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

Author

Listed:
  • 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
    †Present addresses: Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China (F.-L.M.); Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China (L.-S.Y.); Agenus Inc., 3 Forbes Road, Lexington, Massachusetts 02421, USA (F.L., M.G.).)

  • 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
    †Present addresses: Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China (F.-L.M.); Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China (L.-S.Y.); Agenus Inc., 3 Forbes Road, Lexington, Massachusetts 02421, USA (F.L., M.G.).)

  • 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
    †Present addresses: Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China (F.-L.M.); Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China (L.-S.Y.); Agenus Inc., 3 Forbes Road, Lexington, Massachusetts 02421, USA (F.L., M.G.).)

  • Chiara Ambrogio

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Claudia Voena

    (Children’s Hospital Boston and Harvard Medical School
    University of Torino)

  • 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
    †Present addresses: Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China (F.-L.M.); Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China (L.-S.Y.); Agenus Inc., 3 Forbes Road, Lexington, Massachusetts 02421, USA (F.L., M.G.).)

  • 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
    University of Torino)

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.

Suggested Citation

  • 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 & A, 2017. "Phosphatidylinositol 3-kinase δ blockade increases genomic instability in B cells," Nature, Nature, vol. 542(7642), pages 489-493, February.
    • Handle: RePEc:nat:nature:v:542:y:2017:i:7642:d:10.1038_nature21406
    DOI: 10.1038/nature21406
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