Phosphatidylinositol 3-kinase δ blockade increases genomic instability in B cells

Mara Compagno, Qi Wang, Chiara Pighi, Taek-Chin Cheong, Fei-Long Meng, Teresa Poggio, Leng-Siew Yeap, Elif Karaca, Rafael B. Blasco, Fernanda Langellotto, Chiara Ambrogio, Claudia Voena, Adrian Wiestner, Siddha N. Kasar, Jennifer R. Brown, Jing Sun, Catherine J. Wu, Monica Gostissa, Frederick W. Alt and Roberto Chiarle ()
Additional contact information
Mara Compagno: Children’s Hospital Boston and Harvard Medical School
Qi Wang: Children’s Hospital Boston and Harvard Medical School
Chiara Pighi: Children’s Hospital Boston and Harvard Medical School
Taek-Chin Cheong: Children’s Hospital Boston and Harvard Medical School
Fei-Long Meng: Howard Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children’s Hospital, Harvard Medical School
Teresa Poggio: University of Torino
Leng-Siew Yeap: Howard Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children’s Hospital, Harvard Medical School
Elif Karaca: Children’s Hospital Boston and Harvard Medical School
Rafael B. Blasco: Children’s Hospital Boston and Harvard Medical School
Fernanda Langellotto: Children’s Hospital Boston and Harvard Medical School
Chiara Ambrogio: Dana-Farber Cancer Institute, Harvard Medical School
Claudia Voena: Children’s Hospital Boston and Harvard Medical School
Adrian Wiestner: Hematology Branch, National Heart, Lung, and Blood Institute
Siddha N. Kasar: Dana-Farber Cancer Institute, Harvard Medical School
Jennifer R. Brown: Dana-Farber Cancer Institute, Harvard Medical School
Jing Sun: Dana-Farber Cancer Institute, Harvard Medical School
Catherine J. Wu: Dana-Farber Cancer Institute, Harvard Medical School
Monica Gostissa: Howard Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children’s Hospital, Harvard Medical School
Frederick W. Alt: Howard Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children’s Hospital, Harvard Medical School
Roberto Chiarle: Children’s Hospital Boston and Harvard Medical School

Nature, 2017, vol. 542, issue 7642, 489-493

Abstract: PI3Kδ controls the expression of the recombinogenic enzyme AID; excessive AID activity caused by PI3Kδ inhibition can induce genomic instability in leukaemia and lymphoma cells, as well as in patients with chronic lymphocytic leukaemia treated with PI3Kδ inhibitors.

Date: 2017
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DOI: 10.1038/nature21406

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