Immunohistochemical analysis of expression and allelotype of mismatch repair genes ( and ) in bladder cancer
Mutation of human homologues of DNA mismatch repair (MMR) genes in tumours has been shown to be associated with the phenomenon of microsatellite instability (MSI). Several studies have reported the occurrence of MSI in bladder cancer, but evidence of involvement of MMR genes in the pathogenesis of t...
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| Veröffentlicht in: | British journal of cancer 2001-02, Vol.84 (3), p.321-328 |
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| creator | Kassem, H Sh Varley, J M Hamam, S M Margison, G P |
| description | Mutation of human homologues of DNA mismatch repair (MMR) genes in tumours has been shown to be associated with the phenomenon of microsatellite instability (MSI). Several studies have reported the occurrence of MSI in bladder cancer, but evidence of involvement of MMR genes in the pathogenesis of this cancer is still unclear. We therefore utilized quantitative immunohistochemical (IHC) image analysis and PCR-based allelotype analysis to determine
hMLH1
and
hMSH2
genes alteration in a cohort of Egyptian bladder cancer samples. IHC analysis of 24 TCC and 12 SCC revealed marked- intra and intertumour heterogeneity in the levels of expression of the two MMR proteins. One TCC lost MLH1 expression and one lost MSH2, (1/24, 4%), and one SCC lost MSH2 (1/12, 8%). A large proportion of analysed tumours revealed a percentage positivity of less than 50% for MLH1 and MSH2 expression (44% and 69%, respectively). Complete loss of heterozygosity in three dinucleotide repeats lying within, or in close proximity to,
hMLH1
and
hMSH2
was rare (2/57, (4%) for
MLH1
; and 1/55, (2%) for
MSH2
), however allelic imbalance was detected in 11/57 (
hMLH1
) and 10/55 (
hMSH2
) at any of the informative microsatellite loci. These alterations in structure and expression of DNA MMR genes suggest their possible involvement in the tumorigenesis and/or progression of bladder cancer. © 2001 Cancer Research Campaign
http://www.bjcancer.com |
| doi_str_mv | 10.1054/bjoc.2000.1595 |
| format | Article |
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hMLH1
and
hMSH2
genes alteration in a cohort of Egyptian bladder cancer samples. IHC analysis of 24 TCC and 12 SCC revealed marked- intra and intertumour heterogeneity in the levels of expression of the two MMR proteins. One TCC lost MLH1 expression and one lost MSH2, (1/24, 4%), and one SCC lost MSH2 (1/12, 8%). A large proportion of analysed tumours revealed a percentage positivity of less than 50% for MLH1 and MSH2 expression (44% and 69%, respectively). Complete loss of heterozygosity in three dinucleotide repeats lying within, or in close proximity to,
hMLH1
and
hMSH2
was rare (2/57, (4%) for
MLH1
; and 1/55, (2%) for
MSH2
), however allelic imbalance was detected in 11/57 (
hMLH1
) and 10/55 (
hMSH2
) at any of the informative microsatellite loci. These alterations in structure and expression of DNA MMR genes suggest their possible involvement in the tumorigenesis and/or progression of bladder cancer. © 2001 Cancer Research Campaign
http://www.bjcancer.com</description><identifier>ISSN: 0007-0920</identifier><identifier>ISSN: 1532-1827</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1054/bjoc.2000.1595</identifier><identifier>PMID: 11161395</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adaptor Proteins, Signal Transducing ; Adult ; Aged ; Alleles ; Allelic Imbalance ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Bladder cancer ; Cancer Research ; Carrier Proteins ; DNA, Neoplasm - genetics ; DNA-Binding Proteins ; Drug Resistance ; Epidemiology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Loss of Heterozygosity ; Male ; Medical sciences ; Microsatellite Repeats - genetics ; Middle Aged ; Molecular Medicine ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein ; Neoplasm Proteins - analysis ; Neoplasm Proteins - genetics ; Nephrology. Urinary tract diseases ; Nuclear Proteins ; Oncology ; Polymerase Chain Reaction ; Proto-Oncogene Proteins - analysis ; Proto-Oncogene Proteins - genetics ; Regular ; regular-article ; Tumors of the urinary system ; Urinary Bladder Neoplasms - genetics ; Urinary Bladder Neoplasms - metabolism ; Urinary Bladder Neoplasms - pathology ; Urinary tract. Prostate gland</subject><ispartof>British journal of cancer, 2001-02, Vol.84 (3), p.321-328</ispartof><rights>The Author(s) 2001</rights><rights>2001 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Feb 2001</rights><rights>Copyright © 2001 Cancer Research Campaign 2001 Cancer Research Campaign</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c536t-c1ad7e3547213d2fc205394143928ac3a128f3ad53d53cee9b26ecc48d1c7edc3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2363732/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2363732/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,2727,27924,27925,41488,42557,51319,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1081396$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11161395$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kassem, H Sh</creatorcontrib><creatorcontrib>Varley, J M</creatorcontrib><creatorcontrib>Hamam, S M</creatorcontrib><creatorcontrib>Margison, G P</creatorcontrib><title>Immunohistochemical analysis of expression and allelotype of mismatch repair genes ( and ) in bladder cancer</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Mutation of human homologues of DNA mismatch repair (MMR) genes in tumours has been shown to be associated with the phenomenon of microsatellite instability (MSI). Several studies have reported the occurrence of MSI in bladder cancer, but evidence of involvement of MMR genes in the pathogenesis of this cancer is still unclear. We therefore utilized quantitative immunohistochemical (IHC) image analysis and PCR-based allelotype analysis to determine
hMLH1
and
hMSH2
genes alteration in a cohort of Egyptian bladder cancer samples. IHC analysis of 24 TCC and 12 SCC revealed marked- intra and intertumour heterogeneity in the levels of expression of the two MMR proteins. One TCC lost MLH1 expression and one lost MSH2, (1/24, 4%), and one SCC lost MSH2 (1/12, 8%). A large proportion of analysed tumours revealed a percentage positivity of less than 50% for MLH1 and MSH2 expression (44% and 69%, respectively). Complete loss of heterozygosity in three dinucleotide repeats lying within, or in close proximity to,
hMLH1
and
hMSH2
was rare (2/57, (4%) for
MLH1
; and 1/55, (2%) for
MSH2
), however allelic imbalance was detected in 11/57 (
hMLH1
) and 10/55 (
hMSH2
) at any of the informative microsatellite loci. These alterations in structure and expression of DNA MMR genes suggest their possible involvement in the tumorigenesis and/or progression of bladder cancer. © 2001 Cancer Research Campaign
http://www.bjcancer.com</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Adult</subject><subject>Aged</subject><subject>Alleles</subject><subject>Allelic Imbalance</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bladder cancer</subject><subject>Cancer Research</subject><subject>Carrier Proteins</subject><subject>DNA, Neoplasm - genetics</subject><subject>DNA-Binding Proteins</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Loss of Heterozygosity</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsatellite Repeats - genetics</subject><subject>Middle Aged</subject><subject>Molecular Medicine</subject><subject>MutL Protein Homolog 1</subject><subject>MutS Homolog 2 Protein</subject><subject>Neoplasm Proteins - analysis</subject><subject>Neoplasm Proteins - genetics</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nuclear Proteins</subject><subject>Oncology</subject><subject>Polymerase Chain Reaction</subject><subject>Proto-Oncogene Proteins - analysis</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Regular</subject><subject>regular-article</subject><subject>Tumors of the urinary system</subject><subject>Urinary Bladder Neoplasms - genetics</subject><subject>Urinary Bladder Neoplasms - metabolism</subject><subject>Urinary Bladder Neoplasms - pathology</subject><subject>Urinary tract. 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Urinary tract diseases</topic><topic>Nuclear Proteins</topic><topic>Oncology</topic><topic>Polymerase Chain Reaction</topic><topic>Proto-Oncogene Proteins - analysis</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Regular</topic><topic>regular-article</topic><topic>Tumors of the urinary system</topic><topic>Urinary Bladder Neoplasms - genetics</topic><topic>Urinary Bladder Neoplasms - metabolism</topic><topic>Urinary Bladder Neoplasms - pathology</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kassem, H Sh</creatorcontrib><creatorcontrib>Varley, J M</creatorcontrib><creatorcontrib>Hamam, S M</creatorcontrib><creatorcontrib>Margison, G P</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kassem, H Sh</au><au>Varley, J M</au><au>Hamam, S M</au><au>Margison, G P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunohistochemical analysis of expression and allelotype of mismatch repair genes ( and ) in bladder cancer</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2001-02-02</date><risdate>2001</risdate><volume>84</volume><issue>3</issue><spage>321</spage><epage>328</epage><pages>321-328</pages><issn>0007-0920</issn><issn>1532-1827</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Mutation of human homologues of DNA mismatch repair (MMR) genes in tumours has been shown to be associated with the phenomenon of microsatellite instability (MSI). Several studies have reported the occurrence of MSI in bladder cancer, but evidence of involvement of MMR genes in the pathogenesis of this cancer is still unclear. We therefore utilized quantitative immunohistochemical (IHC) image analysis and PCR-based allelotype analysis to determine
hMLH1
and
hMSH2
genes alteration in a cohort of Egyptian bladder cancer samples. IHC analysis of 24 TCC and 12 SCC revealed marked- intra and intertumour heterogeneity in the levels of expression of the two MMR proteins. One TCC lost MLH1 expression and one lost MSH2, (1/24, 4%), and one SCC lost MSH2 (1/12, 8%). A large proportion of analysed tumours revealed a percentage positivity of less than 50% for MLH1 and MSH2 expression (44% and 69%, respectively). Complete loss of heterozygosity in three dinucleotide repeats lying within, or in close proximity to,
hMLH1
and
hMSH2
was rare (2/57, (4%) for
MLH1
; and 1/55, (2%) for
MSH2
), however allelic imbalance was detected in 11/57 (
hMLH1
) and 10/55 (
hMSH2
) at any of the informative microsatellite loci. These alterations in structure and expression of DNA MMR genes suggest their possible involvement in the tumorigenesis and/or progression of bladder cancer. © 2001 Cancer Research Campaign
http://www.bjcancer.com</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>11161395</pmid><doi>10.1054/bjoc.2000.1595</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing Adult Aged Alleles Allelic Imbalance Biological and medical sciences Biomedical and Life Sciences Biomedicine Bladder cancer Cancer Research Carrier Proteins DNA, Neoplasm - genetics DNA-Binding Proteins Drug Resistance Epidemiology Female Gene Expression Regulation, Neoplastic Humans Immunohistochemistry Loss of Heterozygosity Male Medical sciences Microsatellite Repeats - genetics Middle Aged Molecular Medicine MutL Protein Homolog 1 MutS Homolog 2 Protein Neoplasm Proteins - analysis Neoplasm Proteins - genetics Nephrology. Urinary tract diseases Nuclear Proteins Oncology Polymerase Chain Reaction Proto-Oncogene Proteins - analysis Proto-Oncogene Proteins - genetics Regular regular-article Tumors of the urinary system Urinary Bladder Neoplasms - genetics Urinary Bladder Neoplasms - metabolism Urinary Bladder Neoplasms - pathology Urinary tract. Prostate gland |
| title | Immunohistochemical analysis of expression and allelotype of mismatch repair genes ( and ) in bladder cancer |
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