Colorectal and extracolonic cancer variations in MLH1/MSH2 hereditary nonpolyposis colorectal cancer kindreds and the general population
This clinical case review aimed to identify phenotypic variations in colorectal and extracolonic cancer expression between hereditary nonpolyposis colorectal cancer (HNPCC) families with MLH1 and MSH2 germline mutations and the general population. Colorectal cancer onset and site distribution were c...
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| Veröffentlicht in: | Diseases of the colon & rectum 1998-04, Vol.41 (4), p.428-433 |
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| creator | LIN, K. M SHASHIDHARAN, M TERNENT, C. A THORSON, A. G BLATCHFORD, G. J CHRISTENSEN, M. A LANSPA, S. J LEMON, S. J WATSON, P LYNCH, H. T |
| description | This clinical case review aimed to identify phenotypic variations in colorectal and extracolonic cancer expression between hereditary nonpolyposis colorectal cancer (HNPCC) families with MLH1 and MSH2 germline mutations and the general population.
Colorectal cancer onset and site distribution were compared among 67 members of MLH1 kindreds, 45 members of MSH2 kindreds, and 1,189 patients from the general population. Synchronous and metachronous cancer rates, tumor stage, extracolonic cancer incidence, and survival were also compared.
Mean ages of colorectal cancer onset were 44, 46, and 69 years for MLH1, MSH2, and the general population, respectively (P < 0.001). More proximal and fewer distal colon cancers were noted in HNPCC than the general population (P < 0.001, P = 0.04). Site distribution showed disparity of rectal cancers (8 percent MLH1 vs. 28 percent MSH2; P = 0.01) based on genotypes. Overall, synchronous colorectal cancer rates were 7.4, 6.7, and 2.4 percent for MLH1, MSH2, and the general population, respectively (P = 0.016). Annual metachronous colorectal cancer rates were 2.1, 1.7, and 0.33 percent for MLH1, MSH2, and the general population, respectively (P = 0.041). Colorectal cancer stage presentation was lower in HNPCC than the general population (P = 0.0028). Extracolonic cancers were noted in 33 percent of MSH2 patients, compared with 12 percent of MLH1 patients and 7.3 percent of the general population with colorectal cancers (P < 0.001). Combined MLH1 and MSH2 ten-year survival was 68.7 percent compared with 47.8 percent for the general population (P = 0.009 stage stratified, hazard ratio 0.57).
The presence of rectal cancer should not preclude the diagnosis of HNPCC, because the incidence of rectal cancer in MSH2 was comparable with that in the general population. Phenotypic variations, including the preponderance of extracolonic cancers in MSH2 patients, did not result in survival differences between genotypic subgroups. These phenotypic features of HNPCC genotypes may have clinical significance in the design of specific screening, surveillance, and follow-up for affected individuals. |
| doi_str_mv | 10.1007/BF02235755 |
| format | Article |
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Colorectal cancer onset and site distribution were compared among 67 members of MLH1 kindreds, 45 members of MSH2 kindreds, and 1,189 patients from the general population. Synchronous and metachronous cancer rates, tumor stage, extracolonic cancer incidence, and survival were also compared.
Mean ages of colorectal cancer onset were 44, 46, and 69 years for MLH1, MSH2, and the general population, respectively (P < 0.001). More proximal and fewer distal colon cancers were noted in HNPCC than the general population (P < 0.001, P = 0.04). Site distribution showed disparity of rectal cancers (8 percent MLH1 vs. 28 percent MSH2; P = 0.01) based on genotypes. Overall, synchronous colorectal cancer rates were 7.4, 6.7, and 2.4 percent for MLH1, MSH2, and the general population, respectively (P = 0.016). Annual metachronous colorectal cancer rates were 2.1, 1.7, and 0.33 percent for MLH1, MSH2, and the general population, respectively (P = 0.041). Colorectal cancer stage presentation was lower in HNPCC than the general population (P = 0.0028). Extracolonic cancers were noted in 33 percent of MSH2 patients, compared with 12 percent of MLH1 patients and 7.3 percent of the general population with colorectal cancers (P < 0.001). Combined MLH1 and MSH2 ten-year survival was 68.7 percent compared with 47.8 percent for the general population (P = 0.009 stage stratified, hazard ratio 0.57).
The presence of rectal cancer should not preclude the diagnosis of HNPCC, because the incidence of rectal cancer in MSH2 was comparable with that in the general population. Phenotypic variations, including the preponderance of extracolonic cancers in MSH2 patients, did not result in survival differences between genotypic subgroups. These phenotypic features of HNPCC genotypes may have clinical significance in the design of specific screening, surveillance, and follow-up for affected individuals.</description><identifier>ISSN: 0012-3706</identifier><identifier>EISSN: 1530-0358</identifier><identifier>DOI: 10.1007/BF02235755</identifier><identifier>PMID: 9559626</identifier><identifier>CODEN: DICRAG</identifier><language>eng</language><publisher>Secaucus, NJ: Springer</publisher><subject>Adaptor Proteins, Signal Transducing ; Adult ; Age of Onset ; Aged ; Biological and medical sciences ; Carrier Proteins ; Colorectal Neoplasms - epidemiology ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Colorectal Neoplasms, Hereditary Nonpolyposis - epidemiology ; Colorectal Neoplasms, Hereditary Nonpolyposis - genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis - pathology ; DNA Repair ; DNA-Binding Proteins ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Genotype ; Germ-Line Mutation ; Humans ; Incidence ; Male ; Medical sciences ; Middle Aged ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein ; Neoplasm Proteins - genetics ; Neoplasm Staging ; Neoplasms - epidemiology ; Neoplasms - genetics ; Neoplasms - pathology ; Neoplasms, Multiple Primary - epidemiology ; Neoplasms, Multiple Primary - genetics ; Neoplasms, Multiple Primary - pathology ; Neoplasms, Second Primary - epidemiology ; Neoplasms, Second Primary - genetics ; Neoplasms, Second Primary - pathology ; Nuclear Proteins ; Proto-Oncogene Proteins - genetics ; Statistics as Topic ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Survival Rate ; Tumors</subject><ispartof>Diseases of the colon & rectum, 1998-04, Vol.41 (4), p.428-433</ispartof><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c311t-c8a43c60753f996fa781324299e5977dcb984d27831e236f6555d847ca14388c3</citedby><cites>FETCH-LOGICAL-c311t-c8a43c60753f996fa781324299e5977dcb984d27831e236f6555d847ca14388c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2208156$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9559626$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LIN, K. M</creatorcontrib><creatorcontrib>SHASHIDHARAN, M</creatorcontrib><creatorcontrib>TERNENT, C. A</creatorcontrib><creatorcontrib>THORSON, A. G</creatorcontrib><creatorcontrib>BLATCHFORD, G. J</creatorcontrib><creatorcontrib>CHRISTENSEN, M. A</creatorcontrib><creatorcontrib>LANSPA, S. J</creatorcontrib><creatorcontrib>LEMON, S. J</creatorcontrib><creatorcontrib>WATSON, P</creatorcontrib><creatorcontrib>LYNCH, H. T</creatorcontrib><title>Colorectal and extracolonic cancer variations in MLH1/MSH2 hereditary nonpolyposis colorectal cancer kindreds and the general population</title><title>Diseases of the colon & rectum</title><addtitle>Dis Colon Rectum</addtitle><description>This clinical case review aimed to identify phenotypic variations in colorectal and extracolonic cancer expression between hereditary nonpolyposis colorectal cancer (HNPCC) families with MLH1 and MSH2 germline mutations and the general population.
Colorectal cancer onset and site distribution were compared among 67 members of MLH1 kindreds, 45 members of MSH2 kindreds, and 1,189 patients from the general population. Synchronous and metachronous cancer rates, tumor stage, extracolonic cancer incidence, and survival were also compared.
Mean ages of colorectal cancer onset were 44, 46, and 69 years for MLH1, MSH2, and the general population, respectively (P < 0.001). More proximal and fewer distal colon cancers were noted in HNPCC than the general population (P < 0.001, P = 0.04). Site distribution showed disparity of rectal cancers (8 percent MLH1 vs. 28 percent MSH2; P = 0.01) based on genotypes. Overall, synchronous colorectal cancer rates were 7.4, 6.7, and 2.4 percent for MLH1, MSH2, and the general population, respectively (P = 0.016). Annual metachronous colorectal cancer rates were 2.1, 1.7, and 0.33 percent for MLH1, MSH2, and the general population, respectively (P = 0.041). Colorectal cancer stage presentation was lower in HNPCC than the general population (P = 0.0028). Extracolonic cancers were noted in 33 percent of MSH2 patients, compared with 12 percent of MLH1 patients and 7.3 percent of the general population with colorectal cancers (P < 0.001). Combined MLH1 and MSH2 ten-year survival was 68.7 percent compared with 47.8 percent for the general population (P = 0.009 stage stratified, hazard ratio 0.57).
The presence of rectal cancer should not preclude the diagnosis of HNPCC, because the incidence of rectal cancer in MSH2 was comparable with that in the general population. Phenotypic variations, including the preponderance of extracolonic cancers in MSH2 patients, did not result in survival differences between genotypic subgroups. These phenotypic features of HNPCC genotypes may have clinical significance in the design of specific screening, surveillance, and follow-up for affected individuals.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Adult</subject><subject>Age of Onset</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Carrier Proteins</subject><subject>Colorectal Neoplasms - epidemiology</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - epidemiology</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - genetics</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - pathology</subject><subject>DNA Repair</subject><subject>DNA-Binding Proteins</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genotype</subject><subject>Germ-Line Mutation</subject><subject>Humans</subject><subject>Incidence</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>MutL Protein Homolog 1</subject><subject>MutS Homolog 2 Protein</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Staging</subject><subject>Neoplasms - epidemiology</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - pathology</subject><subject>Neoplasms, Multiple Primary - epidemiology</subject><subject>Neoplasms, Multiple Primary - genetics</subject><subject>Neoplasms, Multiple Primary - pathology</subject><subject>Neoplasms, Second Primary - epidemiology</subject><subject>Neoplasms, Second Primary - genetics</subject><subject>Neoplasms, Second Primary - pathology</subject><subject>Nuclear Proteins</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Statistics as Topic</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Survival Rate</subject><subject>Tumors</subject><issn>0012-3706</issn><issn>1530-0358</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkL1OwzAURi0EglJY2JE8IAakgH_i2B6hohSpiAGYI9dxqCG1g50g-gY8NoZGZbKuv6NzdT8ATjC6xAjxq5spIoQyztgOGGFGUYYoE7tghBAmGeWoOACHMb6lERHE98G-ZEwWpBiB74lvfDC6Uw1UroLmqwtKpz9nNdTKaRPgpwpWdda7CK2DD_MZvnp4mhG4NMFUtlNhDZ13rW_WrY82Qv2vHAzv1lWJjX8ruqWBr8aZkPLWt33z5z4Ce7Vqojke3jF4md4-T2bZ_PHufnI9zzTFuMu0UDnVBeKM1lIWteICU5ITKQ2TnFd6IUVeES4oNoQWdcEYq0TOtcI5FULTMTjfeNvgP3oTu3JlozZNo5zxfSy5FBjngifwYgPq4GMMpi7bYFfp2BKj8rf28r_2BJ8O1n6xMtUWHXpO-dmQq6hVU4fUi41bjBAkMCvoD93Rims</recordid><startdate>19980401</startdate><enddate>19980401</enddate><creator>LIN, K. M</creator><creator>SHASHIDHARAN, M</creator><creator>TERNENT, C. A</creator><creator>THORSON, A. G</creator><creator>BLATCHFORD, G. J</creator><creator>CHRISTENSEN, M. A</creator><creator>LANSPA, S. J</creator><creator>LEMON, S. J</creator><creator>WATSON, P</creator><creator>LYNCH, H. T</creator><general>Springer</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><scope>7X8</scope></search><sort><creationdate>19980401</creationdate><title>Colorectal and extracolonic cancer variations in MLH1/MSH2 hereditary nonpolyposis colorectal cancer kindreds and the general population</title><author>LIN, K. M ; SHASHIDHARAN, M ; TERNENT, C. A ; THORSON, A. G ; BLATCHFORD, G. J ; CHRISTENSEN, M. A ; LANSPA, S. J ; LEMON, S. J ; WATSON, P ; LYNCH, H. T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c311t-c8a43c60753f996fa781324299e5977dcb984d27831e236f6555d847ca14388c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Adult</topic><topic>Age of Onset</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Carrier Proteins</topic><topic>Colorectal Neoplasms - epidemiology</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - epidemiology</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - genetics</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - pathology</topic><topic>DNA Repair</topic><topic>DNA-Binding Proteins</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genotype</topic><topic>Germ-Line Mutation</topic><topic>Humans</topic><topic>Incidence</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>MutL Protein Homolog 1</topic><topic>MutS Homolog 2 Protein</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Staging</topic><topic>Neoplasms - epidemiology</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - pathology</topic><topic>Neoplasms, Multiple Primary - epidemiology</topic><topic>Neoplasms, Multiple Primary - genetics</topic><topic>Neoplasms, Multiple Primary - pathology</topic><topic>Neoplasms, Second Primary - epidemiology</topic><topic>Neoplasms, Second Primary - genetics</topic><topic>Neoplasms, Second Primary - pathology</topic><topic>Nuclear Proteins</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Statistics as Topic</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Survival Rate</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LIN, K. M</creatorcontrib><creatorcontrib>SHASHIDHARAN, M</creatorcontrib><creatorcontrib>TERNENT, C. A</creatorcontrib><creatorcontrib>THORSON, A. G</creatorcontrib><creatorcontrib>BLATCHFORD, G. J</creatorcontrib><creatorcontrib>CHRISTENSEN, M. A</creatorcontrib><creatorcontrib>LANSPA, S. J</creatorcontrib><creatorcontrib>LEMON, S. J</creatorcontrib><creatorcontrib>WATSON, P</creatorcontrib><creatorcontrib>LYNCH, H. T</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>Diseases of the colon & rectum</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LIN, K. M</au><au>SHASHIDHARAN, M</au><au>TERNENT, C. A</au><au>THORSON, A. G</au><au>BLATCHFORD, G. J</au><au>CHRISTENSEN, M. A</au><au>LANSPA, S. J</au><au>LEMON, S. J</au><au>WATSON, P</au><au>LYNCH, H. T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Colorectal and extracolonic cancer variations in MLH1/MSH2 hereditary nonpolyposis colorectal cancer kindreds and the general population</atitle><jtitle>Diseases of the colon & rectum</jtitle><addtitle>Dis Colon Rectum</addtitle><date>1998-04-01</date><risdate>1998</risdate><volume>41</volume><issue>4</issue><spage>428</spage><epage>433</epage><pages>428-433</pages><issn>0012-3706</issn><eissn>1530-0358</eissn><coden>DICRAG</coden><abstract>This clinical case review aimed to identify phenotypic variations in colorectal and extracolonic cancer expression between hereditary nonpolyposis colorectal cancer (HNPCC) families with MLH1 and MSH2 germline mutations and the general population.
Colorectal cancer onset and site distribution were compared among 67 members of MLH1 kindreds, 45 members of MSH2 kindreds, and 1,189 patients from the general population. Synchronous and metachronous cancer rates, tumor stage, extracolonic cancer incidence, and survival were also compared.
Mean ages of colorectal cancer onset were 44, 46, and 69 years for MLH1, MSH2, and the general population, respectively (P < 0.001). More proximal and fewer distal colon cancers were noted in HNPCC than the general population (P < 0.001, P = 0.04). Site distribution showed disparity of rectal cancers (8 percent MLH1 vs. 28 percent MSH2; P = 0.01) based on genotypes. Overall, synchronous colorectal cancer rates were 7.4, 6.7, and 2.4 percent for MLH1, MSH2, and the general population, respectively (P = 0.016). Annual metachronous colorectal cancer rates were 2.1, 1.7, and 0.33 percent for MLH1, MSH2, and the general population, respectively (P = 0.041). Colorectal cancer stage presentation was lower in HNPCC than the general population (P = 0.0028). Extracolonic cancers were noted in 33 percent of MSH2 patients, compared with 12 percent of MLH1 patients and 7.3 percent of the general population with colorectal cancers (P < 0.001). Combined MLH1 and MSH2 ten-year survival was 68.7 percent compared with 47.8 percent for the general population (P = 0.009 stage stratified, hazard ratio 0.57).
The presence of rectal cancer should not preclude the diagnosis of HNPCC, because the incidence of rectal cancer in MSH2 was comparable with that in the general population. Phenotypic variations, including the preponderance of extracolonic cancers in MSH2 patients, did not result in survival differences between genotypic subgroups. These phenotypic features of HNPCC genotypes may have clinical significance in the design of specific screening, surveillance, and follow-up for affected individuals.</abstract><cop>Secaucus, NJ</cop><pub>Springer</pub><pmid>9559626</pmid><doi>10.1007/BF02235755</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Diseases of the colon & rectum, 1998-04, Vol.41 (4), p.428-433 |
| issn | 0012-3706 1530-0358 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_79811487 |
| source | MEDLINE; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Adaptor Proteins, Signal Transducing Adult Age of Onset Aged Biological and medical sciences Carrier Proteins Colorectal Neoplasms - epidemiology Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Colorectal Neoplasms, Hereditary Nonpolyposis - epidemiology Colorectal Neoplasms, Hereditary Nonpolyposis - genetics Colorectal Neoplasms, Hereditary Nonpolyposis - pathology DNA Repair DNA-Binding Proteins Female Gastroenterology. Liver. Pancreas. Abdomen Genotype Germ-Line Mutation Humans Incidence Male Medical sciences Middle Aged MutL Protein Homolog 1 MutS Homolog 2 Protein Neoplasm Proteins - genetics Neoplasm Staging Neoplasms - epidemiology Neoplasms - genetics Neoplasms - pathology Neoplasms, Multiple Primary - epidemiology Neoplasms, Multiple Primary - genetics Neoplasms, Multiple Primary - pathology Neoplasms, Second Primary - epidemiology Neoplasms, Second Primary - genetics Neoplasms, Second Primary - pathology Nuclear Proteins Proto-Oncogene Proteins - genetics Statistics as Topic Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Survival Rate Tumors |
| title | Colorectal and extracolonic cancer variations in MLH1/MSH2 hereditary nonpolyposis colorectal cancer kindreds and the general population |
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