
Chelsea L. Dieck: Institute for Cancer Genetics, Columbia University
Koichi Oshima: Institute for Cancer Genetics, Columbia University
Alberto Ambesi-Impiombato: Institute for Cancer Genetics, Columbia University
Marta Sánchez-Martín: Institute for Cancer Genetics, Columbia University
Chioma J. Madubata: Columbia University
Hossein Khiabanian: Rutgers Cancer Institute, Rutgers University
Jiangyan Yu: Princess Maxima Center for Pediatric Oncology
Esme Waanders: Princess Maxima Center for Pediatric Oncology
Ilaria Iacobucci: St. Jude Children’s Research Hospital
Maria Luisa Sulis: Columbia University Medical Center
Motohiro Kato: Saitama Children's Medical Center
Katsuyoshi Koh: Saitama Children's Medical Center
Maddalena Paganin: Salute della Donna e del Bambino (SDB), University of Padua
Giuseppe Basso: Salute della Donna e del Bambino (SDB), University of Padua
Julie M. Gastier-Foster: Nationwide Children’s Hospital
Mignon L. Loh: University of California
Renate Kirschner-Schwabe: Charité-Universitätsmedizin Berlin
Charles G. Mullighan: St. Jude Children’s Research Hospital
Raul Rabadan: Columbia University
Adolfo A. Ferrando: Institute for Cancer Genetics, Columbia University

Nature, 2018, vol. 553, issue 7689, 511-514

Abstract: Mutations in the nucleotidase-encoding gene NT5C2 drive chemotherapy resistance in relapsed acute lymphoid leukaemia but the mutations also lead to a loss-of-fitness phenotype and to collateral drug sensitivity, which could be exploited for therapy.

Date: 2018
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DOI: 10.1038/nature25186

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