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Allelic imbalance within the E‐cadherin gene is an infrequent event in prostate carcinogenesis
Author(s) -
Murant Susan J.,
Rolley Nicky,
Phillips Stewart M.A.,
Stower Michael,
Maitland Norman J.
Publication year - 2000
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(200001)27:1<104::aid-gcc13>3.0.co;2-6
Subject(s) - locus (genetics) , allele , biology , single nucleotide polymorphism , loss of heterozygosity , genetics , carcinogenesis , prostate cancer , gene , microsatellite , cancer research , microbiology and biotechnology , cancer , genotype
By exploiting two single nucleotide polymorphisms (SNPs) located within the E‐cadherin gene, at 16q22, we have determined the frequency of allelic imbalance at this proposed tumor suppressor locus in a series of human prostatic carcinoma DNA samples. Whereas results with seven highly polymorphic microsatellite markers flanking the E‐cadherin locus confirmed the existence of three separate loci on chromosome 16, at which allelic imbalance increased with increasing loss of tumor cell differentiation, no allelic imbalance within the E‐cadherin gene was detected either by single‐strand conformational polymorphism analysis or by direct sequencing. We conclude that the loss of E‐cadherin function observed in prostate cancer is not a result of allelic deletion. Genes Chromosomes Cancer 27:104–109, 2000. © 2000 Wiley‐Liss, Inc.