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Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis.
Loss of the RB1 gene is an important event in the initiation and progression of many tumours. Prostate tissue from 43 patients with prostate cancers and ten with benign prostatic hypertrophy (BPH) were studied for loss of heterozygosity of the RB1 gene. Four intragenic polymorphic loci were studied...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
1994
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033690/ https://www.ncbi.nlm.nih.gov/pubmed/7526887 |
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author | Phillips, S. M. Barton, C. M. Lee, S. J. Morton, D. G. Wallace, D. M. Lemoine, N. R. Neoptolemos, J. P. |
author_facet | Phillips, S. M. Barton, C. M. Lee, S. J. Morton, D. G. Wallace, D. M. Lemoine, N. R. Neoptolemos, J. P. |
author_sort | Phillips, S. M. |
collection | PubMed |
description | Loss of the RB1 gene is an important event in the initiation and progression of many tumours. Prostate tissue from 43 patients with prostate cancers and ten with benign prostatic hypertrophy (BPH) were studied for loss of heterozygosity of the RB1 gene. Four intragenic polymorphic loci were studied with two techniques. These were restriction fragment length polymorphism (RFLP). Southern blotting and hybridisation with the p123m1.8 and p68RS2.0 probes (to introns 1 and 17 respectively) and also the polymerase chain reaction (PCR) to amplify loci within introns 17 and 20. Protein product (pRB) expression was determined by immunohistochemistry using the NCL-RB antibody in nine patients with cancer and four patients with BPH. Loss of heterozygosity was found in 24 out of 40 (60%) informative patients with cancer. Loss of RB1 occurred with a similar frequency in early-stage and low-grade cancers as in more advanced cancers. Loss of RB1 was also found in one patient with BPH. Expression of pRB was completely absent from seven cancers and markedly reduced in the other two, while nuclear pRB staining was always present in areas of BPH, whether alongside cancer-containing tissue or with BPH alone. We conclude that loss of RB1 is an early event in prostatic tumorigenesis. IMAGES: |
format | Text |
id | pubmed-2033690 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1994 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-20336902009-09-10 Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis. Phillips, S. M. Barton, C. M. Lee, S. J. Morton, D. G. Wallace, D. M. Lemoine, N. R. Neoptolemos, J. P. Br J Cancer Research Article Loss of the RB1 gene is an important event in the initiation and progression of many tumours. Prostate tissue from 43 patients with prostate cancers and ten with benign prostatic hypertrophy (BPH) were studied for loss of heterozygosity of the RB1 gene. Four intragenic polymorphic loci were studied with two techniques. These were restriction fragment length polymorphism (RFLP). Southern blotting and hybridisation with the p123m1.8 and p68RS2.0 probes (to introns 1 and 17 respectively) and also the polymerase chain reaction (PCR) to amplify loci within introns 17 and 20. Protein product (pRB) expression was determined by immunohistochemistry using the NCL-RB antibody in nine patients with cancer and four patients with BPH. Loss of heterozygosity was found in 24 out of 40 (60%) informative patients with cancer. Loss of RB1 occurred with a similar frequency in early-stage and low-grade cancers as in more advanced cancers. Loss of RB1 was also found in one patient with BPH. Expression of pRB was completely absent from seven cancers and markedly reduced in the other two, while nuclear pRB staining was always present in areas of BPH, whether alongside cancer-containing tissue or with BPH alone. We conclude that loss of RB1 is an early event in prostatic tumorigenesis. IMAGES: Nature Publishing Group 1994-12 /pmc/articles/PMC2033690/ /pubmed/7526887 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 Phillips, S. M. Barton, C. M. Lee, S. J. Morton, D. G. Wallace, D. M. Lemoine, N. R. Neoptolemos, J. P. Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis. |
title | Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis. |
title_full | Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis. |
title_fullStr | Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis. |
title_full_unstemmed | Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis. |
title_short | Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis. |
title_sort | loss of the retinoblastoma susceptibility gene (rb1) is a frequent and early event in prostatic tumorigenesis. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033690/ https://www.ncbi.nlm.nih.gov/pubmed/7526887 |
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