ABO blood groups and pancreatic cancer risk and survival: Results from the PANcreatic Disease ReseArch (PANDoRA) consortium
There is strong epidemiologic evidence indicating that common genetic variability could be implicated in pancreatic cancer risk and, to date, various loci have been proposed. In particular, there is increasing evidence of the involvement of ABO gene variability and pancreatic cancer risk. In a large...
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| Veröffentlicht in: | Oncology reports 2013-04, Vol.29 (4), p.1637-1644 |
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| creator | RIZZATO, COSMERI CAMPA, DANIELE PEZZILLI, RAFFAELE SOUCEK, PAVEL GREENHALF, WILLIAM CAPURSO, GABRIELE TALAR-WOJNAROWSKA, RENATA HELLER, ANETTE JAMROZIAK, KRZYSZTOF KHAW, KAY-TEE KEY, TIM J BAMBI, FRANCO LANDI, STEFANO MOHELNIKOVA-DUCHONOVA, BEATRICE VODICKOVA, LUDMILA BÜCHLER, MARKUS W BUGERT, PETER VODICKA, PAVEL NEOPTOLEMOS, JOHN P WERNER, JENS HOHEISEL, JÖRG D BAUER, ANDREA S GIESE, NATHALIA CANZIAN, FEDERICO |
| description | There is strong epidemiologic evidence indicating that common genetic variability could be implicated in pancreatic cancer risk and, to date, various loci have been proposed. In particular, there is increasing evidence of the involvement of ABO gene variability and pancreatic cancer risk. In a large multicentric study of 1,028 pancreatic ductal adenocarcinoma cases and 2,257 controls in the context of the PANcreatic Disease ReseArch (PANDoRA) consortium, we investigated the suggested association with increased risk for carriers of single nucleotide polymorphisms (SNPs) determining the A or B allele in comparison with the O allele, which encodes for a non-functional enzyme. Since glycosyltransferase activity, encoded by ABO, is higher for the A1 variant compared with the A2 variant, we investigated the hypothesis that A1 carriers were at an increased risk of pancreatic cancer. In our analysis, carriers of the A1 were indeed at greater risk of developing the disease. In addition, we investigated the possible influence that genetic variability at the ABO locus may have in pancreatic cancer survival, but we observed no effect in our population. |
| doi_str_mv | 10.3892/or.2013.2285 |
| format | Article |
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In particular, there is increasing evidence of the involvement of ABO gene variability and pancreatic cancer risk. In a large multicentric study of 1,028 pancreatic ductal adenocarcinoma cases and 2,257 controls in the context of the PANcreatic Disease ReseArch (PANDoRA) consortium, we investigated the suggested association with increased risk for carriers of single nucleotide polymorphisms (SNPs) determining the A or B allele in comparison with the O allele, which encodes for a non-functional enzyme. Since glycosyltransferase activity, encoded by ABO, is higher for the A1 variant compared with the A2 variant, we investigated the hypothesis that A1 carriers were at an increased risk of pancreatic cancer. In our analysis, carriers of the A1 were indeed at greater risk of developing the disease. In addition, we investigated the possible influence that genetic variability at the ABO locus may have in pancreatic cancer survival, but we observed no effect in our population.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2013.2285</identifier><identifier>PMID: 23403949</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>ABO ; ABO Blood-Group System - genetics ; Age ; Alleles ; Amino acids ; Antigens ; Blood groups ; cancer risk ; Carcinoma, Pancreatic Ductal - genetics ; Cell adhesion & migration ; Confidence intervals ; Consortia ; Enzymes ; Family medical history ; Gender ; Genes ; Genetic Association Studies ; Genetic Predisposition to Disease ; genetic susceptibility ; Glycosyltransferases - genetics ; Health risk assessment ; Humans ; Medical prognosis ; Mutation ; Pancreatic cancer ; Pancreatic Neoplasms - epidemiology ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Polymorphism, Single Nucleotide ; Population ; Risk Factors ; Studies ; Survival Analysis</subject><ispartof>Oncology reports, 2013-04, Vol.29 (4), p.1637-1644</ispartof><rights>Copyright © 2013, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-696188404bba1d14fa26869aa28ca8a73f88811834fb3759b1674ab231f407013</citedby><cites>FETCH-LOGICAL-c497t-696188404bba1d14fa26869aa28ca8a73f88811834fb3759b1674ab231f407013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23403949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>RIZZATO, COSMERI</creatorcontrib><creatorcontrib>CAMPA, DANIELE</creatorcontrib><creatorcontrib>PEZZILLI, RAFFAELE</creatorcontrib><creatorcontrib>SOUCEK, PAVEL</creatorcontrib><creatorcontrib>GREENHALF, WILLIAM</creatorcontrib><creatorcontrib>CAPURSO, GABRIELE</creatorcontrib><creatorcontrib>TALAR-WOJNAROWSKA, RENATA</creatorcontrib><creatorcontrib>HELLER, ANETTE</creatorcontrib><creatorcontrib>JAMROZIAK, KRZYSZTOF</creatorcontrib><creatorcontrib>KHAW, KAY-TEE</creatorcontrib><creatorcontrib>KEY, TIM J</creatorcontrib><creatorcontrib>BAMBI, FRANCO</creatorcontrib><creatorcontrib>LANDI, STEFANO</creatorcontrib><creatorcontrib>MOHELNIKOVA-DUCHONOVA, BEATRICE</creatorcontrib><creatorcontrib>VODICKOVA, LUDMILA</creatorcontrib><creatorcontrib>BÜCHLER, MARKUS W</creatorcontrib><creatorcontrib>BUGERT, PETER</creatorcontrib><creatorcontrib>VODICKA, PAVEL</creatorcontrib><creatorcontrib>NEOPTOLEMOS, JOHN P</creatorcontrib><creatorcontrib>WERNER, JENS</creatorcontrib><creatorcontrib>HOHEISEL, JÖRG D</creatorcontrib><creatorcontrib>BAUER, ANDREA S</creatorcontrib><creatorcontrib>GIESE, NATHALIA</creatorcontrib><creatorcontrib>CANZIAN, FEDERICO</creatorcontrib><title>ABO blood groups and pancreatic cancer risk and survival: Results from the PANcreatic Disease ReseArch (PANDoRA) consortium</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>There is strong epidemiologic evidence indicating that common genetic variability could be implicated in pancreatic cancer risk and, to date, various loci have been proposed. In particular, there is increasing evidence of the involvement of ABO gene variability and pancreatic cancer risk. In a large multicentric study of 1,028 pancreatic ductal adenocarcinoma cases and 2,257 controls in the context of the PANcreatic Disease ReseArch (PANDoRA) consortium, we investigated the suggested association with increased risk for carriers of single nucleotide polymorphisms (SNPs) determining the A or B allele in comparison with the O allele, which encodes for a non-functional enzyme. Since glycosyltransferase activity, encoded by ABO, is higher for the A1 variant compared with the A2 variant, we investigated the hypothesis that A1 carriers were at an increased risk of pancreatic cancer. In our analysis, carriers of the A1 were indeed at greater risk of developing the disease. In addition, we investigated the possible influence that genetic variability at the ABO locus may have in pancreatic cancer survival, but we observed no effect in our population.</description><subject>ABO</subject><subject>ABO Blood-Group System - genetics</subject><subject>Age</subject><subject>Alleles</subject><subject>Amino acids</subject><subject>Antigens</subject><subject>Blood groups</subject><subject>cancer risk</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Cell adhesion & migration</subject><subject>Confidence intervals</subject><subject>Consortia</subject><subject>Enzymes</subject><subject>Family medical history</subject><subject>Gender</subject><subject>Genes</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>genetic susceptibility</subject><subject>Glycosyltransferases - genetics</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Medical prognosis</subject><subject>Mutation</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - epidemiology</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Population</subject><subject>Risk Factors</subject><subject>Studies</subject><subject>Survival Analysis</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpd0UFLHTEQB_BQWqq1vXmWQKFY6D4zSd4m6W2rrQpSRVroLWSzWV3d3bxmdgXplzevTz14ysD8ZgjzJ2QX2EJoww9iWnAGYsG5Xr4i26AMFFwKeJ1rxqEQYvlni7xDvGGMK1aat2SLC8mEkWab_Ku-ndO6j7GhVynOK6RubOjKjT4FN3We-lyGRFOHt_9bOKe77s71X-llwLmfkLYpDnS6DvSi-vk0ddRhcBjWJlTJX9P93DyKl9Vn6uOIMU3dPLwnb1rXY_jw-O6Q3z--_zo8Kc7Oj08Pq7PCS6OmojQlaC2ZrGsHDcjW8VKXxjmuvdNOiVZrDaCFbGuhlqaGUklXcwGtZCqfZofsb_auUvw7B5zs0KEPfe_GEGe0IIDn_UtuMv34gt7EOY35dxaM4KUSgrGsvmyUTxExhdauUje4dG-B2XUoNia7DsWuQ8l873HpXA-hecZPKWTwaQMwH77pmojPJqaCm4LJAkqhxAPli5H7</recordid><startdate>20130401</startdate><enddate>20130401</enddate><creator>RIZZATO, COSMERI</creator><creator>CAMPA, DANIELE</creator><creator>PEZZILLI, RAFFAELE</creator><creator>SOUCEK, PAVEL</creator><creator>GREENHALF, WILLIAM</creator><creator>CAPURSO, GABRIELE</creator><creator>TALAR-WOJNAROWSKA, RENATA</creator><creator>HELLER, ANETTE</creator><creator>JAMROZIAK, KRZYSZTOF</creator><creator>KHAW, KAY-TEE</creator><creator>KEY, TIM J</creator><creator>BAMBI, FRANCO</creator><creator>LANDI, STEFANO</creator><creator>MOHELNIKOVA-DUCHONOVA, BEATRICE</creator><creator>VODICKOVA, LUDMILA</creator><creator>BÜCHLER, MARKUS W</creator><creator>BUGERT, PETER</creator><creator>VODICKA, PAVEL</creator><creator>NEOPTOLEMOS, JOHN P</creator><creator>WERNER, JENS</creator><creator>HOHEISEL, JÖRG D</creator><creator>BAUER, ANDREA S</creator><creator>GIESE, NATHALIA</creator><creator>CANZIAN, FEDERICO</creator><general>D.A. 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In particular, there is increasing evidence of the involvement of ABO gene variability and pancreatic cancer risk. In a large multicentric study of 1,028 pancreatic ductal adenocarcinoma cases and 2,257 controls in the context of the PANcreatic Disease ReseArch (PANDoRA) consortium, we investigated the suggested association with increased risk for carriers of single nucleotide polymorphisms (SNPs) determining the A or B allele in comparison with the O allele, which encodes for a non-functional enzyme. Since glycosyltransferase activity, encoded by ABO, is higher for the A1 variant compared with the A2 variant, we investigated the hypothesis that A1 carriers were at an increased risk of pancreatic cancer. In our analysis, carriers of the A1 were indeed at greater risk of developing the disease. In addition, we investigated the possible influence that genetic variability at the ABO locus may have in pancreatic cancer survival, but we observed no effect in our population.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>23403949</pmid><doi>10.3892/or.2013.2285</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1021-335X |
| ispartof | Oncology reports, 2013-04, Vol.29 (4), p.1637-1644 |
| issn | 1021-335X 1791-2431 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1312840529 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | ABO ABO Blood-Group System - genetics Age Alleles Amino acids Antigens Blood groups cancer risk Carcinoma, Pancreatic Ductal - genetics Cell adhesion & migration Confidence intervals Consortia Enzymes Family medical history Gender Genes Genetic Association Studies Genetic Predisposition to Disease genetic susceptibility Glycosyltransferases - genetics Health risk assessment Humans Medical prognosis Mutation Pancreatic cancer Pancreatic Neoplasms - epidemiology Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Polymorphism, Single Nucleotide Population Risk Factors Studies Survival Analysis |
| title | ABO blood groups and pancreatic cancer risk and survival: Results from the PANcreatic Disease ReseArch (PANDoRA) consortium |
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