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The t(6;16)(p21;q22) Chromosome Translocation in the LNCaP Prostate Carcinoma Cell Line Results in a tpc/hpr Fusion Gene¹

Jefferson Cancer Center, Jefferson Cancer Institute and Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107

Very little is known about the molecular and genetic mechanisms involved in prostate cancer. Previous studies have shown frequent loss of heterozygosity (40%) at chromosomal regions 8p, 10q, and 16q, suggesting the presence of tumor suppressor genes in these regions. The LNCaP cell line, established from a metastatic lesion of human prostatic adenocarcinoma, carries a t(6;16)(p21;q22) translocation. To determine whether this translocation involved genes important in the process of malignant transformation, we cloned and sequenced the t(6;16) breakpoint of this cell line. Sequence analysis showed that the breakpoint is within the haptoglobin gene cluster on chromosome 16, and that, on chromosome 6, the break occurs within a novel gene, tpc, similar to the prokaryotic S10 ribosomal protein gene. The translocation results in the production of a fusion transcript, tpc/hpr.

¹ This work was supported by an Outstanding Investigator Award from the National Cancer Institute (CA39860) (C. M. C.), National Research Fellowship Award NCI 5 F3I CA60352-02 (F. B.), and an AIDS fellowship (D.M. 4.16.92, 2601/SAP 7.2) from the Instituto Superiore di Sanita (Italy: M. L. V.).

² To whom requests for reprints should be addressed, Jefferson Cancer Center, Thomas Jefferson Medical College, BLSB, Room 1050, 233 South 10^th Street, Philadelphia, PA 19107, Phone: (215) 955-4645; Fax: 923-3528.

Received 12/15/95. Accepted 1/ 2/96.

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