Common colorectal cancer risk alleles contribute to the multiple colorectal adenoma phenotype, but do not influence colonic polyposis in FAP View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-02

AUTHORS

Timothy H T Cheng, Maggie Gorman, Lynn Martin, Ella Barclay, Graham Casey, Polly A Newcomb, Graham Casey, David V Conti, Fred Schumacher, Steve Gallinger, Noralane M Lindor, John Hopper, Mark Jenkins, David J Hunter, Peter Kraft, Kevin B Jacobs, David G Cox, Meredith Yeager, Susan E Hankinson, Sholom Wacholder, Zhaoming Wang, Robert Welch, Amy Hutchinson, Junwen Wang, Kai Yu, Nilanjan Chatterjee, Nick Orr, Walter C Willett, Graham A Colditz, Regina G Ziegler, Christine D Berg, Saundra S Buys, Catherine A McCarty, Heather Spencer Feigelson, Eugenia E Calle, Michael J Thun, Richard B Hayes, Margaret Tucker, Daniela S Gerhard, Joseph F Fraumeni, Robert N Hoover, Gilles Thomas, Stephen J Chanock, Meredith Yeager, Nilanjan Chatterjee, Julia Ciampa, Kevin B Jacobs, Jesus Gonzalez-Bosquet, Richard B Hayes, Peter Kraft, Sholom Wacholder, Nick Orr, Sonja Berndt, Kai Yu, Amy Hutchinson, Zhaoming Wang, Laufey Amundadottir, Heather Spencer Feigelson, Michael J Thun, W Ryan Diver, Demetrius Albanes, Jarmo Virtamo, Stephanie Weinstein, Fredrick R Schumacher, Geraldine Cancel-Tassin, Olivier Cussenot, Antoine Valeri, Gerald L Andriole, E David Crawford, Christopher A Haiman, Brian Henderson, Laurence Kolonel, Loic Le Marchand, Afshan Siddiq, Elio Riboli, Timothy J Key, Rudolf Kaaks, William Isaacs, Sarah Isaacs, Kathleen E Wiley, Henrik Gronberg, Fredrik Wiklund, Pär Stattin, Jianfeng Xu, S Lilly Zheng, Jielin Sun, Lars J Vatten, Kristian Hveem, Merethe Kumle, Margaret Tucker, Daniela S Gerhard, Robert N Hoover, Joseph F Fraumeni, David J Hunter, Gilles Thomas, Stephen J Chanock, Mark P Purdue, Mattias Johansson, Diana Zelenika, Jorge R Toro, Ghislaine Scelo, Lee E Moore, Egor Prokhortchouk, Xifeng Wu, Lambertus A Kiemeney, Valerie Gaborieau, Kevin B Jacobs, Wong-Ho Chow, David Zaridze, Vsevolod Matveev, Jan Lubinski, Joanna Trubicka, Neonila Szeszenia-Dabrowska, Jolanta Lissowska, Péter Rudnai, Eleonora Fabianova, Alexandru Bucur, Vladimir Bencko, Lenka Foretova, Vladimir Janout, Paolo Boffetta, Joanne S Colt, Faith G Davis, Kendra L Schwartz, Rosamonde E Banks, Peter J Selby, Patricia Harnden, Christine D Berg, Ann W Hsing, Robert L Grubb III, Heiner Boeing, Paolo Vineis, Françoise Clavel-Chapelon, Domenico Palli, Rosario Tumino, Vittorio Krogh, Salvatore Panico, Eric J Duell, José Ramón Quirós, Maria-José Sanchez, Carmen Navarro, Eva Ardanaz, Miren Dorronsoro, Kay-Tee Khaw, Naomi E Allen, H Bas Bueno-de-Mesquita, Petra H M Peeters, Dimitrios Trichopoulos, Jakob Linseisen, Börje Ljungberg, Kim Overvad, Anne Tjønneland, Isabelle Romieu, Elio Riboli, Anush Mukeria, Oxana Shangina, Victoria L Stevens, Michael J Thun, W Ryan Diver, Susan M Gapstur, Paul D Pharoah, Douglas F Easton, Demetrius Albanes, Stephanie J Weinstein, Jarmo Virtamo, Lars Vatten, Kristian Hveem, Inger Njølstad, Grethe S Tell, Camilla Stoltenberg, Rajiv Kumar, Kvetoslava Koppova, Olivier Cussenot, Simone Benhamou, Egbert Oosterwijk, Sita H Vermeulen, Katja K H Aben, Saskia L van der Marel, Yuanqing Ye, Christopher G Wood, Xia Pu, Alexander M Mazur, Eugenia S Boulygina, Nikolai N Chekanov, Mario Foglio, Doris Lechner, Ivo Gut, Simon Heath, Hélène Blanche, Amy Hutchinson, Gilles Thomas, Zhaoming Wang, Meredith Yeager, Joseph F Fraumeni, Konstantin G Skryabin, James D McKay, Nathaniel Rothman, Stephen J Chanock, Mark Lathrop, Paul Brennan, Brian Saunders, Huw Thomas, Sue Clark, Ian Tomlinson

ABSTRACT

The presence of multiple (5-100) colorectal adenomas suggests an inherited predisposition, but the genetic aetiology of this phenotype is undetermined if patients test negative for Mendelian polyposis syndromes such as familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP). We investigated whether 18 common colorectal cancer (CRC) predisposition single-nucleotide polymorphisms (SNPs) could help to explain some cases with multiple adenomas who phenocopied FAP or MAP, but had no pathogenic APC or MUTYH variant. No multiple adenoma case had an outlying number of CRC SNP risk alleles, but multiple adenoma patients did have a significantly higher number of risk alleles than population controls (P=5.7 × 10(-7)). The association was stronger in those with ≥10 adenomas. The CRC SNPs accounted for 4.3% of the variation in multiple adenoma risk, with three SNPs (rs6983267, rs10795668, rs3802842) explaining 3.0% of the variation. In FAP patients, the CRC risk score did not differ significantly from the controls, as we expected given the overwhelming effect of pathogenic germline APC variants on the phenotype of these cases. More unexpectedly, we found no evidence that the CRC SNPs act as modifier genes for the number of colorectal adenomas in FAP patients. In conclusion, common colorectal tumour risk alleles contribute to the development of multiple adenomas in patients without pathogenic germline APC or MUTYH variants. This phenotype may have 'polygenic' or monogenic origins. The risk of CRC in relatives of multiple adenoma cases is probably much lower for cases with polygenic disease, and this should be taken into account when counselling such patients. More... »

PAGES

260

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ejhg.2014.74

DOI

http://dx.doi.org/10.1038/ejhg.2014.74

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005915969

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24801760


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