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Research Article Free access | 10.1172/JCI113235

Expression of Bcl-2 and Bcl-2-Ig fusion transcripts in normal and neoplastic cells.

W B Graninger, M Seto, B Boutain, P Goldman, and S J Korsmeyer

Department of Medicine, Microbiology and Immunology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110.

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Department of Medicine, Microbiology and Immunology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110.

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Department of Medicine, Microbiology and Immunology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110.

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Department of Medicine, Microbiology and Immunology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110.

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Department of Medicine, Microbiology and Immunology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110.

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Published November 1, 1987 - More info

Published in Volume 80, Issue 5 on November 1, 1987
J Clin Invest. 1987;80(5):1512–1515. https://doi.org/10.1172/JCI113235.
© 1987 The American Society for Clinical Investigation
Published November 1, 1987 - Version history
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Abstract

We examined the expression of the Bcl-2 gene at chromosome segment 18q21, that is translocated into the Ig heavy chain gene locus in t(14;18) bearing lymphomas. Bcl-2, while B cell associated, is expressed in a variety of hematopoietic lineages including T cells. Bcl-2 mRNA levels are high during pre-B cell development, the time at which the t(14;18) translocation occurs, but are down regulated with maturation. Like certain other oncogenes, Bcl-2 is quiescent in resting B cells but up-regulated with B cell activation. Mature B cell lymphomas with a t(14;18) have log-folds more mRNA than matched counterparts without the translocation. A sensitive S1 protection assay revealed that all transcripts in t(14;18) B cells were Bcl-2-Ig fusion mRNAs and originated from the translocated allele. Thus, there is a marked deregulation of Bcl-2 when it is introduced into the Ig locus in t(14;18) lymphomas.

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