Gastric Polyposis and Cancer in Western Patients With Familial Adenomatous Polyposis: Epidemiology, Detection, and Management.

Gregory E Idos, Sonia S Kupfer, Evelien Dekker, William M Grady, Jennifer M Weiss, Arnold J Markowitz, Matthew B Yurgelun, Carol A Burke, N Jewel Samadder, Arthur S Aelvoet, Michael W Cruise, Kaitlyn Kelly, AnnMarie Kieber-Emmons

Journal: Journal of the National Comprehensive Cancer Network : JNCCN 2025;23(6):

PMID: 40499589

Full Text on Sheridan PubFactory View on PubMed

Abstract

Patients with familial adenomatous polyposis (FAP) are at increased risk of developing cancer, with the most common sites being colorectal, duodenal/ampullary and thyroid. In the last decade, an alarming increase in gastric cancer has been reported in the Western FAP population. These cancers are often diagnosed at an advanced stage with poor prognosis, even in patients undergoing regular upper endoscopic surveillance. Most gastric cancers in Western patients with FAP occur in the proximal stomach, where a carpeting of fundic gland polyposis hampers visualization of gastric cancer and its precursor lesions during endoscopic surveillance. Although fundic gland polyps are the most prevalent proximal polyp, several different dysplastic lesions can be found in the stomachs of patients with FAP. including fundic gland polyps with dysplasia, foveolar-type adenomas, pyloric gland adenomas, and intestinal-type adenomas. Although adenomas are the most likely precursors to gastric cancer, the exact lesions responsible for gastric cancer in FAP are not yet fully understood. This review focuses on gastric polyposis and the characteristics of gastric cancer in Western patients with FAP, including risk factors, lesion detection, surveillance and management of gastric polyposis, and areas for future research.

Address: 1Department of Gastroenterology and Hepatology, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.; 2Cancer Center Amsterdam, Amsterdam, the Netherlands.; 3Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, the Netherlands.; 4Department of Pathology and Laboratory Medicine, Cleveland Clinic, Cleveland, OH.; 5Sanford R. Weiss, MD Center for Hereditary Colorectal Neoplasia, Cleveland Clinic, Cleveland, OH.; 6Translational Science and Therapeutics Division, Fred Hutchinson Cancer Center, Seattle, WA.; 7Division of Gastroenterology, University of Washington School of Medicine, Seattle, WA.; 8Division of Gastroenterology, City of Hope National Medical Center, Duarte, CA.; 9Division of Clinical Cancer Genomics, City of Hope National Medical Center, Duarte, CA.; 10Department of Surgery, University of Wisconsin-Madison, Madison, WI.; 11Division of Gastroenterology, Duke University, Durham, NC.; 12Section of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Chicago, Chicago, IL.; 13Gastroenterology, Hepatology and Nutrition Service, Memorial Sloan Kettering Cancer Center, New York, NY.; 14Mayo Clinic Comprehensive Cancer Center, Phoenix, AZ.; 15Division of Gastroenterology and Hepatology, Mayo Clinic Arizona, Phoenix, AZ.; 16Department of Gastroenterology and Hepatology, University of Wisconsin School of Medicine and Public Health, Madison, WI.; 17University of Wisconsin Carbone Cancer Center, Madison, WI.; 18Dana-Farber Cancer Institute, Brigham & Women's Hospital, Boston, MA.; 5Sanford R. Weiss, MD Center for Hereditary Colorectal Neoplasia, Cleveland Clinic, Cleveland, OH.; 18Harvard Medical School, Boston, MA.

DOI: 10.6004/jnccn.2025.7027

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https://medlineplus.gov/stomachcancer.html

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Full Text Sources:

https://jnccn.org/doi/10.6004/jnccn.2025.7027

MeSH Terms: Humans, Adenomatous Polyposis Coli, Stomach Neoplasms, Risk Factors, Disease Management, Adenomatous Polyps