Gastric adenocarcinoma and dysplasia in fundic gland polyps of a patient with attenuated adenomatous polyposis coli

Zwick, Andrew; Munir, M; Ryan, CK; Gian, John; Burt, RW; Leppert, M.; Spirio, Lisa; Wy, Chey

doi:10.1053/gast.1997.v113.pm9247488

Cited by 160 publications

(78 citation statements)

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“…The progression of gastric adenoma to adenocarcinoma is known as by the adenoma-carcinoma sequence, and recently, the cases that progress from fundic gland polyp to gastric cancer have been reported. [7][8][9]18 Maybe, it is by the dysplasiacarcinoma pathway, Bianchi et al 19 reported the half of the fundic gland polyp in FAP patients showed dysplasia. In this study, one patient with fundic gland polyps had gastric adenocarcinoma in cardia after 15 years, but it is unclear that gastric adenocarcinoma was developed from fundic gland polyp because the surgical specimen is not available.…”

Section: Discussionmentioning

confidence: 99%

“…6 In general, gastric cancer arises from adenomatous polyps via the adenomacarcinoma sequence, but several recent reports have shown that gastric adenocarcinoma can be developed from fundic gland polyp in FAP patients. [7][8][9] In this study, we investigated the prevalence of gastric polyps and adenocarcinoma, the changing pattern through follow-up endoscopy and the precancerous possibility of gastric polyp in FAP patients. Also, we described the prevalence of duodenal polyps and adenocarcinoma, progression through follow-up endoscopy, and the factors related to the occurrence of duodenal neoplasm.…”

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Prevalence of Gastric and Duodenal Polyps and Risk Factors for Duodenal Neoplasm in Korean Patients with Familial Adenomatous Polyposis

Park¹,

Ryu²,

Park³

et al. 2011

Gut Liver

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Background/Aims: The prevalence of gastric polyps, duodenal adenoma and duodenal cancer has been reported as being high among familial adenomatous polyposis (FAP) patients, but there have been no reports of this association in Korea. This study evaluated the prevalence of gastric and duodenal polyps and risk factors for duodenal neoplasm in FAP patients in Korea. Methods: We reviewed both initial and follow-up endoscopic results from FAP patients. We also investigated the treatment modality of duodenal adenomas and analyzed the risk factors of duodenal neoplasms by logistic regression analysis. Results: A total of 148 patients with FAP underwent esophagogastroduodenoscopy (EGD), and the fi ndings were as follows: gastric polyp 39.9% (fundic gland polyp 25.7% and gastric adenoma 14.2%), duodenal adenoma 15.5%, gastric cancer 2.7%, and duodenal cancer 0.7%. There were two cases of gastric cancer that developed from benign gastric polyps. There were progressions of duodenal adenomatosis during follow-up, and some degree of relapse occurred after endoscopic resection. Patients with gastric polyps showed a correlation with the occurrence of duodenal neoplasm (odds ratio, 2.814; p=0.024). Conclusions: In Korean FAP patients, gastric cancer was detected more frequently, but fundic gland polyps, duodenal adenoma and duodenal cancer were detected less frequently than in Western patients. FAP patients with gastric polyps should undergo regular EGD, particularly for the early detection of duodenal neoplasia. (Gut Liver 2011;5:46-51) Key Words: Familial adenomatous polyposis; Duodenal cancer; Polyps; Adenomas; Gastric cancer INTRODUCTIONFamilial adenomatous polyposis (FAP) is characterized by the presence of at least one-hundred colorectal polyps and an earlyprogression to the colon cancer. Duodenum is the second most commonly affected site of polyp development in FAP patients. 1Duodenal polyps developed in FAP patients are adenomatous polyps, known as pre-cancerous lesions for duodenal adenocarcinoma.2 While prophylactic proctocolectomy has decreased the proportion of colorectal cancer as a cause of death in FAP patients, duodenal cancer has become a more important cause of death for these patients. 3,4 Therefore, endoscopic surveillance is important for the early detection of duodenal cancer and can improve the prognosis of FAP patients. 5The stomach is also known as a common site of polyps in FAP patients. Fundic gland polyps are the most prevalent gastric lesions, followed by adenomatous polyps. 6 In general, gastric cancer arises from adenomatous polyps via the adenomacarcinoma sequence, but several recent reports have shown that gastric adenocarcinoma can be developed from fundic gland polyp in FAP patients. [7][8][9] In this study, we investigated the prevalence of gastric polyps and adenocarcinoma, the changing pattern through follow-up endoscopy and the precancerous possibility of gastric polyp in FAP patients. Also, we described the prevalence of duodenal polyps and adenocarcinoma, progression through follow-up...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Prevalence of Gastric and Duodenal Polyps and Risk Factors for Duodenal Neoplasm in Korean Patients with Familial Adenomatous Polyposis

Park¹,

Ryu²,

Park³

et al. 2011

Gut Liver

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“…[9][10][11][12][13] These reports suggest that FAP-associated fundic gland polyp is a potential premalignant lesion, although malignant progression is quite rare.…”

Section: -3mentioning

confidence: 99%

High-grade dysplasia associated with fundic gland polyposis in a familial adenomatous polyposis patient, with special reference to APC mutation profiles

Sekine¹,

Shimoda²,

Nimura³

et al. 2004

Modern Pathology

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We report a patient with familial adenomatous polyposis who developed high-grade dysplasia against a background of fundic gland polyposis. Two large high-grade dysplasia lesions were found in the gastric body, where numerous fundic gland polyps were present. In both lesions, the dysplastic epithelium covered nonneoplastic oxyntic glands that occasionally exhibit cystic changes. A genetic analysis for APC (adenomatous polyposis coli) revealed a somatic 50-bp deletion involving codons 1502-1517 and 2-bp deletion at codon 1465 in each lesion of high-grade dysplasia. In contrast, six of the 18 fundic gland polyps were found to harbor an identical mutation: 1-bp insertion at codon 1556. Both lesions of high-grade dysplasia and the fundic gland polyps were similarly located in the fundic gland area and were caused by the inactivation of APC; however, their mutation profiles of APC were different. These results imply that fundic gland polyps and high-grade dysplasia of the stomach have distinct preferences for APC genotypes in their development. Modern Pathology (2004) 17, 1421-1426. doi:10.1038/modpathol.3800178Keywords: gastric dysplasia; familial adenomatous polyposis; APC Fundic gland polyp is the most common type of gastric polyp and has long been thought to be a hamartomatous lesion with no malignant potential. Fundic gland polyp occurs sporadically or in association with familial adenomatous polyposis (FAP). Fundic gland polyps are found in 26-43% of FAP patients, and tend to be more numerous in FAP-associated cases.1-3 FAP patients carry germline mutations of APC (adenomatous polyposis coli), and tumors associated with FAP develop through the biallelic inactivation of APC by germline and somatic mutations. Previous studies have revealed the presence of somatic APC mutations in FAPassociated fundic gland polyps, indicating that FAPassociated fundic gland polyps are a neoplastic lesion caused by the inactivation of both APC alleles, similar to the mechanism of other FAPassociated tumors. 4,5 FAP-associated fundic gland polyps have been reported to frequently develop dysplasia in their foveolar epithelium, whereas this rarely occurs in sporadic fundic gland polyps. 5,6 However, even in FAP-associated fundic gland polyps, the occurrence of adenocarcinoma or high-grade dysplasia is extremely rare. We present an FAP patient who developed two large high-grade dysplasia lesions against a background of fundic gland polyposis and report the results of a genetic analysis for APC mutations.

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“…Moreover, some case reports of development of gastric adenocarcinoma from FGPs in FAP patients have been reported in the literature. 7,8 It is against this background that the paper by Abraham et al really has shed new light on the pathology of syndromic FGPs. They have found the occurrence of somatic APC gene mutation in the FGPs of 12 of 17 FAP-AFAP patients.…”

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Are Syndromic Fundic Gland Polyps True Neoplasms?

Declich¹,

Porcellati²,

Bellone³

et al. 2001

The American Journal of Pathology

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We read with great interest the article by Abraham et al, 1 which recently appeared in your Journal. In their seminal article, the authors have elegantly demonstrated the frequent occurrence of somatic APC gene mutations in fundic gland polyps (FGPs) associated with familial adenomatous polyposis (FAP).FGPs were originally described in two different clinical settings. Sporadic FGPs are prevalent in middleaged women without any other pathological association. 2,3 On the other hand, FGPs with identical histology were described in association with FAP and attenuated variants (AFAP), 4,5 with both sexes equally affected at an earlier age.Both sporadic and syndromic FGPs were initially considered harmless, until Wu et al 6 demonstrated a high percentage of dysplastic change in syndromic FGPs compared to sporadic ones (20% versus 1%). Moreover, some case reports of development of gastric adenocarcinoma from FGPs in FAP patients have been reported in the literature. 7,8 It is against this background that the paper by Abraham et al really has shed new light on the pathology of syndromic FGPs. They have found the occurrence of somatic APC gene mutation in the FGPs of 12 of 17 FAP-AFAP patients. No somatic APC mutation of the normal control mucosa from each patient was demonstrated. Only 1 of 13 patients with sporadic FGPs showed an APC gene mutation.Moreover, the somatic APC gene mutations were not correlated with the development of dysplasia. Therefore, FGPs in FAP-AFAP patients represent a unique example of gastrointestinal polyps with somatic APC gene mutation without adenomatous morphology.We would like to comment on two points. The first one is related to the significance of the term "neoplastic." If we interpret neoplastic (benign or malignant) in a strict histological sense, we could not consider syndromic FGPs as neoplastic until the overt development of dysplasia (FGP plus adenomatous change). On the other hand, if one considers the term in a biological sense, we can agree with the authors that mutated yet histologically "benign" FGPs are neoplasms.The second point concerns the kind citation by Abraham et al of one of our papers. 9 We would like to point out that we reported only about the proliferative rate of a case series of sporadic FGPs, so our interpretation of FGPs as hyperplastic lesions was not by any means extended to syndromic polyps.In conclusion, we feel that the paper by Abraham et al 1 has really shed light on the understanding of the biology of these lesions: syndromic FGPs, histologically identical to sporadic ones, show somatic APC gene mutations. This finding not only may warrant close endoscopic surveillance of the upper GI tract in FAP patients, but in our opinion every new patient with FGPs should have a thorough clinicopathological study to exclude the possible association with FAP-AFAP.

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Gastric adenocarcinoma and dysplasia in fundic gland polyps of a patient with attenuated adenomatous polyposis coli

Cited by 160 publications

References 4 publications

Prevalence of Gastric and Duodenal Polyps and Risk Factors for Duodenal Neoplasm in Korean Patients with Familial Adenomatous Polyposis

Prevalence of Gastric and Duodenal Polyps and Risk Factors for Duodenal Neoplasm in Korean Patients with Familial Adenomatous Polyposis

High-grade dysplasia associated with fundic gland polyposis in a familial adenomatous polyposis patient, with special reference to APC mutation profiles

Are Syndromic Fundic Gland Polyps True Neoplasms?

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