Hyperplastic (Metaplastic) Polyposis of the Colorectum Associated with Adenomas and an Adenocarcinoma

Orii, Seishi; Nakamura, Shinichi; Sugai, Tamotu; Habano, Wataru; Akasaka, Iichiro; Nakasima, Fumie; Kazama, Hiromasa; Hasimoto, Yasuto; Takahasi, Hiroshi; Sugawara, Michinobu; Sato, Syunichi

doi:10.1097/00004836-199707000-00018

Cited by 30 publications

(13 citation statements)

References 20 publications

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“…5,14,18 In short, despite similar histologic appearances, there seems to be a subset of these polyps that may be far more ominous and carry a significant risk of developing into a colorectal cancer, or at least serve as a marker for the development of colorectal cancer. 8,12,[19][20][21][22] In contradistinction to the ubiquitous scenario of several small distal hyperplastic polyps, patients with hyperplastic polyposis are demonstrably unique. A variety of definitions of hyperplastic polyposis have been proposed.…”

Section: Discussionmentioning

confidence: 99%

Hyperplastic Polyposis and the Risk of Colorectal Cancer

Hyman

Anderson

Blasyk

2004

Diseases of the Colon &Amp; Rectum

134

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Section: Discussionmentioning

confidence: 99%

Hyperplastic Polyposis and the Risk of Colorectal Cancer

Hyman

Anderson

Blasyk

2004

Diseases of the Colon &Amp; Rectum

134

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“…Polyp numbers range from 5 to well over 100, with most cases having between 40 and 100 lesions (51). A characteristic feature of HPP is the diverse range of polyp types, ranging from diminutive hyperplastic polyps to larger SSA, SA, and MP as well as traditional adenomas (52)(53)(54). Recently, Burt and Jass (55) developed a working definition of HPP, namely (a) at least five proximal hyperplastic polyps two of which are >10 mm in diameter, or (b) any number of HPs proximal to the sigmoid colon in an individual with a first-degree relative with HPP, or (c) >20 hyperplastic polyps distributed throughout the colon.…”

Section: Hyperplastic Polyposis As a Predisposition To Serrated Neoplmentioning

confidence: 99%

The Case for a Genetic Predisposition to Serrated Neoplasia in the Colorectum: Hypothesis and Review of the Literature

Young

Jass

2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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In recent years, an alternative pathway of colorectal cancer development has been described in which serrated polyps replace the traditional adenoma as the precursor lesion. Importantly, serrated polyps and a subset of colorectal cancer show largely nonoverlapping mutation profiles to those found in adenomas and the majority of colorectal cancer. These genetic alterations include activating mutation of the BRAF proto-oncogene and widespread gene promoter hypermethylation (CpG island methylator phenotype or CIMP). Up to 15% of colorectal cancer is likely to develop on the basis of a strong genetic predisposition. The two most wellcharacterized syndromes, familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer (Lynch syndrome), both develop via the adenoma-carcinoma pathway and together account for approximately one third of familial colorectal cancer. We have recently described 11 families in which there is evidence that the genetic predisposition to autosomal dominant colorectal cancer is linked to the serrated pathway. This condition, serrated pathway syndrome, and the related condition, hyperplastic polyposis, the presentation of which suggests a recessive mode of inheritance, represent two syndromes in which BRAF mutation and methylation co-occur within serrated precursor lesions. Further, CIMP is observed in the normal colonic mucosa of individuals with hyperplastic polyposis consistent with a field defect in epigenetic regulation. The spectrum of serrated neoplasia may also implicate the apparently sporadic and later onset subset of colorectal cancer with high levels of microsatellite instability. The tendency for these lesions to be multiple, associated with smoking, and to show frequent BRAF mutation and CIMP points to a defect that may result from interactions between the environment and a weakly penetrant genetic alteration. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1778 -84)

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“…15 Not surprisingly, the finding of multiple serrated adenomas in the setting of HPS has led to speculation that individuals with this condition also share a significant increase in cancer risk that is analogous to the increased risk seen in adenomatous polyposis. 4,8 This contention is supported by the fact that 18 of the 49 cases (35%) of hyperplastic polyposis or serrated adenomatous polyposis reported in the literature have been associated with synchronous colorectal carcinomas.…”

mentioning

confidence: 94%

“…11 Although seen only rarely in sporadic lesions, it has been reported to a greater though variable extent in HPS, 8,10 often as foci of adenomatous dysplasia. 4,[12][13][14] It has been suggested that the atypia seen in sporadic serrated adenomas reflects neoplastic progression in an otherwise hyperplastic or metaplastic lesion and that such lesions may represent an alternative pathway to colorectal carcinogenesis. 15 Not surprisingly, the finding of multiple serrated adenomas in the setting of HPS has led to speculation that individuals with this condition also share a significant increase in cancer risk that is analogous to the increased risk seen in adenomatous polyposis.…”

mentioning

confidence: 99%

Colorectal Carcinomas Arising in the Hyperplastic Polyposis Syndrome Progress through the Chromosomal Instability Pathway

Hawkins

Gorman

Tomlinson³

et al. 2000

The American Journal of Pathology

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The hyperplastic polyposis syndrome is characterized by the presence within the colon of multiple large hyperplastic polyps. We describe a case of hyperplastic polyposis syndrome associated with two synchronous carcinomas , one of which arises within a pre-existing hyperplastic lesion. Comparative genomic hybridization was used to determine genetic changes in both carcinomas and several associated hyperplastic lesions. Microsatellite analysis at five loci was performed on carcinomas and representative hyperplastic polyps , and p53 status was analyzed by immunohistochemistry. Both carcinomas showed multiple genetic aberrations , including high level gains of 8q and 13q , and loss of 5q. These changes were not seen in the hyperplastic polyps. Microsatellite instability was not seen in the carcinomas , four separate hyperplastic polyps , the hyperplastic polyp with mild adenomatous change associated with the carcinoma , or a separate serrated adenoma. Allelic imbalance in the cancers at D5S346 and D17S938 suggested allelic loss of both p53 and APC , as well as at the loci D13S263 , D13S174 , D13S159 , and D18S49. An early invasive carcinoma in one hyperplastic polyp stained for p53 protein , but the associated hyperplastic polyp was negative. In this case , neoplastic progression followed the typical genetic pathway of common colorectal carcinoma and occurred synchronously with mutation of p53. (Am J Pathol 2000, 157:385-392)

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Hyperplastic (Metaplastic) Polyposis of the Colorectum Associated with Adenomas and an Adenocarcinoma

Cited by 30 publications

References 20 publications

Hyperplastic Polyposis and the Risk of Colorectal Cancer

Hyperplastic Polyposis and the Risk of Colorectal Cancer

The Case for a Genetic Predisposition to Serrated Neoplasia in the Colorectum: Hypothesis and Review of the Literature

Colorectal Carcinomas Arising in the Hyperplastic Polyposis Syndrome Progress through the Chromosomal Instability Pathway

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