Microsatellite instability, Epstein–Barr virus, mutation of type II transforming growth factor β receptor and BAX in gastric carcinomas in Hong Kong Chinese
Summary Microsatellite instability (MI), the phenotypic manifestation of mismatch repair failure, is found in a proportion of gastric carcinomas. Little is known of the links between MI and Epstein–Barr virus (EBV) status and clinicopathological elements. Examination of genes mutated through the MI...
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| Veröffentlicht in: | British journal of cancer 1999-02, Vol.79 (3), p.582-588 |
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| creator | Leung, S Y Yuen, S T Chung, L P Chu, K M Wong, M P Branicki, F J Ho, J C I |
| description | Summary
Microsatellite instability (MI), the phenotypic manifestation of mismatch repair failure, is found in a proportion of gastric carcinomas. Little is known of the links between MI and Epstein–Barr virus (EBV) status and clinicopathological elements. Examination of genes mutated through the MI mechanism could also be expected to reveal important information on the carcinogenic pathway. Seventy-nine gastric carcinomas (61 EBV negative, 18 EBV positive) from local Hong Kong Chinese population, an intermediate-incidence area, were examined. Eight microsatellite loci, inclusive of the A10 tract of type II transforming growth factor β receptor (TβR-II), were used to evaluate the MI status. MI in the BAX and insulin-like growth factor II receptor (IGF-IIR) genes were also examined. High-level MI (>40% unstable loci) was detected in ten cases (12.7%) and low-level MI (1–40% unstable loci) in three (3.8%). High-level MI was detected in two EBV-associated cases (11%) and the incidence was similar for the EBV-negative cases (13%). The high-level MIs were significantly associated with intestinal-type tumours (
P
= 0.03) and a more prominent lymphoid infiltrate (
P
= 0.04). Similar associations were noted in the EBV-positive carcinomas. The high-level MIs were more commonly located in the antrum, whereas the EBV-associated carcinomas were mostly located in body. Thirteen cardia cases were negative for both high-level MI and EBV. All patients aged below 55 were MI negative (
P
= 0.049). Of the high-level MIs, 80% had mutation in TβR-II, 40% in BAX and 0% in IGF-IIR. Of low-level MIs, 33% also had TβR-II mutation. These mutations were absent in the MI-negative cases. Of three lymphoepithelioma-like carcinomas, two cases were EBV positive and MI negative, one case was EBV negative but with high-level MI. In conclusion, high-level MIs were present regardless of the EBV status, and were found in a particular clinicopathological subset of gastric carcinoma patient. Inactivation of important growth regulatory genes observed in these carcinomas confirms the importance of MI in carcinogenesis. |
| doi_str_mv | 10.1038/sj.bjc.6690092 |
| format | Article |
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Microsatellite instability (MI), the phenotypic manifestation of mismatch repair failure, is found in a proportion of gastric carcinomas. Little is known of the links between MI and Epstein–Barr virus (EBV) status and clinicopathological elements. Examination of genes mutated through the MI mechanism could also be expected to reveal important information on the carcinogenic pathway. Seventy-nine gastric carcinomas (61 EBV negative, 18 EBV positive) from local Hong Kong Chinese population, an intermediate-incidence area, were examined. Eight microsatellite loci, inclusive of the A10 tract of type II transforming growth factor β receptor (TβR-II), were used to evaluate the MI status. MI in the BAX and insulin-like growth factor II receptor (IGF-IIR) genes were also examined. High-level MI (>40% unstable loci) was detected in ten cases (12.7%) and low-level MI (1–40% unstable loci) in three (3.8%). High-level MI was detected in two EBV-associated cases (11%) and the incidence was similar for the EBV-negative cases (13%). The high-level MIs were significantly associated with intestinal-type tumours (
P
= 0.03) and a more prominent lymphoid infiltrate (
P
= 0.04). Similar associations were noted in the EBV-positive carcinomas. The high-level MIs were more commonly located in the antrum, whereas the EBV-associated carcinomas were mostly located in body. Thirteen cardia cases were negative for both high-level MI and EBV. All patients aged below 55 were MI negative (
P
= 0.049). Of the high-level MIs, 80% had mutation in TβR-II, 40% in BAX and 0% in IGF-IIR. Of low-level MIs, 33% also had TβR-II mutation. These mutations were absent in the MI-negative cases. Of three lymphoepithelioma-like carcinomas, two cases were EBV positive and MI negative, one case was EBV negative but with high-level MI. In conclusion, high-level MIs were present regardless of the EBV status, and were found in a particular clinicopathological subset of gastric carcinoma patient. Inactivation of important growth regulatory genes observed in these carcinomas confirms the importance of MI in carcinogenesis.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6690092</identifier><identifier>PMID: 10027334</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adult ; Aged ; bcl-2-Associated X Protein ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Carcinoma - genetics ; Carcinoma - pathology ; Carcinoma - virology ; Cell Transformation, Neoplastic - genetics ; DNA Mutational Analysis ; DNA, Neoplasm - genetics ; Drug Resistance ; Epidemiology ; Epstein-Barr virus ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Genes, Tumor Suppressor - genetics ; Herpesviridae Infections - complications ; Herpesvirus 4, Human - pathogenicity ; Hong Kong ; Humans ; Male ; Medical sciences ; Microsatellite Repeats - genetics ; Middle Aged ; Molecular Medicine ; Oncology ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins c-bcl-2 ; Receptors, Transforming Growth Factor beta - genetics ; Regular ; regular-article ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Stomach Neoplasms - virology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumor Virus Infections - complications ; Tumors</subject><ispartof>British journal of cancer, 1999-02, Vol.79 (3), p.582-588</ispartof><rights>The Author(s) 1999</rights><rights>1999 INIST-CNRS</rights><rights>Copyright © 1999 Cancer Research Campaign 1999 Cancer Research Campaign</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-2bb77fce5a4850de726476161def848757f2e6cb3107951eead2208fc13e4e353</citedby><cites>FETCH-LOGICAL-c455t-2bb77fce5a4850de726476161def848757f2e6cb3107951eead2208fc13e4e353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362448/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362448/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1664910$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10027334$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Leung, S Y</creatorcontrib><creatorcontrib>Yuen, S T</creatorcontrib><creatorcontrib>Chung, L P</creatorcontrib><creatorcontrib>Chu, K M</creatorcontrib><creatorcontrib>Wong, M P</creatorcontrib><creatorcontrib>Branicki, F J</creatorcontrib><creatorcontrib>Ho, J C I</creatorcontrib><title>Microsatellite instability, Epstein–Barr virus, mutation of type II transforming growth factor β receptor and BAX in gastric carcinomas in Hong Kong Chinese</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Summary
Microsatellite instability (MI), the phenotypic manifestation of mismatch repair failure, is found in a proportion of gastric carcinomas. Little is known of the links between MI and Epstein–Barr virus (EBV) status and clinicopathological elements. Examination of genes mutated through the MI mechanism could also be expected to reveal important information on the carcinogenic pathway. Seventy-nine gastric carcinomas (61 EBV negative, 18 EBV positive) from local Hong Kong Chinese population, an intermediate-incidence area, were examined. Eight microsatellite loci, inclusive of the A10 tract of type II transforming growth factor β receptor (TβR-II), were used to evaluate the MI status. MI in the BAX and insulin-like growth factor II receptor (IGF-IIR) genes were also examined. High-level MI (>40% unstable loci) was detected in ten cases (12.7%) and low-level MI (1–40% unstable loci) in three (3.8%). High-level MI was detected in two EBV-associated cases (11%) and the incidence was similar for the EBV-negative cases (13%). The high-level MIs were significantly associated with intestinal-type tumours (
P
= 0.03) and a more prominent lymphoid infiltrate (
P
= 0.04). Similar associations were noted in the EBV-positive carcinomas. The high-level MIs were more commonly located in the antrum, whereas the EBV-associated carcinomas were mostly located in body. Thirteen cardia cases were negative for both high-level MI and EBV. All patients aged below 55 were MI negative (
P
= 0.049). Of the high-level MIs, 80% had mutation in TβR-II, 40% in BAX and 0% in IGF-IIR. Of low-level MIs, 33% also had TβR-II mutation. These mutations were absent in the MI-negative cases. Of three lymphoepithelioma-like carcinomas, two cases were EBV positive and MI negative, one case was EBV negative but with high-level MI. In conclusion, high-level MIs were present regardless of the EBV status, and were found in a particular clinicopathological subset of gastric carcinoma patient. Inactivation of important growth regulatory genes observed in these carcinomas confirms the importance of MI in carcinogenesis.</description><subject>Adult</subject><subject>Aged</subject><subject>bcl-2-Associated X Protein</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - pathology</subject><subject>Carcinoma - virology</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>DNA Mutational Analysis</subject><subject>DNA, Neoplasm - genetics</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Epstein-Barr virus</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genes, Tumor Suppressor - genetics</subject><subject>Herpesviridae Infections - complications</subject><subject>Herpesvirus 4, Human - pathogenicity</subject><subject>Hong Kong</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microsatellite Repeats - genetics</subject><subject>Middle Aged</subject><subject>Molecular Medicine</subject><subject>Oncology</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>Receptors, Transforming Growth Factor beta - genetics</subject><subject>Regular</subject><subject>regular-article</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Stomach Neoplasms - virology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumor Virus Infections - complications</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAQxy1ERZeFK0fkA-qp2drOh5MLUrsqdEURF5C4WY4zyTpK7MV2ivbGO_AAvAMPwkPwJHW0KygHLv6Y-c1_7Pkj9IKSFSVpeeH7Vd2rVVFUhFTsEVrQPGUJLRl_jBaEEJ7EMDlFT73v47UiJX-CTikhjKdptkA_3mvlrJcBhkEHwNr4IGsdz_tzfL3zAbT5_e37lXQO32k3-XM8TkEGbQ22LQ77HeDNBgcnjW-tG7XpcOfs17DFrVTBOvzrJ3agYDefpWnw1eXn2AV30genFVbSKW3sKP0cvbGx_t28rLfagIdn6KSVg4fnx32JPr25_ri-SW4_vN2sL28TleV5SFhdc94qyGVW5qQBzoqMF7SgDbRlVvKctwwKVaeU8CqnALJhjJStoilkkObpEr0-6O6meoRGgYlfGsTO6VG6vbBSi38zRm9FZ-8ESwuWZWUUODsKOPtlAh_EqL2KU5UG7OQF5SwrK1ZEcHUA57l7B-2fJpSI2VPhexE9FUdPY8HLh097gB9MjMCrIyC9kkMbvVDa_-WKIqui8BJdHDAfM6YDJ3o7OROn-r_O95o-v_4</recordid><startdate>19990201</startdate><enddate>19990201</enddate><creator>Leung, S Y</creator><creator>Yuen, S T</creator><creator>Chung, L P</creator><creator>Chu, K M</creator><creator>Wong, M P</creator><creator>Branicki, F J</creator><creator>Ho, J C I</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>19990201</creationdate><title>Microsatellite instability, Epstein–Barr virus, mutation of type II transforming growth factor β receptor and BAX in gastric carcinomas in Hong Kong Chinese</title><author>Leung, S Y ; Yuen, S T ; Chung, L P ; Chu, K M ; Wong, M P ; Branicki, F J ; Ho, J C I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-2bb77fce5a4850de726476161def848757f2e6cb3107951eead2208fc13e4e353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Aged</topic><topic>bcl-2-Associated X Protein</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Carcinoma - genetics</topic><topic>Carcinoma - pathology</topic><topic>Carcinoma - virology</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>DNA Mutational Analysis</topic><topic>DNA, Neoplasm - genetics</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Epstein-Barr virus</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genes, Tumor Suppressor - genetics</topic><topic>Herpesviridae Infections - complications</topic><topic>Herpesvirus 4, Human - pathogenicity</topic><topic>Hong Kong</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microsatellite Repeats - genetics</topic><topic>Middle Aged</topic><topic>Molecular Medicine</topic><topic>Oncology</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>Receptors, Transforming Growth Factor beta - genetics</topic><topic>Regular</topic><topic>regular-article</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><topic>Stomach Neoplasms - virology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumor Virus Infections - complications</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Leung, S Y</creatorcontrib><creatorcontrib>Yuen, S T</creatorcontrib><creatorcontrib>Chung, L P</creatorcontrib><creatorcontrib>Chu, K M</creatorcontrib><creatorcontrib>Wong, M P</creatorcontrib><creatorcontrib>Branicki, F J</creatorcontrib><creatorcontrib>Ho, J C I</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>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research 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>Leung, S Y</au><au>Yuen, S T</au><au>Chung, L P</au><au>Chu, K M</au><au>Wong, M P</au><au>Branicki, F J</au><au>Ho, J C I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microsatellite instability, Epstein–Barr virus, mutation of type II transforming growth factor β receptor and BAX in gastric carcinomas in Hong Kong Chinese</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>1999-02-01</date><risdate>1999</risdate><volume>79</volume><issue>3</issue><spage>582</spage><epage>588</epage><pages>582-588</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Summary
Microsatellite instability (MI), the phenotypic manifestation of mismatch repair failure, is found in a proportion of gastric carcinomas. Little is known of the links between MI and Epstein–Barr virus (EBV) status and clinicopathological elements. Examination of genes mutated through the MI mechanism could also be expected to reveal important information on the carcinogenic pathway. Seventy-nine gastric carcinomas (61 EBV negative, 18 EBV positive) from local Hong Kong Chinese population, an intermediate-incidence area, were examined. Eight microsatellite loci, inclusive of the A10 tract of type II transforming growth factor β receptor (TβR-II), were used to evaluate the MI status. MI in the BAX and insulin-like growth factor II receptor (IGF-IIR) genes were also examined. High-level MI (>40% unstable loci) was detected in ten cases (12.7%) and low-level MI (1–40% unstable loci) in three (3.8%). High-level MI was detected in two EBV-associated cases (11%) and the incidence was similar for the EBV-negative cases (13%). The high-level MIs were significantly associated with intestinal-type tumours (
P
= 0.03) and a more prominent lymphoid infiltrate (
P
= 0.04). Similar associations were noted in the EBV-positive carcinomas. The high-level MIs were more commonly located in the antrum, whereas the EBV-associated carcinomas were mostly located in body. Thirteen cardia cases were negative for both high-level MI and EBV. All patients aged below 55 were MI negative (
P
= 0.049). Of the high-level MIs, 80% had mutation in TβR-II, 40% in BAX and 0% in IGF-IIR. Of low-level MIs, 33% also had TβR-II mutation. These mutations were absent in the MI-negative cases. Of three lymphoepithelioma-like carcinomas, two cases were EBV positive and MI negative, one case was EBV negative but with high-level MI. In conclusion, high-level MIs were present regardless of the EBV status, and were found in a particular clinicopathological subset of gastric carcinoma patient. Inactivation of important growth regulatory genes observed in these carcinomas confirms the importance of MI in carcinogenesis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>10027334</pmid><doi>10.1038/sj.bjc.6690092</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged bcl-2-Associated X Protein Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Research Carcinoma - genetics Carcinoma - pathology Carcinoma - virology Cell Transformation, Neoplastic - genetics DNA Mutational Analysis DNA, Neoplasm - genetics Drug Resistance Epidemiology Epstein-Barr virus Female Gastroenterology. Liver. Pancreas. Abdomen Genes, Tumor Suppressor - genetics Herpesviridae Infections - complications Herpesvirus 4, Human - pathogenicity Hong Kong Humans Male Medical sciences Microsatellite Repeats - genetics Middle Aged Molecular Medicine Oncology Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins c-bcl-2 Receptors, Transforming Growth Factor beta - genetics Regular regular-article Stomach Neoplasms - genetics Stomach Neoplasms - pathology Stomach Neoplasms - virology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumor Virus Infections - complications Tumors |
| title | Microsatellite instability, Epstein–Barr virus, mutation of type II transforming growth factor β receptor and BAX in gastric carcinomas in Hong Kong Chinese |
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