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Critical Role for Cyclin D2 in BCR/ABL-induced Proliferation of Hematopoietic Cells¹

Whitehead Institute, Cambridge, Massachusetts 02142 [N. J., M. D., G. Q. D.]; Dana-Farber Cancer Institute and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115 [E. S., P. S.]; Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115 [E. S.]; and Division of Hematology/Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114 [G. Q. D.]

Chronic myeloid leukemia is caused by the tyrosine kinase oncoprotein BCR/ABL. Using oligonucleotide arrays to assay mRNAs at different phases of the cell cycle in BCR/ABL-transformed cells, we found that cyclin D2 mRNA was constitutively expressed at high levels throughout the cell cycle, a pattern confirmed by immunoblotting of protein lysates. Bone marrow cells from cyclin D2-deficient strains of mice failed to proliferate in response to infection with a retrovirus carrying BCR/ABL and failed to generate transformed lymphoid cell lines in vitro. These results establish that BCR/ABL promotes cell cycle progression by altering expression of cyclin D2 and that cyclin D2 induction plays a critical role in proliferation of hematopoietic cells by BCR/ABL.

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