Hyperplastic polyps, adenomatous polyps, and mixed hyperplastic adenomatous polyps of the colon: definitions.
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Adenoma↗
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A truncated poisson regression model with applications to occurrence of adenomatous polyps.
Adenomatous polyps are considered as the dominant precursor lesion of colorectal cancer. A phase III colorectal cancer prevention trial, conducted by the Arizona Cancer Center, concerns the ability of wheat bran fibre supplement to reduce the recurrence of adenomatous polyps. All participants in the study are to have had colorectal polyps detected and removed during a baseline (qualifying) colonoscopy within three months prior to enrolment. In this paper, our interest focuses on occurrence of adenomatous polyps at the baseline colonoscopy. We use a truncated Poisson model to fit these types of data. We develop a regression model to assess the effects of explanatory factors on the positive counting variable. We fit truncated Poisson parameters by a log-linear regression model and estimate regression parameters by the maximum likelihood procedure. Finally, we apply it to the baseline colonoscopy data from the Wheat Bran Fiber study.
Adenomatous Polyps↗
Gastrointestinal adenomatous polyps.
Adenomatous polyps of the gastrointestinal tract are dysplastic precursor lesions of adenocarcinoma. The features of an adenoma that are associated with a greater tendency to progress to carcinoma include larger polyp size, high grade dysplasia, and increased villous glandular architecture. Alterations in particular oncogenes and tumor-suppressor genes have been correlated with various stages of colonic adenoma formation, thereby facilitating our knowledge of adenoma pathogenesis. Heredity and environment contribute to the risk of developing adenomatous polyps of the colon. The incidence of colorectal cancer can be decreased by the endoscopic removal of adenomas, thereby providing good rationale for screening and surveillance programs.
Adenoma↗
Metastatic melanomatous colonic polyps simulating adenomatous polyps.
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Aged↗
Differential activation of ornithine decarboxylase and tyrosine kinase in the rectal mucosa of patients with hyperplastic and adenomatous polyps.
Hyperplastic polyps are considered to be benign colonic lesions with almost no potential for malignant transformation. Recent reports have shown an increased association of hyperplastic polyps with adenomatous polyps and have advocated a full colonoscopy in patients who harbor hyperplastic polyps. Hyperproliferative mucosa is known to be associated with adenomatous polyps, but its relationship to hyperplastic polyps is unknown. In the present pilot study, it is determined whether a change in mucosal proliferative patterns is observed in patients who harbor only hyperplastic polyps or a history of hyperplastic polyps relative to those who harbor both hyperplastic polyps and adenomatous polyps by measuring ornithine decarboxylase and tyrosine kinase activity in macroscopically normal rectal mucosa. Fifteen patients had either adenomatous polyps proximally or harbored adenomatous polyps and hyperplastic polyps. Seven patients had hyperplastic polyps and 15 patients had a prior history of hyperplastic polyps with no polyps found during the current examination. The ornithine decarboxylase activity of the rectal mucosa with proximal adenomatous polyps or both polyp types was significantly higher than that of hyperplastic polyps, the history of hyperplastic polyps, or controls, and values for hyperplastic polyps and the history of hyperplastic polyps were similar to controls. On the other hand, tyrosine kinase activity in the rectal mucosa of patients with both or either polyp type was elevated without any significant difference between hyperplastic and adenomatous polyps. Thus, it is concluded that although increased ornithine decarboxylase activity in rectal mucosa suggests the presence of adenomatous polyps or a combination of adenomatous with hyperplastic polyps, increased tyrosine kinase activity suggests the presence of any type of polyp.
Colonic Polyps↗
Microsatellite instability in hyperplastic and adenomatous polyps of the stomach.
BACKGROUND: Few studies have focused on the presence and significance of microsatellite instability (MSI) in gastric polyps, and the results on record are conflicting. The aim of the current study was to address this issue, taking into consideration the 2 main types of gastric polyps, the coexistence of foci of malignant transformation, and the expression of p53 and ERBB-2. METHODS: Six hyperplastic polyps, 10 adenomatous polyps, and 4 adenomatous polyps displaying foci of malignant transformation (intestinal-type carcinoma) were studied for MSI. The authors analyzed a mononucleotide repeat microsatellite (BAT-26) and 5 dinucleotide repeats in microdissected formalin fixed, paraffin embedded tissue sections that were representative of the lesions. Expression of p53 and ERBB-2 were evaluated by immunohistochemistry. RESULTS: BAT-26 positivity was detected in 1 of 6 hyperplastic polyps (16.7%) and in 2 of 10 adenomas (20%) without malignant transformation. In the 4 adenomatous polyps with carcinomatous foci, BAT-26 positivity was detected in 2 cases (50%) in both (adenomatous and carcinomatous) components of the lesions. p53 immunoreactivity was observed in 6 adenomatous polyps, 2 of them with malignant transformation. Overexpression of the ERBB-2 protein was detected in 1 adenomatous polyp with malignant transformation. CONCLUSIONS: Replication error (RER+) phenotype occurs in both hyperplastic and adenomatous polyps of the stomach. The highest frequency is observed in adenomatous polyps with carcinomatous foci, suggesting that MSI may play a role in the process of malignant transformation in this setting. No significant association was observed between RER+ phenotype and overexpression of p53 or ERBB-2 proteins.
Adenomatous Polyps↗
Colorectal polyps in autopsy material. Part I. Adenomatous polyps.
In prospective studies specimens of the large bowel were obtained from 733 autopsy cases. After fixing they were examined under illuminated magnifying lens and all polypous lesions were excised for histological analysis and classified according to Correa's criteria (8). Adenomatous polyps were found in 280 cases (38.2%) and their prevalence increased with age in both sexes. Adenomatous polyps, also multiple were found most frequently in the transverse colon, and then ascending colon, sigmoid, descending colon and rectum. The mean number of adenomatous polyps per positive specimen was 2.33 for men and 2.60 for women. In 6.8% their diameter was > or = 10 mm. The prevalence of polyps with severe degree of dysplasia (III degree) increased from proximal to distal segments of the colon in both sexes and their prevalence is significantly higher in the ascending colon in women. In the whole series there were 6 adenocarcinomas of 5-18 mm in size, all in women over 80 years of age. The results of the present study were compared with the data concerning other populations of the world. In the light of a repeatedly confirmed a generally accepted relationship between adenoma and adenocarcinoma of the large intestine the results of our study seem to underestimate the prevalence of colon adenocarcinoma in the population of Cracow and Cracow district.
Adenocarcinoma↗
Gastric polyposis due to multiple hyperplastic adenomatous polyps.
Four cases of gastric polyposis in which the multiple polyps were hyperplastic adenomatous polyps are presented with endoscopic and histologic description. The multiple hyperplastic adenomatous polyps in our cases showed more diffuse involvement of specific regions of the stomach than is usual with papillary adenomatous polyps. Hyperplastic adenomatous polyps have a low potential for malignancy, and it is suggested that they may be followed by periodic observation rather than fulguration or removal.
Adenoma↗
Mixed hyperplastic adenomatous polyps--an underdiagnosed entity. Report of a case of adenocarcinoma arising within a mixed hyperplastic adenomatous polyp.
We report a case of colonic adenocarcinoma arising within a polyp with mixed morphology of a hyperplastic polyp and tubular adenoma. Despite the relatively small size of the polyp, two isolated foci of adenocarcinoma in situ were present and tumor islands invaded the submucosa. Isolated areas, morphologically resembling hyperplastic glands, and varying degrees of atypia. Though rare, some hyperplastic polyps may be precursors of adenomas.
Adenocarcinoma↗
Cigarettes, alcohol, coffee, and caffeine as risk factors for colorectal adenomatous polyps.
The possible association of colorectal adenomatous polyps, a precursor lesion for colorectal cancer, with cigarette smoking, alcohol consumption, and coffee and caffeine consumption was investigated in a case-control study. Between April 1986 and March 1988, 271 cases of patients with pathologically confirmed incident colorectal adenomatous polyps and 457 control subjects were collected from three colonoscopy practices in New York City. Information on exposure was obtained by structured interviews. After adjustment of age, statistically significant odds ratios (highest-lowest quartile) were found for cigarette smoking in males (2.2; 95% confidence interval (CI), 1.2 to 3.8) and coffee consumption in females (2.0%; 95% CI, 1.0 to 3.9). No significant associations were obtained for cigarette smoking in females, for coffee consumption in males, or for alcohol or caffeine consumption. After adjustments for alcohol, coffee, and caffeine consumption, the association of adenomas with cigarette smoking remained in males and significant associations were also observed in subcategory analysis for both left-side and right-side adenomatous polyps. Adjustment for cigarette smoking eliminated the association between colorectal adenomatous polyps and coffee consumption in females. Cigarette smoking appears to be a significant risk factor for colorectal adenomatous polyps in males.
Adenomatous Polyps↗
Histochemical and morphological analysis of colonic epithelium from children with Gardner's syndrome and adults bearing adenomatous polyps.
Normal and adenomatous colonic tissues from children with Gardner's syndrome were compared to analogous tissues from adults bearing adenomatous polyps using mucin histochemical and lectin-binding techniques. Adenomatous tissue from children exhibited general morphological similarity to its adult homologue, but showed less dysplasia. Its goblet cells stained weaker for mucins and the lectins Dolichos biflorus agglutinin (DBA) and peanut agglutinin (PNA). This suggested underglycosylation of side chains of mucins in these childhood adenomas. The weak DBA and relatively intense sulfomucin staining in these adenomas suggested that they arose from deep crypt cells. Adult adenomas shared certain histochemical properties with carcinomas, namely, increased affinity for periodic acid-Schiff (PAS) and focally for PNA. There is evidence based on the effects of saponification and sialidase treatments that the weak initial PAS reaction in normal and adenomatous colonic goblet cells from both age groups results from substituents on sialic acid and, in the case of normal colon from children, on other monosaccharides as well. Finally, there was a frequent lack of parellelism between PAS and lectin staining suggesting that different groups within the sugars are responsible for reactivity with those compounds.
Acetylgalactosamine↗
High prevalence of adenomatous polyps of the duodenal papilla in familial adenomatous polyposis.
Eighteen consecutive asymptomatic patients with familial adenomatous polyposis (both familial polyposis coli and Gardener's syndrome) were studied over a 12-month period; side-viewing upper endoscopy and biopsy were used to assess the frequency of adenomatous polyps of the duodenal papilla. Nine of the 18 patients demonstrated adenomatous polyps of the papilla, varying in size and appearance from microadenomas in normal-appearing duodenal papillae (two) to a sessile polyp 3 cm in diameter. Two were tubulovillous adenomas (0.5 cm and 2 cm in diameter) and the remainder were tubular adenomas. Severe atypia and malignancy were not encountered. These findings reveal that adenomas of the duodenal papilla are common in individuals with familial adenomatous polyposis. Because of these findings and because of the known risk of periampullary adenocarcinomas and nonmalignant complications of polyps of the duodenal papilla in patients with familial adenomatous polyposis, upper gastrointestinal screening of such patients should include examination of the duodenal papilla with a side-viewing endoscope.
Adenomatous Polyposis Coli↗
Effects of sulindac on sporadic colorectal adenomatous polyps.
BACKGROUND: Although sulindac is known to cause regression of colorectal adenomatous polyps in familial adenomatous polyposis, less is known about the effect of sulindac on sporadic adenomas. The precise mechanisms of these effects also remain to be determined. AIMS: Sulindac was given to patients with sporadic colorectal adenomatous polyps to evaluate its effects on them, and histological analysis was performed to elucidate the mechanism of the polyp regression, as well the kind of adenomatous polys that are susceptible to the agent. SUBJECTS: 20 adenomatous polyps in 15 patients were studied. METHODS: Sulindac (300 mg daily) was given for four months, followed by colonoscopy with removal of the residual polyps. Polyp size, degree of atypia, inflammatory cell infiltration in the polyps, and immunostaining for mutant p53 product were evaluated before and after treatment. RESULTS: 13 of the 20 polyps shrank or disappeared. Patient sex, polyp location, size, degree of atypia, or p53 mutation did not affect the response, but polyps in older patients were more sensitive to sulindac. The degree of atypia or inflammatory cell infiltration was not affected by the treatment. A polyp containing a focal cancer was unresponsive. CONCLUSIONS: Sulindac can cause regression of sporadic colorectal adenomatous polyps.
Adenomatous Polyps↗
Adenomatous polyps develop commonly in the ileal pouch of patients with familial adenomatous polyposis.
PURPOSE: The aim of this study was to establish the prevalence of adenomatous polyps in the ileal pouch of patients with familial adenomatous polyposis. METHOD: Forty-three patients who had an ileal pouch for familial adenomatous polyposis were invited to have a careful endoscopic examination of their pouch, including dye spraying. The number of polyps was recorded, and up to ten were biopsied. In addition, four random biopsy specimens were taken from the proximal and four from the distal pouch. RESULTS: Thirty-three patients with a median age of 36 (range, 14-63) years who had a pouch (5 Kock and 28 pelvic) for a median of 7 (range, 1-19) years accepted the invitation. Twenty-one patients (64 percent) had endoscopically identified polyps, the number of polyps ranging from 1 to 100 (median, 10) and varying in size from 1 to 3 mm. Fourteen patients (42 percent) had adenomatous polyps and 4 of these also had microadenomas on random biopsies. Nine of the 14 patients with adenomas also had lymphoid polyps. Seven patients had lymphoid polyps only and two of these patients had a microadenoma on random biopsy. Four of 12 patients with no visible polyps had microadenomas in their random biopsies. The presence of adenomatous polyps (Pearson's correlation; P < 0.01) increased with the age of the pouch. In total, 20 of 33 (60 percent) patients had adenomas and or microadenomas. CONCLUSION: Adenomatous polyps occur frequently in ileal pouches. These findings are of concern, and therefore, regular surveillance seems warranted until the natural history of these adenomatous polyps is determined.
Adenomatous Polyposis Coli↗
Correlation of nuclear ploidy with histology in adenomatous polyps of colon.
Histological sections of adenomatous polyps of the colon showing carcinoma were studied by video image analysis. Nuclear DNA content and morphology were measured in regions identified as either dysplasia, carcinoma confined to the mucosa, or carcinoma invading the muscularis mucosa. Where carcinoma was present, areas of dysplasia in the same polyp were found to have similar distributions of nuclear DNA content and size, supporting the notion that adenomatous polyps becomes cancer. The method can be used to detect those regions in sections of adenomatous polyps with the most severe nuclear abnormality.
Adenocarcinoma↗
Cancer and adenomatous polyp distribution in the colorectum.
OBJECTIVE: To examine the possible role of adenomatous polyps in colorectal cancer development, this study focused on the relationship of the distribution between adenomatous polyps and cancer in the colorectum. METHODS: The distribution of 753 adenomatous polyps was compared with that of 35 colorectal cancer lesions in 510 male patients ranging from 45 to 55 yr of age who underwent a total colonoscopy. RESULTS: The incidence of cancer significantly increased with a distal shift in the colorectal sites in comparison with that of adenomatous polyps (p < 0.02). CONCLUSION: The different distribution between adenomatous polyps and cancer thus suggested that adenomatous polyps at various colorectal sites appear to have a different malignant potential for cancer development.
Adenocarcinoma↗
Colon cancer specific nuclear matrix protein alterations in human colonic adenomatous polyps.
Most colon cancers arise within preexisting adenomatous polyps or adenomas. The slow evolution from the non-invasive premalignant lesion, the adenomatous polyp, to invasive cancer supports a strategy of early detection. Recently, we identified unique nuclear matrix proteins (NMPs) specific for colon cancer (CC2, CC3, CC4, CC5). Most of the NMPs identified are common to all cell types, but several identified NMPs are tissue and cell line specific. The objective of this study is to describe and characterize the NMP profile of premalignant adenomatous colon polyps. Specifically when in the adenoma-carcinoma sequence four specific colon cancer NMPs, previously described, appear. Using two-dimensional (2-D) gel analysis 20 colon polyps (one juvenile polyp, six tubular adenoma (TA), seven tubulovillous adenoma (TVA), six TVA with focal high-grade dysplasia (HGD), were analyzed for the presence of four (CC2, CC3, CC4, CC5) specific NMPs. CC2 was not seen in any of the premalignant polyps. CC5 was present in only two premalignant TVA with HGD and in one TA. CC3 and CC4 were present in most adenomas. None of the NMPs were seen in the juvenile polyp, which is not considered to be a precursor of colon cancer. CC2 and CC5 are NMPs expressed at the junction of an advanced adenoma and invasive colorectal cancer. CC3 and CC4 are expressed earlier in the evolution of adenomatous polyps. Development of an assay to these proteins may serve as a new method for early detection of colorectal cancer.
Adenomatous Polyps↗
The adenomatous polyp and the hereditary polyposis syndromes.
Adenomatous polyps are the benign precursors of colorectal adenocarcinoma. Colonic adenomas occur commonly in adults in Western countries. There is recent evidence that inheritance may play an important role in the etiology of these adenomatous polyps. Colonic adenomatous polyposis (numerous colonic adenomas) is the central feature of several rare inherited syndromes that give rise to colorectal cancer. There also appears to be a risk of gastrointestinal and other malignancies in the rare inherited syndromes of hamartomatous polyposis.
Adenomatous Polyposis Coli↗