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Loss of heterozygosity of DPC4 tumor suppressor gene in human sporadic colon cancer
We investigated the prevalence of DPC4 loss of heterozygosity in sporadic colorectal cancer. Thirty-six cases of human sporadic colon carcinoma and corresponding normal tissue samples were examined to evaluate loss of heterozygosity at the DPC4 tumor suppressor locus using variable nucleotide tandem...
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Published in: | Journal of molecular medicine (Berlin, Germany) Germany), 2001-04, Vol.79 (2-3), p.128-132 |
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container_title | Journal of molecular medicine (Berlin, Germany) |
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creator | HADZIJA, Marijana Popovic KAPITANOVIC, Sanja RADOSEVIC, Senka CACEV, Tamara MIRT, Mirela KOVACEVIC, Duje LUKAC, Josip HADZIJA, Mirko SPAVENTI, Radan PAVELIC, Kresimir |
description | We investigated the prevalence of DPC4 loss of heterozygosity in sporadic colorectal cancer. Thirty-six cases of human sporadic colon carcinoma and corresponding normal tissue samples were examined to evaluate loss of heterozygosity at the DPC4 tumor suppressor locus using variable nucleotide tandem repeat (VNTR) analysis and three polymorphic markers. From 36 analyzed samples 35 (97%) were heterozygous or informative. Loss of heterozygosity at the DPC4 locus was detected in 18 (51%) of informative tumor DNAs. The DPC4 LOH was more frequent in smaller tumors ( |
doi_str_mv | 10.1007/s001090000179 |
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Thirty-six cases of human sporadic colon carcinoma and corresponding normal tissue samples were examined to evaluate loss of heterozygosity at the DPC4 tumor suppressor locus using variable nucleotide tandem repeat (VNTR) analysis and three polymorphic markers. From 36 analyzed samples 35 (97%) were heterozygous or informative. Loss of heterozygosity at the DPC4 locus was detected in 18 (51%) of informative tumor DNAs. The DPC4 LOH was more frequent in smaller tumors (<5 cm) than in larger ones. There was no correlation between DPC4 LOH and age or sex of patients. There was a negative correlation between DPC4 LOH and histological grade or Dukes' stage of tumors, but without statistic significance. Observed results are in agreement with the view that malignant progression is consequence of many genetic changes. It can be concluded that inactivation of the DPC4 gene plays a role in a multistep process of outgrowth and progression of colon cancer.</description><identifier>ISSN: 0946-2716</identifier><identifier>EISSN: 1432-1440</identifier><identifier>DOI: 10.1007/s001090000179</identifier><identifier>PMID: 11357936</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Aged ; Aged, 80 and over ; Biological and medical sciences ; Colonic Neoplasms - genetics ; DNA-Binding Proteins - genetics ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Genes, Tumor Suppressor ; Heterozygote ; Humans ; Male ; Medical sciences ; Middle Aged ; Smad4 Protein ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Trans-Activators - genetics ; Tumors</subject><ispartof>Journal of molecular medicine (Berlin, Germany), 2001-04, Vol.79 (2-3), p.128-132</ispartof><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c233t-cf4a07ee422137abf3c1d16767891dbaf6cd0dcbaafa567a79adbc8159f07d453</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1013806$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11357936$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HADZIJA, Marijana Popovic</creatorcontrib><creatorcontrib>KAPITANOVIC, Sanja</creatorcontrib><creatorcontrib>RADOSEVIC, Senka</creatorcontrib><creatorcontrib>CACEV, Tamara</creatorcontrib><creatorcontrib>MIRT, Mirela</creatorcontrib><creatorcontrib>KOVACEVIC, Duje</creatorcontrib><creatorcontrib>LUKAC, Josip</creatorcontrib><creatorcontrib>HADZIJA, Mirko</creatorcontrib><creatorcontrib>SPAVENTI, Radan</creatorcontrib><creatorcontrib>PAVELIC, Kresimir</creatorcontrib><title>Loss of heterozygosity of DPC4 tumor suppressor gene in human sporadic colon cancer</title><title>Journal of molecular medicine (Berlin, Germany)</title><addtitle>J Mol Med (Berl)</addtitle><description>We investigated the prevalence of DPC4 loss of heterozygosity in sporadic colorectal cancer. Thirty-six cases of human sporadic colon carcinoma and corresponding normal tissue samples were examined to evaluate loss of heterozygosity at the DPC4 tumor suppressor locus using variable nucleotide tandem repeat (VNTR) analysis and three polymorphic markers. From 36 analyzed samples 35 (97%) were heterozygous or informative. Loss of heterozygosity at the DPC4 locus was detected in 18 (51%) of informative tumor DNAs. The DPC4 LOH was more frequent in smaller tumors (<5 cm) than in larger ones. There was no correlation between DPC4 LOH and age or sex of patients. There was a negative correlation between DPC4 LOH and histological grade or Dukes' stage of tumors, but without statistic significance. Observed results are in agreement with the view that malignant progression is consequence of many genetic changes. It can be concluded that inactivation of the DPC4 gene plays a role in a multistep process of outgrowth and progression of colon cancer.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Colonic Neoplasms - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genes, Tumor Suppressor</subject><subject>Heterozygote</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Smad4 Protein</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Liver. Pancreas. Abdomen</topic><topic>Genes, Tumor Suppressor</topic><topic>Heterozygote</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Smad4 Protein</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Trans-Activators - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HADZIJA, Marijana Popovic</creatorcontrib><creatorcontrib>KAPITANOVIC, Sanja</creatorcontrib><creatorcontrib>RADOSEVIC, Senka</creatorcontrib><creatorcontrib>CACEV, Tamara</creatorcontrib><creatorcontrib>MIRT, Mirela</creatorcontrib><creatorcontrib>KOVACEVIC, Duje</creatorcontrib><creatorcontrib>LUKAC, Josip</creatorcontrib><creatorcontrib>HADZIJA, Mirko</creatorcontrib><creatorcontrib>SPAVENTI, Radan</creatorcontrib><creatorcontrib>PAVELIC, Kresimir</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><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HADZIJA, Marijana Popovic</au><au>KAPITANOVIC, Sanja</au><au>RADOSEVIC, Senka</au><au>CACEV, Tamara</au><au>MIRT, Mirela</au><au>KOVACEVIC, Duje</au><au>LUKAC, Josip</au><au>HADZIJA, Mirko</au><au>SPAVENTI, Radan</au><au>PAVELIC, Kresimir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of heterozygosity of DPC4 tumor suppressor gene in human sporadic colon cancer</atitle><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle><addtitle>J Mol Med (Berl)</addtitle><date>2001-04</date><risdate>2001</risdate><volume>79</volume><issue>2-3</issue><spage>128</spage><epage>132</epage><pages>128-132</pages><issn>0946-2716</issn><eissn>1432-1440</eissn><abstract>We investigated the prevalence of DPC4 loss of heterozygosity in sporadic colorectal cancer. Thirty-six cases of human sporadic colon carcinoma and corresponding normal tissue samples were examined to evaluate loss of heterozygosity at the DPC4 tumor suppressor locus using variable nucleotide tandem repeat (VNTR) analysis and three polymorphic markers. From 36 analyzed samples 35 (97%) were heterozygous or informative. Loss of heterozygosity at the DPC4 locus was detected in 18 (51%) of informative tumor DNAs. The DPC4 LOH was more frequent in smaller tumors (<5 cm) than in larger ones. There was no correlation between DPC4 LOH and age or sex of patients. There was a negative correlation between DPC4 LOH and histological grade or Dukes' stage of tumors, but without statistic significance. Observed results are in agreement with the view that malignant progression is consequence of many genetic changes. It can be concluded that inactivation of the DPC4 gene plays a role in a multistep process of outgrowth and progression of colon cancer.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>11357936</pmid><doi>10.1007/s001090000179</doi><tpages>5</tpages></addata></record> |
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subjects | Aged Aged, 80 and over Biological and medical sciences Colonic Neoplasms - genetics DNA-Binding Proteins - genetics Female Gastroenterology. Liver. Pancreas. Abdomen Genes, Tumor Suppressor Heterozygote Humans Male Medical sciences Middle Aged Smad4 Protein Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Trans-Activators - genetics Tumors |
title | Loss of heterozygosity of DPC4 tumor suppressor gene in human sporadic colon cancer |
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