A therapeutically targetable mechanism of BCR-ABL–independent imatinib resistance in chronic myeloid leukemia

Author:

Ma Leyuan1,Shan Yi2,Bai Robert1,Xue Liting3,Eide Christopher A.4,Ou Jianhong3,Zhu Lihua J.35,Hutchinson Lloyd6,Cerny Jan2,Khoury Hanna Jean7,Sheng Zhi89,Druker Brian J.4,Li Shaoguang2,Green Michael R.1

Affiliation:

1. Howard Hughes Medical Institute, Programs in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

2. Division of Hematology/Oncology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

3. Programs in Gene Function and Expression and Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

4. Howard Hughes Medical Institute, Knight Cancer Institute, Division of Hematology and Medical Oncology, Oregon Health and Science University, Portland, OR 97239, USA.

5. Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.

6. Department of Pathology, University of Massachusetts Medical School, Worcester, MA 01605, USA.

7. Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA 30332, USA.

8. Virginia Tech Carilion Research Institute, Roanoke, VA 24016, USA.

9. Department of Biomedical Sciences and Pathobiology, Virginia Tech, Blacksburg, VA 24061, USA.

Abstract

A large-scale RNA interference screen reveals a new mechanism of imatinib resistance in chronic myeloid leukemia that can be therapeutically targeted.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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