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Previous Volume 328:141 January 14, 1993 Number 2 Next

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To the Editor: The editorial by Cheson (Aug. 6 issue)¹ mentions the bcl-2 oncogene in follicular B-cell non-Hodgkin's lymphoma. The chromosomal location of this oncogene is incorrectly identified. This oncogene was cloned at the site of the t(14;18) (q32;q21) breakpoint² rather than at the t(11;14) translocation. The bcl-1 oncogene has been characterized at the t(11;14) (q13;q32) breakpoint³.

The product of the fusion of the PML gene to the retinoic acid receptor-alpha gene that results from the t(15;17) translocation is similar to the product of the fusion of bcr and abl, in that perturbation of both genes may contribute to pathogenesis, whereas the disruption of the normal expression of the bcl-2 locus alone appears to contribute to the development of lymphoma.

Stanley R. Frankel, M.D.
Roswell Park Cancer Institute
Buffalo, NY 14263

References

1. Cheson BD. The maturation of differentiation therapy. N Engl J Med 1992;327:422-424. [Medline]
2. Tsujimoto Y, Finger LR, Yunis J, Nowell PC, Croce CM. Cloning of the chromosome breakpoint of neoplastic B cells with the t(14;18) chromosome translocation. Science 1984;226:1097-1099. [Free Full Text]
3. Tsujimoto Y, Yunis J, Onorato-Showe L, Erikson J, Nowell PC, Croce CM. Molecular cloning of the chromosomal breakpoint of B-cell lymphomas and leukemias with the t(11;14) chromosome translocation. Science 1984;224:1403-1406. [Free Full Text]

To the Editor: I appreciate Dr. Frankel's correction of the inadvertent substitution of the translocation of bcl-1 for that of bcl-2. This mistake was missed despite intensive proofreading by me and several colleagues.

Bruce D. Cheson, M.D.
National Cancer Institute
Bethesda, MD 20892

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