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Joleen M. Hubbard and Axel Grothey

, Crohn disease, and regional enteritis), familial adenomatous polyposis (FAP), or hereditary nonpolyposis colorectal cancer (HNPCC) syndrome, and 22% had family history of CRC. 6 The 2 major known familial syndromes associated with CRC in young adults

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Al B. Benson III, Alan P. Venook, Mahmoud M. Al-Hawary, Mustafa A. Arain, Yi-Jen Chen, Kristen K. Ciombor, Stacey A. Cohen, Harry S. Cooper, Dustin A. Deming, Ignacio Garrido-Laguna, Jean L. Grem, Sarah E. Hoffe, Joleen Hubbard, Steven Hunt, Ahmed Kamel, Natalie Kirilcuk, Smitha Krishnamurthi, Wells A. Messersmith, Jeffrey Meyerhardt, Eric D. Miller, Mary F. Mulcahy, Steven Nurkin, Michael J. Overman, Aparna Parikh, Hitendra Patel, Katrina S. Pedersen, Leonard B. Saltz, Charles Schneider, David Shibata, John M. Skibber, Constantinos T. Sofocleous, Elena M. Stoffel, Eden Stotsky-Himelfarb, Christopher G. Willett, Alyse Johnson-Chilla, Kristina M. Gregory and Lisa A. Gurski

adenomatous polyposis (FAP). Therefore, it is recommended that all patients with small bowel cancer be queried regarding their family history and considered for risk assessment, as detailed in the NCCN Guidelines for Colorectal Cancer Screening (available at

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Samir Gupta, Dawn Provenzale, Xavier Llor, Amy L. Halverson, William Grady, Daniel C. Chung, Sigurdis Haraldsdottir, Arnold J. Markowitz, Thomas P. Slavin Jr, Heather Hampel, CGC, Reid M. Ness, Jennifer M. Weiss, Dennis J. Ahnen, Lee-may Chen, Gregory Cooper, Dayna S. Early, Francis M. Giardiello, Michael J. Hall, Stanley R. Hamilton, Priyanka Kanth, Jason B. Klapman, Audrey J. Lazenby, Patrick M. Lynch, Robert J. Mayer, June Mikkelson, CGC, Shajan Peter, Scott E. Regenbogen, Mary A. Dwyer, CGC and Ndiya Ogba

adenomatous polyposis (FAP), and MUTYH –associated polyposis (MAP), 2 , 8 and rare inherited syndromes, including juvenile polyposis syndrome (JPS), Cowden syndrome/PTEN hamartoma tumor syndrome (PHTS), and Peutz-Jeghers syndrome (PJS). 9 , 10 Some

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Dawn Provenzale, Samir Gupta, Dennis J. Ahnen, Travis Bray, Jamie A. Cannon, Gregory Cooper, Donald S. David, Dayna S. Early, Deborah Erwin, James M. Ford, Francis M. Giardiello, William Grady, Amy L. Halverson, Stanley R. Hamilton, Heather Hampel, Mohammad K. Ismail, Jason B. Klapman, David W. Larson, Audrey J. Lazenby, Patrick M. Lynch, Robert J. Mayer, Reid M. Ness, Scott E. Regenbogen, Niloy Jewel Samadder, Moshe Shike, Gideon Steinbach, David Weinberg, Mary Dwyer and Susan Darlow

-defined inherited syndromes such as Lynch syndrome (also known as hereditary nonpolyposis colorectal cancer), familial adenomatous polyposis (FAP), and MutY human homolog (MUTYH)-associated polyposis (MAP). Other entities include Cowden, Bannayan

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Patrick M. Lynch

adenomatous polyposis coli gene . Cell 1991 , 66 : 589 – 600 . 14. Kinzler KW Nilbert MC Su LK . Identification of FAP locus genes from chromosome 5q21 . Science 1991 ; 253 : 661 – 665 . 15. van der Luijt RB Khan PM Vasen HF

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Katrina S. Pedersen, Kanwal Raghav and Michael J. Overman

instability (MSI-H) is indicated and may help predict better therapies, including immune checkpoint therapy, for these patients. 30 , 31 Familial adenomatous polyposis (FAP) has been typically associated with the formation of hundreds of colon polyps and

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different cancer site guidelines. Guidelines for colorectal cancer screening cover several hereditary colon cancer syndromes (Lynch syndrome [LS], familial adenomatous polyposis [FAP], MUTYH -associated polyposis, Peutz-Jeghers, and juvenile polyposis

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Randall W. Burt, Jamie A. Cannon, Donald S. David, Dayna S. Early, James M. Ford, Francis M. Giardiello, Amy L. Halverson, Stanley R. Hamilton, Heather Hampel, Mohammad K. Ismail, Kory Jasperson, Jason B. Klapman, Audrey J. Lazenby, Patrick M. Lynch, Robert J. Mayer, Reid M. Ness, Dawn Provenzale, M. Sambasiva Rao, Moshe Shike, Gideon Steinbach, Jonathan P. Terdiman, David Weinberg, Mary Dwyer and Deborah Freedman-Cass

syndromes such as Lynch syndrome (also known as hereditary nonpolyposis colorectal cancer [HNPCC]), familial adenomatous polyposis (FAP), and MutY human homolog -associated polyposis (MAP). Other entities include Muir-Torre, Turcot, Gardner, Cowden

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Peter F. Coccia, Jessica Altman, Smita Bhatia, Scott C. Borinstein, Joseph Flynn, Suzanne George, Robert Goldsby, Robert Hayashi, Mary S. Huang, Rebecca H. Johnson, Lynda Kwon Beaupin, Michael P. Link, Kevin C. Oeffinger, Kathleen M. Orr, Alberto S. Pappo, Damon Reed, Holly L. Spraker, Deborah A. Thomas, Margaret von Mehren, Daniel S. Wechsler, Kimberly F. Whelan, Bradley J. Zebrack, Hema Sundar and Dorothy A. Shead

colon cancer developing in the AYA population. 12 Familial adenomatous polyposis (FAP) is an autosomal dominant disease caused by germline mutations in the APC gene. This syndrome is associated with thousands of colonic polyps and with the development

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Rishi Jain, Michelle J. Savage, Andrea D. Forman, Reetu Mukherji and Michael J. Hall

adenomatous polyposis: more evidence for disease diversity and genetic heterogeneity . Gut 2001 ; 48 : 508 – 514 . 33. Groves CJ Saunders BP Spigelman AD Phillips RK . Duodenal cancer in patients with familial adenomatous polyposis (FAP