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Inactivation of the retinoblastoma gene in human lymphoid neoplasms
AM Ginsberg, M Raffeld and J Cossman
Laboratory of Pathology, National Cancer Institute, National Institutes of
Health, Bethesda, MD.
The absence of wild type retinoblastoma (Rb) gene expression in a wide
variety of human solid tumors suggests an etiologic role for this tumor
suppressor gene in human cancer. We have evaluated the involvement of Rb
gene inactivation in the pathogenesis and progression of human lymphoma and
leukemia. We examined the genomic configuration and transcription of the Rb
gene in cultured cell lines and primary cases of T- and B-cell lymphomas
and leukemias. By Southern analysis, abnormalities of the Rb locus were
identified in 1 of 5 T-cell acute lymphoblastic lymphoma (T-ALL) cell
lines, 1 of 26 primary cases of T- ALL, 1 of 40 primary cases of chronic
lymphocytic lymphoma/well- differentiated lymphoma (CLL/WDL), and 1 of 15
primary cases of intermediately differentiated lymphoma (IDL). By Northern
analysis, markedly reduced or abnormal expression of the Rb gene was
identified in 2 of 5 T-ALL cell lines, 1 of 7 primary cases of T-ALL, 1 of
5 primary cases of CLL/WDL, and 1 of 6 primary cases of IDL. These findings
show that Rb gene inactivation can be associated with a broad range of
lymphoid neoplasms and that loss of the tumor suppressor function of Rb may
influence the pathogenesis and progression of lymphoma/leukemia.
Volume 77,
Issue 4,
pp. 833-840,
02/15/1991
Copyright © 1991 by The American Society of Hematology
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