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Oncogene. 1996 May 16;12(10):2147-53.

Loss of heterozygosity of chromosome 17 in human borderline and invasive epithelial ovarian tumors.

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  • 1Department of Obsterics, Gynecology and Reproductive Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.


Polymerase chain reaction (PCR) analysis of microsatellite polymorphisms corresponding to four loci which map to chromosome 17p and 11 loci which map to chromosome 17q was performed to screen for loss of heterozygosity (LOH) in paired normal and tumor tissues from 27 cases of borderline epithelial ovarian tumors (BEOT) and 32 cases of invasive epithelial ovarian cancers (IOC). LOH was observed in six of 27 (22%) of the borderline tumors and in 29 of 32 (90%) of the invasive ovarian cancers (P<0.001). At all 15 loci studied, a lower percentage of allelic loss was detected in borderline tumors (0-14%) vs invasive cancer (8-93%). At eight loci this difference was statistically significant. For IOC, one common loss region was identified on chromosome 17p and four distinct common loss regions were on chromosome 17q, which supports the notion that multiple tumor suppressors may reside on chromosome 17 in IOC. These data suggest that LOH on chromosome 17 is an infrequent event in BEOT compared with IOC and therefore may not be important in the distinct pathogenesis of BEOT.

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