Efficacy of JAK/STAT pathway inhibition in murine xenograft models of early T-cell precursor (ETP) acute lymphoblastic leukemia

Author:

Maude Shannon L.12,Dolai Sibasish3,Delgado-Martin Cristina4,Vincent Tiffaney1,Robbins Alissa3,Selvanathan Arthavan3,Ryan Theresa1,Hall Junior1,Wood Andrew C.5,Tasian Sarah K.12,Hunger Stephen P.12,Loh Mignon L.4,Mullighan Charles G.6,Wood Brent L.7,Hermiston Michelle L.4,Grupp Stephan A.12,Lock Richard B.3,Teachey David T.12

Affiliation:

1. Division of Oncology, Children’s Hospital of Philadelphia, Philadelphia, PA;

2. Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA;

3. Leukaemia Biology, Children’s Cancer Institute, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia;

4. Division of Hematology/Oncology, University of California, San Francisco Benioff Children’s Hospital, San Francisco, CA;

5. Molecular Medicine and Pathology, University of Auckland, Auckland, New Zealand;

6. Department of Pathology, St. Jude Children’s Research Hospital, Memphis, TN; and

7. Division of Hematopathology, University of Washington and Seattle Cancer Care Alliance, Seattle, WA

Abstract

Key Points ETP-ALL, a high-risk subtype of T-ALL, is characterized by aberrant activation of the JAK/STAT signaling pathway. The JAK1/2 inhibitor ruxolitinib demonstrates robust activity in patient-derived xenograft models of ETP-ALL.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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