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The gastric adenoma or adenomatous polyp is largely considered a pre-malignant condition in the stomach. A complete surgical removal, either by endoscopic removal or laparascopic wedge resection, is recommended.


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Cyclooxygenase 2, p53, b-Catenin, and APC Protein Expression in Gastric Adenomatous Polyps.

Smith GV, Feakins R, Farthing MJ, Ballinger A.

Academic Department of Adult and Paediatric Gastroenterology, Barts and the London Queen Mary's University of London School, of Medicine and Dentistry, London, England.
Am J Clin Pathol. 2005 Mar;123(3):415-20. Abstract quote  

Gastric adenomatous polyps are rare findings in upper gastrointestinal endoscopy; however, they are associated strongly with malignant transformation. Few series describe the oncogenic characteristics of gastric adenomas.

In the present study, we immunohisto-chemically assessed the expression of cyclooxygenase (COX)-2, b-catenin, p53, and adenomatous polyposis coli (APC) in paraffin-embedded specimens of 14 gastric adenomas. Control samples of normal gastric tissue and gastric adenocarcinoma also were analyzed. Of the adenomas, 7 demonstrated overexpression of COX-2, and all demonstrated nuclear p53 accumulation. Accumulation of b-catenin in the nucleus and cytoplasm was detected in 38% (3/8) of specimens. Loss of APC staining was observed in 50% (4/8). Similar alterations in oncoprotein expression were seen in gastric cancers but not in normal control sections.

Gastric adenomas display alterations in the expression of COX-2, b-catenin, and APC similar to those seen in adenocarcinomas; however, accumulation of p53 was significantly more common in adenomas than in cancers.

Inverse relationship between APC gene mutation in gastric adenomas and development of adenocarcinoma.

Lee JH, Abraham SC, Kim HS, Nam JH, Choi C, Lee MC, Park CS, Juhng SW, Rashid A, Hamilton SR, Wu TT.

Department of Pathology, MD Anderson Cancer Center, Houston, Texas 77030, USA.

Am J Pathol 2002 Aug;161(2):611-8 Abstract quote

Gastric cancer is common among the world, but genetic mechanisms of gastric carcinogenesis are not well understood. Gastric polypoid adenomas and flat dysplasias are regarded as precursor lesions. However, a detailed molecular study of these lesions has not been done to determine their role as precancerous lesions.

We investigated mutations of the APC, beta-catenin, and K-ras genes, and microsatellite instability (MSI) status in 35 adenomas and 47 flat dysplasias without adenocarcinoma, 35 adenomas/dysplasias associated with adenocarcinomas, and 39 adenocarcinomas (20 diffuse type and 19 intestinal type). Somatic APC gene mutations were identified in 76% (59 of 78) of adenomas or flat dysplasias without associated adenocarcinoma, but in only 3% (1 of 30) of adenomas/dysplasias associated with adenocarcinoma, and in only 4% (3 of 69) of adenocarcinomas (P < 0.000001). No mutations of beta-catenin were found in adenocarcinomas, or adenomas/dysplasia without APC mutation. K-ras mutations were detected in 5% (4 of 82) of gastric adenomas/dysplasia without carcinoma, 3% (1 of 39) of adenocarcinomas without associated adenoma/dysplasia, and not in 32 adenocarcinomas with associated adenoma/dysplasia. High level of MSI (MSI-H) was more frequent in gastric adenoma/dysplasia associated with carcinoma (17%, 6 of 35) than in adenomas/dysplasia without carcinoma (3%, 2 of 75; P = 0.01). MSI-H was also more frequent in intestinal type adenocarcinoma (20%, 11 of 54) than in diffuse type (0%, 0 of 20; P = 0.03).

APC gene mutations were present in six of nine (67%) of gastric adenomas/dysplasias with low level of MSI, but in none of the eight adenomas/dysplasia with MSI-H phenotype (P = 0.009). Our results indicate that somatic mutation of the APC gene plays an important role in the pathogenesis of gastric adenoma and dysplasia but has a limited role in neoplastic progression to adenocarcinoma. Gastric adenomas or dysplasias without APC mutations but with or without MSI may have a different biological behavior, and are precursors of intestinal-type of gastric adenocarcinomas.


Genetic alterations in gastric adenomas of intestinal and foveolar phenotypes.

Abraham SC, Park SJ, Lee JH, Mugartegui L, Wu TT.

Department of Pathology, Mayo Clinic, Rochester, MN 55905, USA

Mod Pathol. 2003 Aug;16(8):786-95. Abstract quote

Gastric adenomas are unusual neoplasms that can constitute one of the direct precursors to gastric adenocarcinoma. Most gastric adenomas are comprised of polypoid projections of dysplastic epithelium with at least focal intestinal-type differentiation (containing goblet cells and/or Paneth cells), whereas adenomas comprised entirely of dysplastic foveolar-type epithelium are rare. It has been shown that nearly all intestinal-type adenomas arise in association with background intestinal metaplasia and gastric atrophy, approximately 40% harbor high-grade dysplasia, and nearly one fourth progress to adenocarcinoma. In contrast, foveolar-type adenomas tend to occur in otherwise normal, nonatrophic gastric mucosa and rarely harbor high-grade dysplasia or carcinoma. Potential differences in the genetic alterations between intestinal-type and foveolar-type gastric adenomas have not been systematically studied.

We investigated 11 intestinal-type and 7 foveolar-type gastric adenomas (all from patients without familial adenomatous polyposis) for alterations in APC (using 5q allelic loss assays and direct DNA sequencing of the mutation cluster region), beta-catenin (using direct DNA sequencing of the phosphorylation region in exon 3), K-ras (using direct DNA sequencing of codons 12 and 13), and microsatellite instability (MSI; using fluorescent-based PCR amplification of a standard panel of 5 microsatellite markers). Overall, 10 of 11 (91%) intestinal-type adenomas harbored at least one detectable genetic alteration, whereas only 3 of 7 (43%) of foveolar-type adenomas did (P =.047). However, no statistically significant differences in any particular genetic alteration were found. Among intestinal-type adenomas, APC alterations were present in seven (64%), high-level MSI in three (27%), and K-ras mutations in two (18%). Among foveolar-type adenomas, APC alterations were present in three (43%) and a K-ras mutation in one of six amplifiable polyps (17%). Neither APC nor MSI correlated with the size of the adenoma, but K-ras mutations were found only in lesions of > or = 1 cm. beta-catenin mutations were not present in any gastric adenoma, irrespective of the presence or absence of APC alterations.

These results suggest that the types and frequencies of genetic alterations occurring in gastric and colorectal adenomas are similar. Although intestinal-type and foveolar-type gastric adenomas display divergent biologic behavior, the specific genetic events accounting for these differences in morphology and biologic behavior are unclear.

Allelotype of the adenoma-carcinoma sequence of the stomach.

Kim HS, Woo DK, Bae SI, Kim YI, Kim WH.

Department of Pathology, Seoul National University College of Medicine, Korea.

Cancer Detect Prev 2001;25(3):237-44 Abstract quote

In order to identify the significant allelic loss involving the gastric adenoma-carcinoma sequence, we used 49 genome-wide microsatellite markers in an allelotype study of 30 cases of stomach resections that harbored both adenomas and carcinomas.

Frequent loss of heterozygosity was demonstrated on 12q (53.3%), 2p (50.0%), and 18p (50.0%) in adenomas and on 8q (80.0%), 2p (70.0%), 18p (66.7%), and 17p (61.9%) in carcinomas. Significant difference in the loss of heterozygosity rate between the adenoma and the carcinoma was noted on 17p.

Our results suggested that the critical target of loss of heterozygosity in gastric adenomacarcinoma sequences may be the p53 gene on 17p.


Features of gastritis predisposing to gastric adenoma and early gastric cancer.

Meining A, Riedl B, Stolte M.

Medical Department, University of Munich, 0-80336 Munich, Germany Department of Pathology, Klinikum Bayreuth, D-95445 Bayreuth, Germany Department of Pathology, Klinikum Bayreuth.

J Clin Pathol 2002 Oct;55(10):770-3 Abstract quote

Background/Aims: Helicobacter pylori gastritis is a risk factor for the development of gastric cancer. The results of several studies indicate that gastric adenomas, which are considered premalignant lesions, may also be associated with H pylori gastritis. However, it is not clear whether there are different patterns of gastritis in these patients compared with patients with gastric cancer or patients with H pylori gastritis alone. Therefore, this study was designed to investigate the patterns of gastritis in these three groups of patients.

METHODS: The histological features of gastric mucosa at a distance from the tumour were analysed prospectively in 118 patients with gastric adenoma (mean age, 71.8; female to male ratio, 6 : 4). In addition, for every patient with H pylori associated gastric adenoma an age and sex matched control patient with either H pylori associated early gastric cancer of the intestinal type or H pylori gastritis only was investigated.

RESULTS: Only 60 patients (50.9%) with gastric adenoma were infected with H pylori. In the remaining patients, complete atrophic gastritis predominated. In those patients with adenoma and H pylori infection, the gastritis was similar to that seen in patients with early gastric cancer (median score, 2 for activity and degree of gastritis in the antrum and corpus); intestinal metaplasia was common to both groups. These two groups differed significantly from patients with H pylori gastritis only (median grade and activity of gastritis, 1 in antrum and corpus), in whom intestinal metaplasia was rare.

CONCLUSIONS: It appears that gastric adenomas and gastric intestinal cancer arise by analogous mechanisms. However, owing to severe atrophic gastritis and a lower incidence of H pylori, adenomas do not appear to be definite precursor lesions for gastric cancer.


Clinical usefulness of microsatellite instability for the prediction of gastric adenoma or adenocarcinoma in patients with chronic gastritis.

Kashiwagi K, Watanabe M, Ezaki T, Kanai T, Ishii H, Mukai M, Hibi T.

Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.

Br J Cancer 2000 Jun;82(11):1814-8 Abstract quote

To assess a role of microsatellite instability (MSI) in the development of gastric adenocarcinoma or adenoma from chronic gastritis, we analysed mutations of five microsatellite loci in gastritis, adenoma and adenocarcinoma retrospectively. Gastric mucosa was biopsied from the same area in each patient at different periods and examined for MSI. Only one of 55 patients with chronic gastritis revealed MSI-H phenotype and the other 54 patients showed microsatellite stable (MSS) phenotypes.

In six of 17 patients with gastric adenoma or well-differentiated adenocarcinoma, MSI-positive phenotypes were demonstrated. Interestingly, all of six patients showing MSI, including three high-level MSI (MSI-H) cases and three low-level (MSH-L) cases, had already revealed MSI at the stage of chronic gastritis. In two of three MSI-H cases, the identical MSI patterns had been observed at the stage of gastritis 1.5-7 years before the final diagnosis of adenocarcinoma. The adjacent gastritis mucosa within 10 mm from the carcinoma demonstrated MSI as well. MSI was not found in any of 35 patients with Helicobacter pylori infection, but found in one of 30 patients without infection. Moreover, two of three cases of gastric adenoma or well-differentiated adenocarcinoma with MSI-H at the stage of chronic gastritis showed no evidence of Helicobacter pylori infection throughout the observation periods.

These results indicate that MSI in biopsy specimens at the stage of chronic gastritis may predict the risk of the progression to adenoma and well-differentiated adenocarcinoma, and that Helicobacter pylori infection itself may not induce MSI directly in the gastric mucosa.






Protruding and non-protruding adenomas of the stomach.

Rubio CA, Kato Y, Jonasson JG.

Department of Pathology, Karolinska Institute, Stockholm, Sweden

Anticancer Res 2001 Jul-Aug;21(4B):3037-40 Abstract quote

Sixty-seven gastric adenomas found at gastrectomy in two ethnic groups (53 in Japanese and 14 in Icelandic patients) were investigated. Micrometric measurements were carried out on tissue sections. Adenomas being not higher than twice the measured height of the non-dysplastic adjacent gastric mucosa were regarded as non-protruding (n = 40) and those surpassing that limit as protruding (n=27).

Measurements showed that 59.7% (n=40) of the 67 adenomas were non-protruding. The mean width in protruding adenomas (11.6 mm) surpassed the mean width of non- protruding adenomas (7.1 mm), suggesting that non-protruding adenomas may evolve into protruding forms. On the other hand, 13.6% (3 out of 22) of the protruding adenomas in Japanese patients were very small (< or = 5mm in width), implying that some small gastric adenomas grow from the outset in a protruding fashion. Conversely, 22.5% (n =9) of the 40 non-protruding adenomas measured 10 to 25 mm in width, suggesting that a proportion of the larger gastric adenomas may grow in a non-protruding, horizontal fashion without "becoming" protruding.

Thus, similarly to colorectal adenomas, gastric adenomas may be classified into protruding and non-protruding. Micrometric measurements permit the correct assessment of the type of adenoma.



Diagnostic accuracy of forceps biopsy versus polypectomy for gastric polyps: a prospective multicentre study.

Muehldorfer SM, Stolte M, Martus P, Hahn EG, Ell C; Multicenter Study Group "Gastric Polyps".

Department of Medicine I, University of Erlangen-Nuremberg, Germany.


Gut 2002 Apr;50(4):465-70 Abstract quote

AIMS: To determine whether an adequate histological diagnosis of gastric polyps can be attained on the basis of forceps biopsy.

PATIENTS AND METHODS: In a prospective multicentre study, 194 patients with 222 endoscopically removable gastric polyps (>or=5 mm) underwent forceps biopsy and complete polypectomy. Patients with fundic gland polyps and polyposis syndrome were not included. Specimens were evaluated by primary and reference pathologists, and the complication rate of gastric polypectomy was also determined.

RESULTS: Of the 222 polyps, histological examination of the polypectomy specimens revealed tumour-like lesions in 77% (10% focal foveolar hyperplasia, 59% hyperplastic polyps, 4% inflammatory fibroid polyps, 4% other polyps) and neoplasia in 19% (10% tubular adenoma, 2% tubulovillous adenoma, 1% high grade intraepithelial neoplasia, 6% adenocarcinoma). When biopsy results were compared, complete agreement was found in 124 cases (55.8%) and, in an additional 77 cases (34.7%), the clinically important differentiation between tumour-like lesions and neoplasia was possible. However, relevant differences were found by the reference pathologist in six cases (2.7%), the most common reason being failure of biopsy to reveal foci of carcinoma in hyperplastic polyps. Bleeding was observed after polypectomy in 16 patients (7.2%), in 15 of whom it was managed conservatively.

CONCLUSIONS: We recommend complete removal by an experienced endoscopist of all epithelial gastric polyps larger than 5 mm after thorough individualised risk-benefit analysis.


Serrated neoplasia of the stomach: a new entity.

Rubio CA.

Gastrointestinal and Liver Pathology Research Laboratory, Karolinska Institute and Hospital, 171 76 Stockholm, Sweden.

J Clin Pathol 2001 Nov;54(11):849-53 Abstract quote

AIM: Despite the fact that gastric carcinoma continues to be one of the most common cancers world wide, only dysplasia in flat mucosa and adenomas have been shown to evolve into invasive carcinoma. The aim of this paper is to report a novel histological phenotype of gastric adenoma with early invasive growth.

MATERIAL AND RESULTS: The patient presented with gastric complaints. A barium examination revealed an ulcerated tumour in the corpus, apparently infiltrating the gastric wall. The endoscopic examination showed a pediculated protruding tumour in the greater curvature. Punch biopsies were reported as invasive adenocarcinoma. Because of the poor condition of the patient, a partial gastrectomy was performed. The histological examination revealed elongated fronds with lateral crenated, saw tooth-like notches as a result of scalloped epithelial indentations. Areas with high grade dysplasia, with carcinoma in situ, and invasive carcinoma at the tip of the adenoma were demonstrated. The pedicle of the protruding neoplasia "emerged" from a non-protruding serrated adenoma.

CONCLUSIONS: The protruding serrated neoplasia had apparently evolved from a non-protruding serrated gastric adenoma. This appears to be the first case of gastric serrated neoplasia in the literature.


Gastric adenomas: intestinal-type and gastric-type adenomas differ in the risk of adenocarcinoma and presence of background mucosal pathology.

Abraham SC, Montgomery EA, Singh VK, Yardley JH, Wu TT.


Am J Surg Pathol 2002 Oct;26(10):1276-85 Abstract quote

Gastric adenomas are neoplastic growths characterized by localized, polypoid proliferations of dysplastic epithelium. They frequently arise in stomachs with a background of mucosal atrophy and intestinal metaplasia, and a higher risk of adenocarcinoma elsewhere in the stomach has been reported in patients with gastric adenomas. Additionally, some gastric adenomas themselves demonstrate neoplastic progression to infiltrating adenocarcinoma. However, previous studies have not comprehensively evaluated the background gastric mucosa and risk of adenocarcinoma, particularly in relation to the histologic classification of adenomas as either intestinal-type or gastric-type.

We studied 61 gastric adenomas from 51 patients between 1985 and 2001. The adenomas were classified as intestinal-type (containing at least focal goblet cells and/or Paneth cells), gastric-type (lined entirely by gastric mucin cells on PAS/alcian blue stain), or indeterminate. We evaluated the histologic features of both the adenomas (location, multiplicity, degree of dysplasia, presence of adenocarcinoma within the polyp) and the surrounding gastric mucosa (presence of gastritis, intestinal metaplasia, and adenocarcinoma).

Gastric adenomas were distributed equally throughout the stomach, were most frequently solitary (82%), and contained adenocarcinoma in nine cases (14.8%). There were 34 intestinal-type adenomas (56%) in 31 patients, 25 gastric-type adenomas (41%) in 18 patients (including 10 patients with familial adenomatous polyposis), and 2 of indeterminate type (3%). Intestinal-type adenomas were significantly more likely than gastric-type adenomas to show high-grade dysplasia (p <0.0001), adenocarcinoma within the polyp (p = 0.016), intestinal metaplasia in the surrounding stomach (p <0.000001), and gastritis (p = 0.002). Patients with intestinal-type adenomas were also more likely to have separate adenocarcinomas (five cases vs 0 cases), although this did not reach statistical significance.

Gastric adenomas are rarely truly "sporadic" lesions. In any individual patient complete removal of the adenoma should be performed, and thorough biopsy of the surrounding gastric mucosa is essential to understand the clinicopathologic context of the adenoma.


Risk factors suggesting malignant transformation of gastric adenoma: univariate and multivariate analysis.

Park DI, Rhee PL, Kim JE, Hyun JG, Kim YH, Son HJ, Kim JJ, Paik SW, Rhee JC, Choi KW, Oh YL.

Division of Gastroenterology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.

Endoscopy 2001 Jun;33(6):501-6 Abstract quote

BACKGROUND AND STUDY AIMS: Since gastric adenomas are precancerous lesions, polypectomy is necessary. However, there have been no reports suggesting factors capable of predicting malignant transformation of gastric adenomas removed by endoscopic snare polypectomy (ESP) or endoscopic mucosal resection (EMR) in Korea, a country in which gastric cancer is a major problem. The aim of this paper was to elucidate the risk factors suggesting malignant transformation of gastric adenomas removed by ESP or EMR at our center.

PATIENTS AND METHODS: Between November 1994 and June 1999, 118 gastric adenomas diagnosed on the basis of endoscopy and histological examinations of the forceps biopsy specimens obtained were treated by ESP or EMR at our department. Factors capable of predicting malignancy were searched for in the endoscopy reports, still photographs, and histopathological findings.

RESULTS: Eight of the 118 adenomas ultimately proved to have malignant foci. In the univariate analysis, four of the variables studied--location, histological type, surface redness, and degree of dysplasia--had a statistically significant relationship with malignant transformation. In the multivariate analysis, only the degree of dysplasia had a statistically significant relationship with malignant transformation.

CONCLUSIONS: These results suggest that a diagnosis of high-grade dysplasia in forceps biopsy material should be considered an absolute indication for ESP or EMR.


Laparoscopic wedge resection for benign gastric tumors.

Rothlin M, Schob O.

Department of Surgery, Klinik fur Viszeralchirurgie, Universitatsspital, Ramistrasse 100, CH-8091 Zurich, Switzerland.

Surg Endosc 2001 Aug;15(8):893-5 Abstract quote

BACKGROUND: Both laparoscopic wedge resection and formal laparoscopic resection are used in the treatment of benign and malignant gastric diseases.

METHODS: We performed totally laparoscopic wedge resection using stapling devices and three or four trocars. Patients: Four patients were treated with this technique. All four suffered from gastrointestinal stromal tumors (GIST), and one presented with an additional gastric adenoma. Two were morbidly obese, and two had additional operations performed at the same time. Two patients were admitted for acute upper GI bleeding.

RESULTS: All of the tumors were removed successfully. Operating time ranged from 135 to 215 min. Oral feeding commenced on days 2-4. Postoperative hospital stay ranged from 5 to 11 days.

CONCLUSION: Laparoscopic wedge resection of benign gastric tumors is a safe, reliable method that should be further investigated and used on a broader scale.

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Last Updated March 15, 2005

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