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Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas.
Using a panel of ten polymorphic markers, we examined the frequency of loss of heterozygosity (LOH) on chromosome 17 in 55 sporadic ovarian tumours. LOH on 17p and 17q was observed to be 50% and 62% respectively. LOH at D17S5 was detected in 24/36 (67%) of malignant cases and in 19/43 (44%) at TP53;...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
1996
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2074870/ https://www.ncbi.nlm.nih.gov/pubmed/8932340 |
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author | Papp, J. Csokay, B. Bosze, P. Zalay, Z. Toth, J. Ponder, B. Olah, E. |
author_facet | Papp, J. Csokay, B. Bosze, P. Zalay, Z. Toth, J. Ponder, B. Olah, E. |
author_sort | Papp, J. |
collection | PubMed |
description | Using a panel of ten polymorphic markers, we examined the frequency of loss of heterozygosity (LOH) on chromosome 17 in 55 sporadic ovarian tumours. LOH on 17p and 17q was observed to be 50% and 62% respectively. LOH at D17S5 was detected in 24/36 (67%) of malignant cases and in 19/43 (44%) at TP53; the marker D17S855 intragenic to the BRCA1 gene showed allele loss in 50% (20/40) cases. The data presented here suggest that loss of the whole chromosome 17 is a relatively frequent event (30%) in ovarian carcinomas and this observation is especially frequent for serous, transitional cell and anaplastic histological subtypes. Mucinous and endometrioid ovarian tumours showed only short interstitial deletions (4/11, 36%). The overall frequency of the short deletions was relatively low (7/43, 16%) in our panel of carcinomas. Amplification of c-erbB-2/neu oncogene was detected in 32% (11/34) of the carcinomas tested; the gene was amplified only in those histological subtypes in which high incidence of LOH on chromosome 17 was observed, and was associated with advanced stages of the disease. We conclude that different histological types of tumour may have different aetiological mechanisms, and tumour-suppressor genes on chromosome 17 might be associated specifically with serous and transitional cell ovarian carcinomas. IMAGES: |
format | Text |
id | pubmed-2074870 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1996 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-20748702009-09-10 Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas. Papp, J. Csokay, B. Bosze, P. Zalay, Z. Toth, J. Ponder, B. Olah, E. Br J Cancer Research Article Using a panel of ten polymorphic markers, we examined the frequency of loss of heterozygosity (LOH) on chromosome 17 in 55 sporadic ovarian tumours. LOH on 17p and 17q was observed to be 50% and 62% respectively. LOH at D17S5 was detected in 24/36 (67%) of malignant cases and in 19/43 (44%) at TP53; the marker D17S855 intragenic to the BRCA1 gene showed allele loss in 50% (20/40) cases. The data presented here suggest that loss of the whole chromosome 17 is a relatively frequent event (30%) in ovarian carcinomas and this observation is especially frequent for serous, transitional cell and anaplastic histological subtypes. Mucinous and endometrioid ovarian tumours showed only short interstitial deletions (4/11, 36%). The overall frequency of the short deletions was relatively low (7/43, 16%) in our panel of carcinomas. Amplification of c-erbB-2/neu oncogene was detected in 32% (11/34) of the carcinomas tested; the gene was amplified only in those histological subtypes in which high incidence of LOH on chromosome 17 was observed, and was associated with advanced stages of the disease. We conclude that different histological types of tumour may have different aetiological mechanisms, and tumour-suppressor genes on chromosome 17 might be associated specifically with serous and transitional cell ovarian carcinomas. IMAGES: Nature Publishing Group 1996-11 /pmc/articles/PMC2074870/ /pubmed/8932340 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Research Article Papp, J. Csokay, B. Bosze, P. Zalay, Z. Toth, J. Ponder, B. Olah, E. Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas. |
title | Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas. |
title_full | Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas. |
title_fullStr | Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas. |
title_full_unstemmed | Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas. |
title_short | Allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas. |
title_sort | allele loss from large regions of chromosome 17 is common only in certain histological subtypes of ovarian carcinomas. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2074870/ https://www.ncbi.nlm.nih.gov/pubmed/8932340 |
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