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Author: Ueda, T.; Komiya, A.; Emi, M.; Suzuki, H.; Shiraishi, T.; Yatani,
R.; Masai, M.; Yasuda, K.; Ito, H.
Year: 1997
Title: Allelic losses on 18q21 are associated with progression and
metastasis in human prostate cancer
Journal: Genes Chromosomes Cancer
Volume: 20
Issue: 2
Pages: 140-7
Label: 97472605
Keywords: Adenocarcinoma/*genetics/secondary
Chromosomes, Human, Pair 18/*genetics
Disease Progression
DNA, Neoplasm/analysis
Human
Loss of Heterozygosity
Male
Microsatellite Repeats
Neoplasm Metastasis/genetics
Neoplasm Staging
Polymorphism, Single-Stranded Conformational
Prostatic Neoplasms/*genetics/pathology
Regression Analysis
Support, Non-U.S. Gov't
Abstract: We analyzed normal/tumor DNA pairs obtained from 46 patients
with prostate cancers (stage B, 16 cases; C, 10 cases; D1, 4 cases;
and endocrine therapy-resistant cancer-death, 16 cases) for loss
of heterozygosity using 32 microsatellite markers on chromosome
18. Seventeen of the 46 cases (37%) showed loss of heterozygosity
(LOH) for at least one locus on the long arm. Detailed deletion
mapping in these tumors identified a distinct commonly deleted
region within a 5-cM interval in 18q21.1. There was a statistical
correlation between the frequency of LOH on 18q and clinical stage
(chi 2 = 12.3; P = 0.0064). LOH on 18q was observed more frequently
in Stage D1 cases (4/4; 100%) than in stage B+C cases (5/26; 19%;
P = 0.0046, Fisher's exact test). In 8 of 9 (89%) cancer-death
patients from whom DNAs were available from both primary and metastatic
tumors, the primary tumors had either no detectable abnormality
of chromosome 18 or the region involving loss of heterozygosity
was limited while the metastatic foci showed more frequent and
extended allelic losses on this chromosome. No abnormalities were
detected in the DCC and DPC4 genes when their exons were analyzed
separately by single strand conformation polymorphism assay. These
results suggest that inactivation of one or more putative tumor
suppressor genes on 18q21 other than DCC and DPC4 plays an important
role in the progression of human prostate cancer.