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p16 mutations/deletions are not frequent events in prostate cancer.
Cyclin-dependent kinase-4 inhibitor gene (p16INK4) has recently been mapped to chromosome 9p21. Homozygous deletions of this gene have been found at high frequency in cell lines derived from different types of tumours. These findings suggested therefore, that p16INK4 is a tumour-suppressor gene invo...
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/PMC2074596/ https://www.ncbi.nlm.nih.gov/pubmed/8679444 |
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author | Tamimi, Y. Bringuier, P. P. Smit, F. van Bokhoven, A. Debruyne, F. M. Schalken, J. A. |
author_facet | Tamimi, Y. Bringuier, P. P. Smit, F. van Bokhoven, A. Debruyne, F. M. Schalken, J. A. |
author_sort | Tamimi, Y. |
collection | PubMed |
description | Cyclin-dependent kinase-4 inhibitor gene (p16INK4) has recently been mapped to chromosome 9p21. Homozygous deletions of this gene have been found at high frequency in cell lines derived from different types of tumours. These findings suggested therefore, that p16INK4 is a tumour-suppressor gene involved in a wide variety of human cancers. To investigate the frequency of p16INK mutations/deletions in prostate cancer, we screened 20 primary prostate tumours and four established cell lines by polymerase chain reaction (PCR) and single-strand conformation polymorphism (SSCP) analysis for exon 1 and exon 2. In contrast to most previous reports, no homozygous deletions were found in prostate cancer cell lines, but one cell line (DU145) has revealed to a mutation at codon 76. Only two SSCP shifts were detected in primary tumours: one of them corresponds to a mutation at codon 55 and the other one probably corresponds to a polymorphism. These data suggest that mutation of the p16INK4 gene is not a frequent genetic alteration implicated in prostate cancer development. IMAGES: |
format | Text |
id | pubmed-2074596 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1996 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-20745962009-09-10 p16 mutations/deletions are not frequent events in prostate cancer. Tamimi, Y. Bringuier, P. P. Smit, F. van Bokhoven, A. Debruyne, F. M. Schalken, J. A. Br J Cancer Research Article Cyclin-dependent kinase-4 inhibitor gene (p16INK4) has recently been mapped to chromosome 9p21. Homozygous deletions of this gene have been found at high frequency in cell lines derived from different types of tumours. These findings suggested therefore, that p16INK4 is a tumour-suppressor gene involved in a wide variety of human cancers. To investigate the frequency of p16INK mutations/deletions in prostate cancer, we screened 20 primary prostate tumours and four established cell lines by polymerase chain reaction (PCR) and single-strand conformation polymorphism (SSCP) analysis for exon 1 and exon 2. In contrast to most previous reports, no homozygous deletions were found in prostate cancer cell lines, but one cell line (DU145) has revealed to a mutation at codon 76. Only two SSCP shifts were detected in primary tumours: one of them corresponds to a mutation at codon 55 and the other one probably corresponds to a polymorphism. These data suggest that mutation of the p16INK4 gene is not a frequent genetic alteration implicated in prostate cancer development. IMAGES: Nature Publishing Group 1996-07 /pmc/articles/PMC2074596/ /pubmed/8679444 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 Tamimi, Y. Bringuier, P. P. Smit, F. van Bokhoven, A. Debruyne, F. M. Schalken, J. A. p16 mutations/deletions are not frequent events in prostate cancer. |
title | p16 mutations/deletions are not frequent events in prostate cancer. |
title_full | p16 mutations/deletions are not frequent events in prostate cancer. |
title_fullStr | p16 mutations/deletions are not frequent events in prostate cancer. |
title_full_unstemmed | p16 mutations/deletions are not frequent events in prostate cancer. |
title_short | p16 mutations/deletions are not frequent events in prostate cancer. |
title_sort | p16 mutations/deletions are not frequent events in prostate cancer. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2074596/ https://www.ncbi.nlm.nih.gov/pubmed/8679444 |
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