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Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer.
To examine the hypothesis that colorectal carcinomas with and without TP53 mutations may be characterised by aetiological heterogeneity, we analysed a group of 107 patients with primary Dukes' C colorectal cancer seen at the Memorial Sloan-Kettering Cancer Center (MSKCC) from 1986 to 1990. We a...
Autores principales: | , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
1995
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033726/ https://www.ncbi.nlm.nih.gov/pubmed/7710960 |
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author | Zhang, Z. F. Zeng, Z. S. Sarkis, A. S. Klimstra, D. S. Charytonowicz, E. Pollack, D. Vena, J. Guillem, J. Marshall, J. R. Cordon-Cardo, C. |
author_facet | Zhang, Z. F. Zeng, Z. S. Sarkis, A. S. Klimstra, D. S. Charytonowicz, E. Pollack, D. Vena, J. Guillem, J. Marshall, J. R. Cordon-Cardo, C. |
author_sort | Zhang, Z. F. |
collection | PubMed |
description | To examine the hypothesis that colorectal carcinomas with and without TP53 mutations may be characterised by aetiological heterogeneity, we analysed a group of 107 patients with primary Dukes' C colorectal cancer seen at the Memorial Sloan-Kettering Cancer Center (MSKCC) from 1986 to 1990. We assessed p53 overexpression using the monoclonal antibody PAb 1801, and identified 42 (39%) patients displaying p53-positive phenotype, defined as > or = 25% of positive cells. Patients with two or more first-degree relatives with cancer had an odds ratio (OR) of 2.9 (95% CI 1.0-8.3) for p53 overexpression in comparison with those without a family history of cancer (trend test, P = 0.11). A possible association between body weight and p53 overexpression was observed. The ORs were 1.9 for the second quartile, 1.9 for the third quartile and 3.4 for the highest quartile in comparison with the lowest quartile (trend test, P = 0.06). No association between occupational physical activity, smoking, drinking, parity and p53 overexpression was identified. The results suggest that p53 overexpression may be related to genetic predisposition to colorectal cancer, and p53-positive and p53-negative colorectal cancers may be controlled by different aetiological pathways. IMAGES: |
format | Text |
id | pubmed-2033726 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1995 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-20337262009-09-10 Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer. Zhang, Z. F. Zeng, Z. S. Sarkis, A. S. Klimstra, D. S. Charytonowicz, E. Pollack, D. Vena, J. Guillem, J. Marshall, J. R. Cordon-Cardo, C. Br J Cancer Research Article To examine the hypothesis that colorectal carcinomas with and without TP53 mutations may be characterised by aetiological heterogeneity, we analysed a group of 107 patients with primary Dukes' C colorectal cancer seen at the Memorial Sloan-Kettering Cancer Center (MSKCC) from 1986 to 1990. We assessed p53 overexpression using the monoclonal antibody PAb 1801, and identified 42 (39%) patients displaying p53-positive phenotype, defined as > or = 25% of positive cells. Patients with two or more first-degree relatives with cancer had an odds ratio (OR) of 2.9 (95% CI 1.0-8.3) for p53 overexpression in comparison with those without a family history of cancer (trend test, P = 0.11). A possible association between body weight and p53 overexpression was observed. The ORs were 1.9 for the second quartile, 1.9 for the third quartile and 3.4 for the highest quartile in comparison with the lowest quartile (trend test, P = 0.06). No association between occupational physical activity, smoking, drinking, parity and p53 overexpression was identified. The results suggest that p53 overexpression may be related to genetic predisposition to colorectal cancer, and p53-positive and p53-negative colorectal cancers may be controlled by different aetiological pathways. IMAGES: Nature Publishing Group 1995-04 /pmc/articles/PMC2033726/ /pubmed/7710960 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 Zhang, Z. F. Zeng, Z. S. Sarkis, A. S. Klimstra, D. S. Charytonowicz, E. Pollack, D. Vena, J. Guillem, J. Marshall, J. R. Cordon-Cardo, C. Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer. |
title | Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer. |
title_full | Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer. |
title_fullStr | Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer. |
title_full_unstemmed | Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer. |
title_short | Family history of cancer, body weight, and p53 nuclear overexpression in Duke's C colorectal cancer. |
title_sort | family history of cancer, body weight, and p53 nuclear overexpression in duke's c colorectal cancer. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033726/ https://www.ncbi.nlm.nih.gov/pubmed/7710960 |
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