Title | Allelic loss of 10q23, the PTEN tumour suppressor gene locus, in Barrett's oesophagus-associated adenocarcinoma. |
Publication Type | Journal Article |
Year of Publication | 2001 |
Authors | Kulke MH, Odze RD, Thakore KS, Thomas G, Wang H, Loda M, Eng C |
Journal | Br J Cancer |
Volume | 84 |
Issue | 6 |
Pagination | 748-53 |
Date Published | 2001 Mar 23 |
ISSN | 0007-0920 |
Keywords | Adenocarcinoma, Adult, Aged, Aged, 80 and over, Alleles, Barrett Esophagus, Chromosomes, Human, Pair 10, Female, Genes, Tumor Suppressor, Humans, Loss of Heterozygosity, Male, Middle Aged, Phosphoric Monoester Hydrolases, PTEN Phosphohydrolase, Tumor Suppressor Proteins |
Abstract | PTEN is a putative tumour suppressor gene located on chromosome band 10q23. Mutations in PTEN have been identified in numerous human malignancies, including cancers of the brain, endometrium, ovary, and prostate. In this study, we screened 80 Barrett's oesophagus-associated adenocarcinomas (BOAd) for loss of heterozygosity (LOH) at 10q23, using the microsatellite markers D10S541, D10S219, and D10S551. Tumours demonstrating LOH were then screened for the presence or absence of PTEN mutations. LOH at one or more loci was identified in 17/80 (21%) cases. In none of these cases did we detect mutations in PTEN. The presence of LOH did not correlate with patient age, tumour stage, degree of differentiation, presence of perineural or vascular invasion, or overall survival. We conclude that LOH at chromosome 10q23 is uncommon in BOAd, is not associated with mutations in the PTEN tumour suppressor gene, and does not correlate with the clinical or pathologic features of these tumours. It is possible that PTEN is inactivated through other mechanisms in BOAd. |
DOI | 10.1054/bjoc.2000.1660 |
Alternate Journal | Br J Cancer |
PubMed ID | 11259087 |
PubMed Central ID | PMC2363812 |
Related Faculty:
Massimo Loda, M.D.