LOSS OF HETEROZYGOSITY OF THE RETINOBLASTOMA AND ADENOMATOUS POLYPOSIS SUSCEPTIBILITY GENE LOCI AND IN CHROMOSOMES 10P, 10Q AND 16Q IN HUMAN PROSTATE-CANCER

作者：PHILLIPS SMA^*; MORTON DG; LEE SJ; WALLACE DMA; NEOPTOLEMOS JP

来源：British Journal of Urology, 1994, 73(4): 390-395.

DOI：10.1111/j.1464-410X.1994.tb07602.x

• TUMOR SUPPRESSOR GENES
• POLYMORPHISM
• LOSS OF HETEROZYGOSITY
• DELETION
• ALLELE

Objective To examine prostate tumours for losses of known or suspected tumour suppressor genes to determine some of the important events in the genesis of this common cancer.
Materials and methods Paired tumour and blood samples were obtained from 21 patients who underwent transurethral resection of malignant prostate glands for urinary outflow obstruction. Paired tumour and normal tissue (leucocytes) DNA was extracted and examined for possible losses of several known or suspected tumour suppressor genes, using restriction fragment length polymorphism techniques to detect loss of heterozygosity.
Results Deletions of the retinoblastoma susceptibility gene (RB1) locus were found in six of nine informative cases using two intragenic probes (p68RS2.0 and p123ml.8). The locus related to the familial adenomatous polyposis susceptibility (APC) gene demonstrated loss of heterozygosity in three of seven informative cases using the EF5.44 probe. Losses were also noted in loci on chromosome 10p in four of 19 informative cases (probe cTBQ7), chromosome 10q in eight out of 19 informative cases (probes EFD75 and D10S90) and in 16q in three of 17 informative cases (probe D16S7).
Conclusion These finding suggest that losses of the RB1 and APC tumour suppressor genes and suspected tumour suppressor genes on 10p, 10q and 16q may be important events in the genesis of prostatic tumours.

• 出版日期1994-4