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Human Gliomas with Wild-Type p53 Express bcl-2¹

Molecular Neuro-Oncology Laboratory, Neurology Service [L. M. A., R. L. C., J. W. H.], Neurosurgery Service [G. R. H., D. N. L.], Department of Pathology (Neuropathology) [D. N. L.], and Harvard Medical School [G. R. H., D. N. L., J. W. H.], Massachusetts General Hospital, Charlestown, Massachusetts 02129

Human astrocytomas frequently overexpress wild-type p53, which suggests that gliomas have evolved a mechanism to subvert p53-mediated apoptosis. bcl-2 inhibits apoptosis mediated by p53, and it is expressed in several human cancers. We therefore examined a series of human gliomas to determine whether bcl-2 is expressed and whether this expression is associated with tumors which have wild-type p53. Twenty-eight paraffinembedded gliomas (3 WHO grade II, 13 grade III, 12 grade IV) were immunohistochemically stained for bcl-2 and p53. p53 mutations were identified with single strand conformation polymorphism and DNA sequencing. Sixteen of 28 (57%) tumors expressed bcl-2, and bcl-2 expression was associated with wild-type p53 (P < 0.01). Among gliomas which overexpressed p53, bcl-2 was positive in 7 of 7 tumors with wild-type p53 but in only 1 of 7 with mutant p53 (P < 0.01). We conclude that bcl-2 is frequently expressed in human gliomas and that expression is more common in tumors with wild-type p53.

¹ Supported by NIH Grants NS 01605 (J. W. H.) and CA 57683 (D. N. L.).

² To whom requests for reprints should be addressed, at Molecular Neuro-Oncology Laboratory, CNY6, Massachusetts General Hospital, Charlestown, MA 02129.

Received 11/14/94. Accepted 1/18/95.

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