LOSS OF HETEROZYGOSITY OF THE RETINOBLASTOMA AND ADENOMATOUS POLYPOSIS SUSCEPTIBILITY GENE LOCI AND IN CHROMOSOMES 10P, 10Q AND 16Q IN HUMAN PROSTATE-CANCER
Sma. Phillips et al., LOSS OF HETEROZYGOSITY OF THE RETINOBLASTOMA AND ADENOMATOUS POLYPOSIS SUSCEPTIBILITY GENE LOCI AND IN CHROMOSOMES 10P, 10Q AND 16Q IN HUMAN PROSTATE-CANCER, British Journal of Urology, 73(4), 1994, pp. 390-395
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 transu
rethral resection of malignant prostate glands for urinary outflow obs
truction. Paired tumour and normal tissue (leucocytes) DNA was extract
ed and examined for possible losses of several known or suspected tumo
ur suppressor genes, using restriction fragment length polymorphism te
chniques to detect loss of heterozygosity. Results Deletions of the re
tinoblastoma 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 susceptibili
ty (APC) gene demonstrated loss of heterozygosity in three of seven in
formative cases using the EF5.44 probe. Losses were also noted in loci
on chromosome 10p in four of 19 informative cases (probe cTBQ7), chro
mosome 10q in eight out of 19 informative cases (probes EFD75 and D10S
90) and in 16q in three of 17 informative cases (probe D16S7). Conclus
ion These finding suggest that losses of the RB1 and APC tumour suppre
ssor genes and suspected tumour suppressor genes on 10p, 10q and 16q m
ay be important events in the genesis of prostatic tumours.