Genetic aberrations detected by comparative genomic hybridization in hepatocellular carcinomas: Their relationship to clinicopathological features
To elucidate cytogenetic alterations underlying human hepatocellular carcinomas (HCCs), we used a comparative genomic hybridization (CGH) method to analyze 41 cases of hepatocellular carcinoma (HCC) including 15 well differentiated HCCs, 14 moderately differentiated HCCs, and 12 poorly differentiate...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 1999-06, Vol.29 (6), p.1858-1862 |
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| container_title | Hepatology (Baltimore, Md.) |
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| creator | Kusano, Noriyoshi Shiraishi, Kei Kubo, Keiko Oga, Atsunori Okita, Kiwamu Sasaki, Kohsuke |
| description | To elucidate cytogenetic alterations underlying human hepatocellular carcinomas (HCCs), we used a comparative genomic hybridization (CGH) method to analyze 41 cases of hepatocellular carcinoma (HCC) including 15 well differentiated HCCs, 14 moderately differentiated HCCs, and 12 poorly differentiated HCCs. Of these, 27 patients were chronically infected with hepatitis C virus (HCV), and the remaining patients were positive for hepatitis B virus (HBV). The most common sites of increase in DNA copy number were 1q (78% of the cases) and 8q (66%) with minimal overlapping regions at 1q24‐25 and 8q24, respectively. Frequent decreases in copy number were observed at 17p (51%), 16q (46%), 13q13‐14 (37%), 4q13‐22 (32%), 8p (29%), and 10q (17%). In 6 cases (15%), an amplification was found in the region of 11q13. A gain of 8q24 was significantly associated with well‐differentiated HCCs (P |
| doi_str_mv | 10.1002/hep.510290636 |
| format | Article |
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Of these, 27 patients were chronically infected with hepatitis C virus (HCV), and the remaining patients were positive for hepatitis B virus (HBV). The most common sites of increase in DNA copy number were 1q (78% of the cases) and 8q (66%) with minimal overlapping regions at 1q24‐25 and 8q24, respectively. Frequent decreases in copy number were observed at 17p (51%), 16q (46%), 13q13‐14 (37%), 4q13‐22 (32%), 8p (29%), and 10q (17%). In 6 cases (15%), an amplification was found in the region of 11q13. A gain of 8q24 was significantly associated with well‐differentiated HCCs (P<.05), whereas a loss of 13q13‐14 and amplification of 11q13 were linked to moderately and poorly differentiated HCCs (P<.01). These observations suggest that a gain of 8q24 is an early event and that a loss of 13q13‐14 and amplification of 11q13 are a late event in the course of liver carcinogenesis. A gain of 10q (7/41) was detected exclusively in cases with HCV infection. In contrast, an amplification of 11q13 was preferentially found in HBV‐positive HCCs. These findings raise the hypothesis that, although many genetic alterations are basically common to both HCV–positive and HBV–positive tumors, the process of carcinogenesis may be to some extent different between these two types of tumors.</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.510290636</identifier><identifier>PMID: 10347130</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Philadelphia, PA: W.B. Saunders</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Carcinoma, Hepatocellular - complications ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; Carcinoma, Hepatocellular - surgery ; Chromosome Aberrations ; Chromosome Deletion ; Chromosome Mapping ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatitis B, Chronic - complications ; Hepatitis B, Chronic - pathology ; Hepatitis C, Chronic - complications ; Hepatitis C, Chronic - pathology ; Humans ; In Situ Hybridization ; Liver Neoplasms - complications ; Liver Neoplasms - genetics ; Liver Neoplasms - pathology ; Liver Neoplasms - surgery ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Loss of Heterozygosity ; Male ; Medical sciences ; Middle Aged ; Tumors</subject><ispartof>Hepatology (Baltimore, Md.), 1999-06, Vol.29 (6), p.1858-1862</ispartof><rights>Copyright © 1999 American Association for the Study of Liver Diseases</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4056-3af06148661a325887156a325175f19529f4f670a8e05b7793bb15e731cb2c993</citedby><cites>FETCH-LOGICAL-c4056-3af06148661a325887156a325175f19529f4f670a8e05b7793bb15e731cb2c993</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.510290636$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.510290636$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1804281$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10347130$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kusano, Noriyoshi</creatorcontrib><creatorcontrib>Shiraishi, Kei</creatorcontrib><creatorcontrib>Kubo, Keiko</creatorcontrib><creatorcontrib>Oga, Atsunori</creatorcontrib><creatorcontrib>Okita, Kiwamu</creatorcontrib><creatorcontrib>Sasaki, Kohsuke</creatorcontrib><title>Genetic aberrations detected by comparative genomic hybridization in hepatocellular carcinomas: Their relationship to clinicopathological features</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>To elucidate cytogenetic alterations underlying human hepatocellular carcinomas (HCCs), we used a comparative genomic hybridization (CGH) method to analyze 41 cases of hepatocellular carcinoma (HCC) including 15 well differentiated HCCs, 14 moderately differentiated HCCs, and 12 poorly differentiated HCCs. Of these, 27 patients were chronically infected with hepatitis C virus (HCV), and the remaining patients were positive for hepatitis B virus (HBV). The most common sites of increase in DNA copy number were 1q (78% of the cases) and 8q (66%) with minimal overlapping regions at 1q24‐25 and 8q24, respectively. Frequent decreases in copy number were observed at 17p (51%), 16q (46%), 13q13‐14 (37%), 4q13‐22 (32%), 8p (29%), and 10q (17%). In 6 cases (15%), an amplification was found in the region of 11q13. A gain of 8q24 was significantly associated with well‐differentiated HCCs (P<.05), whereas a loss of 13q13‐14 and amplification of 11q13 were linked to moderately and poorly differentiated HCCs (P<.01). These observations suggest that a gain of 8q24 is an early event and that a loss of 13q13‐14 and amplification of 11q13 are a late event in the course of liver carcinogenesis. A gain of 10q (7/41) was detected exclusively in cases with HCV infection. In contrast, an amplification of 11q13 was preferentially found in HBV‐positive HCCs. These findings raise the hypothesis that, although many genetic alterations are basically common to both HCV–positive and HBV–positive tumors, the process of carcinogenesis may be to some extent different between these two types of tumors.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Hepatocellular - complications</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Carcinoma, Hepatocellular - surgery</subject><subject>Chromosome Aberrations</subject><subject>Chromosome Deletion</subject><subject>Chromosome Mapping</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatitis B, Chronic - complications</subject><subject>Hepatitis B, Chronic - pathology</subject><subject>Hepatitis C, Chronic - complications</subject><subject>Hepatitis C, Chronic - pathology</subject><subject>Humans</subject><subject>In Situ Hybridization</subject><subject>Liver Neoplasms - complications</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - pathology</subject><subject>Liver Neoplasms - surgery</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Loss of Heterozygosity</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Tumors</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90E1PxCAQBmBiNLp-HL0aDl6rQymleDPGr8RED3puKDu1GLY00NWsP8NfLGuNevIECc8MMy8hhwxOGEB-2uFwIhjkCkpebpAZE7nMOBewSWaQS8gU42qH7Mb4AgCqyKttssOAF5JxmJGPa-xxtIbqBkPQo_V9pHMc0Yw4p82KGr8Y9PrhFekz9n6RbLdqgp3b9y9ObU_TEHr0Bp1bOh2o0cHYRHU8o48d2kADuql3Zwc6emqc7a3xqarzzj9box1tUY_LgHGfbLXaRTz4PvfI09Xl48VNdnd_fXtxfpeZAkSZcd1CyYqqLJnmuagqyUS5vjEpWqZErtqiLSXoCkE0UireNEyg5Mw0uVGK75Fs6muCjzFgWw_BLnRY1QzqdbZ1Wqv-yTb5o8kPy2aB8z96CjOB42-gY1qoDbo3Nv66ClL6LDE5sTfrcPX_p_XN5cPvBJ8FS5Tt</recordid><startdate>199906</startdate><enddate>199906</enddate><creator>Kusano, Noriyoshi</creator><creator>Shiraishi, Kei</creator><creator>Kubo, Keiko</creator><creator>Oga, Atsunori</creator><creator>Okita, Kiwamu</creator><creator>Sasaki, Kohsuke</creator><general>W.B. Saunders</general><general>Wiley</general><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></search><sort><creationdate>199906</creationdate><title>Genetic aberrations detected by comparative genomic hybridization in hepatocellular carcinomas: Their relationship to clinicopathological features</title><author>Kusano, Noriyoshi ; Shiraishi, Kei ; Kubo, Keiko ; Oga, Atsunori ; Okita, Kiwamu ; Sasaki, Kohsuke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4056-3af06148661a325887156a325175f19529f4f670a8e05b7793bb15e731cb2c993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Hepatocellular - complications</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Carcinoma, Hepatocellular - surgery</topic><topic>Chromosome Aberrations</topic><topic>Chromosome Deletion</topic><topic>Chromosome Mapping</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatitis B, Chronic - complications</topic><topic>Hepatitis B, Chronic - pathology</topic><topic>Hepatitis C, Chronic - complications</topic><topic>Hepatitis C, Chronic - pathology</topic><topic>Humans</topic><topic>In Situ Hybridization</topic><topic>Liver Neoplasms - complications</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>Liver Neoplasms - surgery</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Loss of Heterozygosity</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kusano, Noriyoshi</creatorcontrib><creatorcontrib>Shiraishi, Kei</creatorcontrib><creatorcontrib>Kubo, Keiko</creatorcontrib><creatorcontrib>Oga, Atsunori</creatorcontrib><creatorcontrib>Okita, Kiwamu</creatorcontrib><creatorcontrib>Sasaki, Kohsuke</creatorcontrib><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><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kusano, Noriyoshi</au><au>Shiraishi, Kei</au><au>Kubo, Keiko</au><au>Oga, Atsunori</au><au>Okita, Kiwamu</au><au>Sasaki, Kohsuke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic aberrations detected by comparative genomic hybridization in hepatocellular carcinomas: Their relationship to clinicopathological features</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>1999-06</date><risdate>1999</risdate><volume>29</volume><issue>6</issue><spage>1858</spage><epage>1862</epage><pages>1858-1862</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>To elucidate cytogenetic alterations underlying human hepatocellular carcinomas (HCCs), we used a comparative genomic hybridization (CGH) method to analyze 41 cases of hepatocellular carcinoma (HCC) including 15 well differentiated HCCs, 14 moderately differentiated HCCs, and 12 poorly differentiated HCCs. Of these, 27 patients were chronically infected with hepatitis C virus (HCV), and the remaining patients were positive for hepatitis B virus (HBV). The most common sites of increase in DNA copy number were 1q (78% of the cases) and 8q (66%) with minimal overlapping regions at 1q24‐25 and 8q24, respectively. Frequent decreases in copy number were observed at 17p (51%), 16q (46%), 13q13‐14 (37%), 4q13‐22 (32%), 8p (29%), and 10q (17%). In 6 cases (15%), an amplification was found in the region of 11q13. A gain of 8q24 was significantly associated with well‐differentiated HCCs (P<.05), whereas a loss of 13q13‐14 and amplification of 11q13 were linked to moderately and poorly differentiated HCCs (P<.01). These observations suggest that a gain of 8q24 is an early event and that a loss of 13q13‐14 and amplification of 11q13 are a late event in the course of liver carcinogenesis. A gain of 10q (7/41) was detected exclusively in cases with HCV infection. In contrast, an amplification of 11q13 was preferentially found in HBV‐positive HCCs. These findings raise the hypothesis that, although many genetic alterations are basically common to both HCV–positive and HBV–positive tumors, the process of carcinogenesis may be to some extent different between these two types of tumors.</abstract><cop>Philadelphia, PA</cop><pub>W.B. Saunders</pub><pmid>10347130</pmid><doi>10.1002/hep.510290636</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hepatology (Baltimore, Md.), 1999-06, Vol.29 (6), p.1858-1862 |
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| subjects | Adult Aged Biological and medical sciences Carcinoma, Hepatocellular - complications Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - pathology Carcinoma, Hepatocellular - surgery Chromosome Aberrations Chromosome Deletion Chromosome Mapping Female Gastroenterology. Liver. Pancreas. Abdomen Hepatitis B, Chronic - complications Hepatitis B, Chronic - pathology Hepatitis C, Chronic - complications Hepatitis C, Chronic - pathology Humans In Situ Hybridization Liver Neoplasms - complications Liver Neoplasms - genetics Liver Neoplasms - pathology Liver Neoplasms - surgery Liver. Biliary tract. Portal circulation. Exocrine pancreas Loss of Heterozygosity Male Medical sciences Middle Aged Tumors |
| title | Genetic aberrations detected by comparative genomic hybridization in hepatocellular carcinomas: Their relationship to clinicopathological features |
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