Gastric Adenocarcinoma and Proximal Polyposis of the Stomach (GAPPS) (PDQ®): Genetics - Health Professional Information [NCI]

Introduction to Gastric Adenocarcinoma and Proximal Polyposis of the Stomach (GAPPS)

Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) is an autosomal dominant syndrome caused by germline pathogenic variants in promoter 1B of the APCgene.[1,2] Of note, large deletions involving promoter 1B of the APC gene are associated with a different syndrome called familial adenomatous polyposis (FAP).[3,4] GAPPS was first described in 2012.[2] This syndrome is characterized by numerous stomach polyps (predominantly fundic gland polyps in the body and fundus of the stomach, sparing the antrum), with regions of dysplasia.[2,5] GAPPS is not typically associated with colorectal polyposis. The risk of intestinal-type gastric adenocarcinoma appears to be significantly elevated in GAPPS, but the exact risk of this is currently unknown.

GAPPS and FAP are both caused by pathogenic or likely pathogenic variants in the APC gene, but they are distinct syndromes with different clinical characteristics. In GAPPS, polyposis and cancer risk are primarily confined to the stomach, while in FAP, polyposis and cancer risk are elevated in the colon. FAP is a hereditary cancer syndrome characterized by colorectal polyposis and a 93% risk of colorectal adenocarcinoma. Pathogenic or likely pathogenic variants in promoter 1B of the APC gene are pathognomonic of GAPPS and do not lead to FAP. In contrast, FAP is caused by germline pathogenic variants elsewhere in the APC gene or large deletions in promoter 1B. For more information about FAP, refer to the FAP section in Genetics of Colorectal Cancer.

Environmental risk factors have not been reported to cause or modify the penetrance of GAPPS. Although studies have speculated that there is an inverse relationship between gastric neoplasia and Helicobacter pylori infection, further research is warranted to clarify how H. pylori impacts gastric neoplasia in individuals with GAPPS.[6]

References:

1. Li J, Woods SL, Healey S, et al.: Point Mutations in Exon 1B of APC Reveal Gastric Adenocarcinoma and Proximal Polyposis of the Stomach as a Familial Adenomatous Polyposis Variant. Am J Hum Genet 98 (5): 830-842, 2016.
2. Worthley DL, Phillips KD, Wayte N, et al.: Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome. Gut 61 (5): 774-9, 2012.
3. Lin Y, Lin S, Baxter MD, et al.: Novel APC promoter and exon 1B deletion and allelic silencing in three mutation-negative classic familial adenomatous polyposis families. Genome Med 7 (1): 42, 2015.
4. Snow AK, Tuohy TM, Sargent NR, et al.: APC promoter 1B deletion in seven American families with familial adenomatous polyposis. Clin Genet 88 (4): 360-5, 2015.
5. Yanaru-Fujisawa R, Nakamura S, Moriyama T, et al.: Familial fundic gland polyposis with gastric cancer. Gut 61 (7): 1103-4, 2012.
6. Tacheci I, Repak R, Podhola M, et al.: Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) - A Helicobacter-opposite point. Best Pract Res Clin Gastroenterol 50-51: 101728, 2021.

Genetics of GAPPS

Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) is caused by germline pathogenic variants in promoter 1B (regulatory region) of the APCtumor suppressor gene.[1] Of note, large deletions involving promoter 1B result in a familial adenomatous polyposis (FAP) phenotype. For more information, see the FAP section in Genetics of Colorectal Cancer.[2,3]

The APCgene is located on chromosome 5q21 and encodes a 2,843–amino acid protein that is important for cell adhesion and signal transduction processes.[4,5] The APC protein regulates intracellular concentrations of beta-catenin, a major mediator of the Wnt signal transduction pathway.[6] For more information about the APC gene, see the Genetics of FAP section in Genetics of Colorectal Cancer.

A 2016 study identified that germline pathogenic variants in promoter 1B of the APC gene cause GAPPS.[1] The study included six families who all previously tested negative for germline pathogenic variants in APC. However, regulatory regions in APC, like promoter 1B, were not included in their original testing.[1,7]Whole genome sequencing was also performed in these families, and it failed to identify novel or rare genetic variants that cosegregated with GAPPS. After a loss of heterozygosity was identified in fundic gland polyps on chromosome 5 in a 46-Mb region containing the APC gene, the researchers pursued Sanger sequencing of the APC gene's promoter 1A and promoter 1B in family members affected with GAPPS.[1] Sanger sequencing identified several pathogenic variants in the promoter 1B region of APC, including APC c.-191T>C variants in four families with GAPPS, an APC c.-192A>G variant in one family with GAPPS, and an APC c.-195A>C variant in one family with GAPPS. These APC pathogenic variants reside within the Ying Yang 1 binding motif of promoter 1B, and hence, reduce transcriptional activity of APC. The study also reported that a second somatic hit in APC occurred in most fundic gland polyps in relatives with GAPPS, either via loss of the wild-type allele or acquisition of protein-truncating variants.

Since GAPPS was first described in the literature, over 20 families with the syndrome have been identified in Australia, North America, Europe, and Japan.[1,7,8,9,10,11,12] However, the population prevalence and geographic distribution of GAPPS is elusive. This phenomenon may be due to the following: 1) disparate access to diagnostic screening modalities that can identify gastric lesions, and 2) few laboratories offer sequencing analysis of APC's promoter 1B.[13,14]

References:

1. Li J, Woods SL, Healey S, et al.: Point Mutations in Exon 1B of APC Reveal Gastric Adenocarcinoma and Proximal Polyposis of the Stomach as a Familial Adenomatous Polyposis Variant. Am J Hum Genet 98 (5): 830-842, 2016.
2. Lin Y, Lin S, Baxter MD, et al.: Novel APC promoter and exon 1B deletion and allelic silencing in three mutation-negative classic familial adenomatous polyposis families. Genome Med 7 (1): 42, 2015.
3. Snow AK, Tuohy TM, Sargent NR, et al.: APC promoter 1B deletion in seven American families with familial adenomatous polyposis. Clin Genet 88 (4): 360-5, 2015.
4. Kinzler KW, Nilbert MC, Su LK, et al.: Identification of FAP locus genes from chromosome 5q21. Science 253 (5020): 661-5, 1991.
5. Nishisho I, Nakamura Y, Miyoshi Y, et al.: Mutations of chromosome 5q21 genes in FAP and colorectal cancer patients. Science 253 (5020): 665-9, 1991.
6. Rubinfeld B, Souza B, Albert I, et al.: Association of the APC gene product with beta-catenin. Science 262 (5140): 1731-4, 1993.
7. Worthley DL, Phillips KD, Wayte N, et al.: Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome. Gut 61 (5): 774-9, 2012.
8. Yanaru-Fujisawa R, Nakamura S, Moriyama T, et al.: Familial fundic gland polyposis with gastric cancer. Gut 61 (7): 1103-4, 2012.
9. Repak R, Kohoutova D, Podhola M, et al.: The first European family with gastric adenocarcinoma and proximal polyposis of the stomach: case report and review of the literature. Gastrointest Endosc 84 (4): 718-25, 2016.
10. Grossman A, Colavito J, Levine J, et al.: Filling in the "GAPPS": an unusual presentation of a child with gastric adenocarcinoma and proximal polyposis of the stomach. Gastric Cancer 25 (2): 468-472, 2022.
11. Foretová L, Navrátilová M, Svoboda M, et al.: GAPPS - Gastric Adenocarcinoma and Proximal Polyposis of the Stomach Syndrome in 8 Families Tested at Masaryk Memorial Cancer Institute - Prevention and Prophylactic Gastrectomies. Klin Onkol 32 (Supplementum2): 109-117, 2019.
12. Iwakawa Y, Yoshikawa K, Okamoto K, et al.: Four cases of gastric adenocarcinoma and proximal polyposis of the stomach treated by robotic total gastrectomy. Surg Case Rep 8 (1): 70, 2022.
13. Herrero R, Park JY, Forman D: The fight against gastric cancer - the IARC Working Group report. Best Pract Res Clin Gastroenterol 28 (6): 1107-14, 2014.
14. National Library of Medicine: Genetic Testing Registry. Bethesda, MD: National Library of Medicine. Available online. Last accessed February 23, 2024.

Genetic Testing for GAPPS

Consensus genetic testing guidelines specific to gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) do not yet exist. Proposed diagnostic criteria for GAPPS include a heterozygous germline APCpathogenic variant in promoter 1B and all of the following:[1,2]

• More than 100 proximal gastric polyps with antral sparing in the proband or more than 30 gastric polyps in an individual who has a first-degree relative with GAPPS.
• The proband's gastric polyps primarily have fundic gland pathology (some with dysplasia), or the proband has a family member with a history of dysplastic fundic gland polyps or gastric adenocarcinoma.
• Proband does not have a history of duodenal or colorectal polyposis.
• Gastric polyps and gastric adenocarcinoma in the family follow an autosomal dominant inheritance pattern.
• Other causes of gastric polyposis have been ruled out (i.e., other heritable gastric polyposis syndromes and the use of proton pump inhibitors).

However, GAPPS should be suspected in patients with 100 or more proximal gastric polyps with antral sparing, the absence of colorectal polyposis, and the presence of a germline pathogenic variant in the promoter 1B region of the APCgene. Individuals are at the greatest risk for GAPPS if they have a biological relative with clinical features of GAPPS and/or a known germline pathogenic variant in promoter 1B of the APC gene. Clinical-grade, diagnostic genetic testing for GAPPS is available at Clinical Laboratory Improvement Amendments (CLIA)-certified laboratories. Although many laboratories in the United States offer germline APC genetic testing, only a few perform sequence analysis of promoter 1B for the pathogenic variants that cause GAPPS.[3] Therefore, when patients have personal and/or family histories that are suggestive of GAPPS, APC genetic testing must be ordered from one of these laboratories.

Primary differential diagnoses for GAPPS include the following:

• Classic and attenuated familial adenomatous polyposis (FAP). In both classic and attenuated FAP, fundic gland polyps are observed in up to 89% of cases (fundic gland polyps carpet the stomach in 25% of cases).[4,5] The hallmark feature of both classic and attenuated FAP is colonic polyposis followed by duodenal polyposis. In GAPPS, affected individuals notably lack duodenal and colorectal polyposis. For more information, see the Familial Adenomatous Polyposis section in Genetics of Colorectal Cancer.
• MUTYH-associated polyposis (MAP). The gastric manifestations of MAP are attenuated when compared with those associated with FAP. However, more research on MAP-related gastric manifestations is necessary. For more information, see the MUTYH-Associated Polyposis section in Genetics of Colorectal Cancer.
• Proton pump inhibitor–induced gastric polyposis. Sporadic fundic gland polyps can be seen in 3% to 5% of patients in the general population who use proton pump inhibitors.[6,7,8] These polyps tend to be isolated, are less than 5 mm in size, and do not show signs of dysplasia. For more information, see the Introduction section in Genetics of Gastric Cancer.
• Hamartomatous polyposis syndromes. The hamartomatous polyposis syndromes include PTEN tumor hamartoma syndromes, juvenile polyposis syndrome, and Peutz-Jeghers syndrome. Patients with these syndromes can present with gastric polyposis (including fundic gland polyps), although pathology usually includes hamartomatous polyps as well. Furthermore, gastric polyposis occurs in the antrum —an area of the stomach that is spared in individuals with GAPPS.[1] For more information, see the PTEN hamartoma tumor syndromes (including Cowden syndrome), Peutz-Jeghers syndrome, and Juvenile polyposis syndrome sections in Genetics of Colorectal Cancer.

References:

1. Rudloff U: Gastric adenocarcinoma and proximal polyposis of the stomach: diagnosis and clinical perspectives. Clin Exp Gastroenterol 11: 447-459, 2018.
2. Worthley DL, Phillips KD, Wayte N, et al.: Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome. Gut 61 (5): 774-9, 2012.
3. National Library of Medicine: Genetic Testing Registry. Bethesda, MD: National Library of Medicine. Available online. Last accessed February 23, 2024.
4. Bianchi LK, Burke CA, Bennett AE, et al.: Fundic gland polyp dysplasia is common in familial adenomatous polyposis. Clin Gastroenterol Hepatol 6 (2): 180-5, 2008.
5. Mankaney G, Leone P, Cruise M, et al.: Gastric cancer in FAP: a concerning rise in incidence. Fam Cancer 16 (3): 371-376, 2017.
6. Torbenson M, Lee JH, Cruz-Correa M, et al.: Sporadic fundic gland polyposis: a clinical, histological, and molecular analysis. Mod Pathol 15 (7): 718-23, 2002.
7. Freeman HJ: Proton pump inhibitors and an emerging epidemic of gastric fundic gland polyposis. World J Gastroenterol 14 (9): 1318-20, 2008.
8. Huang CZ, Lai RX, Mai L, et al.: Relative risk factors associated with the development of fundic gland polyps. Eur J Gastroenterol Hepatol 26 (11): 1217-21, 2014.

Clinical Features of GAPPS

Gastric Manifestations in GAPPS

A key feature of gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) is extensive fundic gland polyposis in the proximal regions of the stomach with antral (distal) sparing. For more information, see the Gastric polyps section in Genetics of Gastric Cancer.[1] Since GAPPS is rare, literature on this syndrome primarily exists in the form of case reports and case series.[2,3,4,5,6] The incidence of gastric adenocarcinoma (intestinal or mixed types) in patients with GAPPS is 12% to 25% with age of diagnosis ranging from 23 years to 75 years.[5,6,7] Fundic gland polyposis (which precedes gastric adenocarcinoma) has occurred as early as 8 years in patients with GAPPS.[8] Gastric polyps range in size, with most polyps measuring less than 1 cm.[5,6,7] However, in GAPPS, gastric polyps can grow up to 4 cm in size. These polyps can be densely packed with extensive carpeting that covers the gastric mucosa without any visible normal mucosa. Most gastric polyps in GAPPS have fundic gland pathology with or without dysplasia. However, other pathologies are also seen, including hyperplastic polyps, adenomas, and hyperproliferative aberrant crypts. In a histological review of 25 patients, 15 patients had abnormal endoscopic biopsies.[6] Of these 15 individuals, 10 had hyperproliferative aberrant crypts, 10 had fundic gland polyps, 6 had gastric adenomas, 1 had an adenoma associated with gastric adenocarcinoma, and 1 had gastric adenocarcinoma. The penetrance of fundic gland polyposis and gastric adenocarcinoma can vary between different families and among family members with the same APCpathogenic variant. In a study of 24 Czech patients from 8 families (all had the same germline c.-191T>C APC promotor 1B variant), some developed gastric polyposis in their 20s while others had not yet developed polyposis at age 65 years.[5] Five individuals in this study developed gastric adenocarcinoma between the ages of 29 years and 64 years.

Colorectal Manifestations in GAPPS

Individuals with GAPPS may also have a propensity to develop colon polyps, although polyps are not thought to develop at an earlier age than those seen in the general population.[7,9] It has been postulated that APC's promoter 1A compensates for promoter 1B's dysfunction in the colonic mucosa, likely sparing the colorectum of polyposis. However, promoter 1A is methylated in the gastric mucosa, resulting in isolated gastric polyposis.[10] Nevertheless, GAPPS is caused by pathogenic variants in the same gene (APC) that causes familial adenomatous polyposis and can therefore, theoretically increase risk of colonic neoplasia.

Clinicopathologic evaluation of two families with GAPPS phenotypes (based on clinical criteria) demonstrated that seven of nine affected individuals had colon pathology.[9] In contrast, the six first-degree relatives (FDRs) in the study without GAPPS diagnoses had normal colonoscopies. In this study, the average age of individuals with GAPPS was 43.9 years (range, 20–71 y), whereas the average age of FDRs without GAPPS was 32.2 years (range, 18–51 y). In the GAPPS group, four of nine individuals had tubular adenomas in the colon, the youngest of whom was 48 years old. The colorectal polyps in individuals with GAPPS had increased beta-catenin, Ki67, and p53 expression. This expression pattern was also noted in the fundic gland polyps of these individuals, suggesting that GAPPS may be responsible. In the first paper that described GAPPS, 13 individuals with GAPPS underwent colonoscopy, in which six individuals (age, 18–37 y) did not have polyps, three individuals (age, 31–56 y) had tubular adenomas (including a 46-year-old individual who developed eight tubular adenomas over 4 years), and four individuals had hyperplastic polyps (one was located in the proximal colon, and the rest were located in the rectosigmoid colon).[7] Notably, none of the individuals had colonic polyposis. Colonoscopy findings were available for eight family members who did not have GAPPS. Three of these individuals (age, 55–77 y) had a single tubular adenoma with or without villous features. The other five individuals were less than 45 years old (age, 29–36 y) and had normal colonoscopies. In contrast to these studies, a report from eight French families with an APC pathogenic variant in promoter 1B revealed colonic polyposis in multiple members, which required colectomy.[10,11] When these data are taken together, it is unclear whether individuals with GAPPS develop colonic neoplasia any earlier than individuals in the general population. However, there appears to be a trend in which individuals with GAPPS develop more polyps than individuals in the general population.

References:

1. Huang CZ, Lai RX, Mai L, et al.: Relative risk factors associated with the development of fundic gland polyps. Eur J Gastroenterol Hepatol 26 (11): 1217-21, 2014.
2. Repak R, Kohoutova D, Podhola M, et al.: The first European family with gastric adenocarcinoma and proximal polyposis of the stomach: case report and review of the literature. Gastrointest Endosc 84 (4): 718-25, 2016.
3. Mitsui Y, Yokoyama R, Fujimoto S, et al.: First report of an Asian family with gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) revealed with the germline mutation of the APC exon 1B promoter region. Gastric Cancer 21 (6): 1058-1063, 2018.
4. Beer A, Streubel B, Asari R, et al.: Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) - a rare recently described gastric polyposis syndrome - report of a case. Z Gastroenterol 55 (11): 1131-1134, 2017.
5. Foretová L, Navrátilová M, Svoboda M, et al.: GAPPS - Gastric Adenocarcinoma and Proximal Polyposis of the Stomach Syndrome in 8 Families Tested at Masaryk Memorial Cancer Institute - Prevention and Prophylactic Gastrectomies. Klin Onkol 32 (Supplementum2): 109-117, 2019.
6. de Boer WB, Ee H, Kumarasinghe MP: Neoplastic Lesions of Gastric Adenocarcinoma and Proximal Polyposis Syndrome (GAPPS) Are Gastric Phenotype. Am J Surg Pathol 42 (1): 1-8, 2018.
7. Worthley DL, Phillips KD, Wayte N, et al.: Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome. Gut 61 (5): 774-9, 2012.
8. Grossman A, Colavito J, Levine J, et al.: Filling in the "GAPPS": an unusual presentation of a child with gastric adenocarcinoma and proximal polyposis of the stomach. Gastric Cancer 25 (2): 468-472, 2022.
9. McDuffie LA, Sabesan A, Allgäeuer M, et al.: β-Catenin activation in fundic gland polyps, gastric cancer and colonic polyps in families afflicted by 'gastric adenocarcinoma and proximal polyposis of the stomach' (GAPPS). J Clin Pathol 69 (9): 826-33, 2016.
10. Li J, Woods SL, Healey S, et al.: Point Mutations in Exon 1B of APC Reveal Gastric Adenocarcinoma and Proximal Polyposis of the Stomach as a Familial Adenomatous Polyposis Variant. Am J Hum Genet 98 (5): 830-842, 2016.
11. Lagarde A, Rouleau E, Ferrari A, et al.: Germline APC mutation spectrum derived from 863 genomic variations identified through a 15-year medical genetics service to French patients with FAP. J Med Genet 47 (10): 721-2, 2010.

Management for GAPPS

Consensus guidelines for management of gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) do not exist, given the rarity of this syndrome and the dearth of GAPPS literature (aside from case reports or case series). Furthermore, the incomplete penetrance of GAPPS and its large age range of polyposis onset/gastric adenocarcinoma incidence makes creating uniform management recommendations challenging. The literature frequently recommends that providers use an individualized management approach for patients with GAPPS, with frequent upper endoscopic surveillance and extensive sampling of gastric polyps.[1] The literature also suggests discussing gastrectomy planning early with a multidisciplinary team.

The goal of gastric endoscopic surveillance is to detect morphological or histological changes that increase risk for gastric adenocarcinoma. Generally, the detection of fundic gland dysplasia in GAPPS prompts heightened gastric cancer surveillance with more frequent endoscopic screening and discussions about risk-reducing gastrectomy with a multidisciplinary team. However, the natural progression in histology from fundic gland polyp to adenocarcinoma (including the precursor lesion to adenocarcinoma) is unknown. It has been hypothesized that hyperproliferative crypts found on pathology may be precursors to fundic gland polyps and adenomas in patients with GAPPS.[2] In addition to understanding the histological precursors of gastric adenocarcinoma, endoscopically identifying them is challenging, since they may easily be hidden or missed in the setting of dense polyp carpeting. For example, in a study, four members of a European family had GAPPS and developed gastric adenocarcinoma while under endoscopic surveillance.[3] In two of these individuals, gastric adenocarcinoma was identified in their gastrectomy specimens.

Given the variable penetrance of GAPPS, the correlation between gastric adenocarcinoma and clinical features (such as age, family history, degree of polyposis, and pathology of polyps) is unknown. However, given the high incidence of gastric adenocarcinoma seen in those with GAPPS (even when patients participate in gastric surveillance), discussion about risk-reducing gastrectomy with a multidisciplinary team may be warranted. Risk-reducing gastrectomy has been recommended when dysplasia is present.[1,4,5]

There are no consensus guidelines for colorectal surveillance in patients with GAPPS. Therefore, patients are managed based on their family histories of colorectal polyps/cancer with consideration of a baseline colonoscopy to exclude colonic polyposis.[6]

Level of evidence: 5

References:

1. Rudloff U: Gastric adenocarcinoma and proximal polyposis of the stomach: diagnosis and clinical perspectives. Clin Exp Gastroenterol 11: 447-459, 2018.
2. de Boer WB, Ee H, Kumarasinghe MP: Neoplastic Lesions of Gastric Adenocarcinoma and Proximal Polyposis Syndrome (GAPPS) Are Gastric Phenotype. Am J Surg Pathol 42 (1): 1-8, 2018.
3. Repak R, Kohoutova D, Podhola M, et al.: The first European family with gastric adenocarcinoma and proximal polyposis of the stomach: case report and review of the literature. Gastrointest Endosc 84 (4): 718-25, 2016.
4. Tacheci I, Repak R, Podhola M, et al.: Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) - A Helicobacter-opposite point. Best Pract Res Clin Gastroenterol 50-51: 101728, 2021.
5. Matsumoto C, Iwatsuki M, Iwagami S, et al.: Prophylactic laparoscopic total gastrectomy for gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): the first report in Asia. Gastric Cancer 25 (2): 473-478, 2022.
6. National Comprehensive Cancer Network: NCCN Clinical Practice Guidelines in Oncology: Genetic/Familial High-Risk Assessment: Colorectal. Version 2.2023 . Plymouth Meeting, PA: National Comprehensive Cancer Network, 2023. Available with free registration. Last accessed March 13, 2024.

Latest Updates to This Summary (04 / 10 / 2024)

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About This PDQ Summary

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the genetics of gastric adenocarcinoma and proximal polyposis of the stomach. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

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This summary is reviewed regularly and updated as necessary by the PDQ Cancer Genetics Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

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The lead reviewers for Gastric Adenocarcinoma and Proximal Polyposis of the Stomach (GAPPS) are:

• Grace-Ann O. Fasaye, ScM, CGC (National Cancer Institute)
• Gautam Mankaney, MD (Virginia Mason Franciscan Health)

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Last Revised: 2024-04-10