Allelic imbalance in familial and sporadic prostate cancer at the putative human prostate cancer susceptibility locus, HPC1
A recent report has provided strong evidence for a major prostate cancer susceptibility locus (HPC1) on chromosome 1q24-25 (Smith et al, 1996). Most inherited cancer susceptibility genes function as tumour-suppressor genes (TSGs). Allelic loss or imbalance in tumour tissue is often the hallmark of a...
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Veröffentlicht in: | British journal of cancer 1998-12, Vol.78 (11), p.1430-1433 |
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creator | Dunsmuir, WD Edwards, SM Lakhani, SR Young, M Corbishley, C Kirby, RS Dearnaley, DP Dowe, A Ardern-Jones, A Kelly, J Eeles, RA |
description | A recent report has provided strong evidence for a major prostate cancer susceptibility locus (HPC1) on chromosome 1q24-25 (Smith et al, 1996). Most inherited cancer susceptibility genes function as tumour-suppressor genes (TSGs). Allelic loss or imbalance in tumour tissue is often the hallmark of a TSG. Studies of allelic loss have not previously implicated the chromosomal region 1q24-25 in prostate cancer. However, analysis of tumour DNA from cases in prostate cancer families has not been reported. In this study, we have evaluated DNA from tissue obtained from small families [3-5 affected members (n = 17)], sibling pairs (n = 15) and sporadic (n = 40) prostate tumours using the three markers from Smith et al (1996) that defined the maximum multipoint linkage lod score. Although widely spaced (12-50 cM), each marker showed evidence of allelic imbalance in only approximately 7.5% of informative tumours. There was no difference between the familial and sporadic cases. We conclude that the incidence of allelic imbalance at HPC1 is low in both sporadic tumours and small prostate cancer families. In this group of patients, HPC1 is unlikely to be acting as a TSG in the development of prostate cancer. |
doi_str_mv | 10.1038/bjc.1998.703 |
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Most inherited cancer susceptibility genes function as tumour-suppressor genes (TSGs). Allelic loss or imbalance in tumour tissue is often the hallmark of a TSG. Studies of allelic loss have not previously implicated the chromosomal region 1q24-25 in prostate cancer. However, analysis of tumour DNA from cases in prostate cancer families has not been reported. In this study, we have evaluated DNA from tissue obtained from small families [3-5 affected members (n = 17)], sibling pairs (n = 15) and sporadic (n = 40) prostate tumours using the three markers from Smith et al (1996) that defined the maximum multipoint linkage lod score. Although widely spaced (12-50 cM), each marker showed evidence of allelic imbalance in only approximately 7.5% of informative tumours. There was no difference between the familial and sporadic cases. We conclude that the incidence of allelic imbalance at HPC1 is low in both sporadic tumours and small prostate cancer families. In this group of patients, HPC1 is unlikely to be acting as a TSG in the development of prostate cancer.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/bjc.1998.703</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Drug Resistance ; Epidemiology ; experimental-oncology ; Medical sciences ; Molecular Medicine ; Nephrology. Urinary tract diseases ; Oncology ; Tumors of the urinary system ; Urinary tract. 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Most inherited cancer susceptibility genes function as tumour-suppressor genes (TSGs). Allelic loss or imbalance in tumour tissue is often the hallmark of a TSG. Studies of allelic loss have not previously implicated the chromosomal region 1q24-25 in prostate cancer. However, analysis of tumour DNA from cases in prostate cancer families has not been reported. In this study, we have evaluated DNA from tissue obtained from small families [3-5 affected members (n = 17)], sibling pairs (n = 15) and sporadic (n = 40) prostate tumours using the three markers from Smith et al (1996) that defined the maximum multipoint linkage lod score. Although widely spaced (12-50 cM), each marker showed evidence of allelic imbalance in only approximately 7.5% of informative tumours. There was no difference between the familial and sporadic cases. We conclude that the incidence of allelic imbalance at HPC1 is low in both sporadic tumours and small prostate cancer families. In this group of patients, HPC1 is unlikely to be acting as a TSG in the development of prostate cancer.</description><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>experimental-oncology</subject><subject>Medical sciences</subject><subject>Molecular Medicine</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oncology</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. 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Urinary tract diseases</topic><topic>Oncology</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dunsmuir, WD</creatorcontrib><creatorcontrib>Edwards, SM</creatorcontrib><creatorcontrib>Lakhani, SR</creatorcontrib><creatorcontrib>Young, M</creatorcontrib><creatorcontrib>Corbishley, C</creatorcontrib><creatorcontrib>Kirby, RS</creatorcontrib><creatorcontrib>Dearnaley, DP</creatorcontrib><creatorcontrib>Dowe, A</creatorcontrib><creatorcontrib>Ardern-Jones, A</creatorcontrib><creatorcontrib>Kelly, J</creatorcontrib><creatorcontrib>Eeles, RA</creatorcontrib><creatorcontrib>The CRC/BPG UK Familial Prostate Cancer Study Collaborators</creatorcontrib><collection>Pascal-Francis</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dunsmuir, WD</au><au>Edwards, SM</au><au>Lakhani, SR</au><au>Young, M</au><au>Corbishley, C</au><au>Kirby, RS</au><au>Dearnaley, DP</au><au>Dowe, A</au><au>Ardern-Jones, A</au><au>Kelly, J</au><au>Eeles, RA</au><aucorp>The CRC/BPG UK Familial Prostate Cancer Study Collaborators</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Allelic imbalance in familial and sporadic prostate cancer at the putative human prostate cancer susceptibility locus, HPC1</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><date>1998-12-01</date><risdate>1998</risdate><volume>78</volume><issue>11</issue><spage>1430</spage><epage>1433</epage><pages>1430-1433</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>A recent report has provided strong evidence for a major prostate cancer susceptibility locus (HPC1) on chromosome 1q24-25 (Smith et al, 1996). Most inherited cancer susceptibility genes function as tumour-suppressor genes (TSGs). Allelic loss or imbalance in tumour tissue is often the hallmark of a TSG. Studies of allelic loss have not previously implicated the chromosomal region 1q24-25 in prostate cancer. However, analysis of tumour DNA from cases in prostate cancer families has not been reported. In this study, we have evaluated DNA from tissue obtained from small families [3-5 affected members (n = 17)], sibling pairs (n = 15) and sporadic (n = 40) prostate tumours using the three markers from Smith et al (1996) that defined the maximum multipoint linkage lod score. Although widely spaced (12-50 cM), each marker showed evidence of allelic imbalance in only approximately 7.5% of informative tumours. There was no difference between the familial and sporadic cases. We conclude that the incidence of allelic imbalance at HPC1 is low in both sporadic tumours and small prostate cancer families. In this group of patients, HPC1 is unlikely to be acting as a TSG in the development of prostate cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><doi>10.1038/bjc.1998.703</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Research Drug Resistance Epidemiology experimental-oncology Medical sciences Molecular Medicine Nephrology. Urinary tract diseases Oncology Tumors of the urinary system Urinary tract. Prostate gland |
title | Allelic imbalance in familial and sporadic prostate cancer at the putative human prostate cancer susceptibility locus, HPC1 |
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