Sporadic and Syndromic Hyperplastic Polyps and Serrated Adenomas of the Colon: Classification, Molecular Genetics, Natural History, and Clinical Management

doi:10.1016/j.gtc.2007.12.014

Gastroenterology Clinics of North America

Volume 37, Issue 1, March 2008, Pages 25-46

https://doi.org/10.1016/j.gtc.2007.12.014 Get rights and content

There is now strong evidence for an alternative pathway of colorectal carcinogenesis implicating hyperplastic polyps and serrated adenomas. This article briefly reviews the evidence for this serrated pathway, provides diagnostic criteria for clinically significant hyperplastic polyps and allied serrated polyps, and suggests how this information may be translated into safe, effective guidelines for colonoscopy-based colon cancer prevention. Consideration also is given to the definition and management of hyperplastic polyposis syndrome. The currently proposed management plan for serrated polyps is tentative because of incomplete knowledge of the nature and behavior of these polyps. This article highlights key areas warranting further research.

Section snippets

Colorectal Cancer: More Than One Disease

The serrated pathway concept evolved based on (1) identification of a subtype of colorectal cancer that could not be conceived to develop within a pre-existing adenoma and (2) demonstration that hyperplastic polyps and related lesions could fill the gap left by the adenoma. Study of rare forms of hereditary colorectal cancer provided the initial evidence of different molecular mechanisms for the evolution of colorectal cancer. Investigation of familial adenomatous polyposis led to the discovery

Hyperplastic Polyps, Serrated Adenomas, and the Serrated Pathway to Colorectal Cancer

For half a century colorectal epithelial polyps were assumed to comprise two main and nonoverlapping groups: hyperplastic polyps and adenomas. Reports of mixed or intermediate types of polyp had occasionally appeared in the pathologic literature, but it was not until 1990 that Longacre and Fenoglio-Preiser [14] explored the concept of an intermediate type of polyp in a detailed survey of more than 18,000 colorectal polyps. Among these polyps, 110 (0.6%) were diagnosed as serrated adenomas. In

Hyperplastic Polyposis and the Sessile Serrated Adenoma

Hyperplastic polyposis originally was perceived as lacking any cancer risk. Its clinical significance lay only in the potential for misdiagnosis as familial adenomatous polyposis [16]. Occasional descriptions of malignancy were explained by the presence of coexisting adenomas. Case reports then appeared showing transitions from hyperplastic polyps through dysplasia (mixed polyps) to carcinoma [17]. In a small series of hyperplastic polyposis, the dysplastic components of such mixed or

Multiple Serrated Pathways to Colorectal Cancer

The existence of distinct types of serrated adenoma (SSA and TSA) raises the question of multiple pathways to what has been termed “serrated adenocarcinoma” [35]. The SSA has been associated with proximal colorectal cancers, BRAF mutation, and extensive DNA methylation. These cancers include a subset of sporadic MSI-H colorectal cancer with methylation and inactivation of the DNA mismatch repair gene MLH1. These colorectal cancers are more common in women [35]. Contrariwise, TSA has been

Diagnosis of Sessile Serrated Adenoma: Recognition and Nomenclature

As previously noted, SSAs originally were labeled as “hyperplastic polyps.” Based on systematic analysis of histologic features in sporadic hyperplastic polyps, Torlakovic and Snover [20] showed that 18% of “hyperplastic polyps” satisfied the criteria for SSA as described in hyperplastic polyposis. Development of a universally acceptable nomenclature for SSA has been problematic because these lesions have subtle differences from hyperplastic polyps and do not display the features of

Sessile Serrated Adenoma and Risk of Colorectal Cancer

Stratification of “hyperplastic polyps” into GCHP, MVHP, and SSA has occurred recently [44]. Without this stratification, the increased risk associated with SSA would be diluted by the negligible risk associated with small, distal hyperplastic polyps [45], [46], [47]. Most right-sided hyperplastic polyps (or SSAs) do not become malignant. In an autopsy study conducted in New Zealand, 43 right-sided hyperplastic polyps (12.9% prevalence) were detected among 333 subjects [48]. Many of these

Detection of Hyperplastic Polyps and Sessile Serrated Adenomas

Detection of hyperplastic polyps has been little analyzed because these lesions were considered to confer negligible risk of advanced colorectal neoplasia [53], [54]. Screening techniques to detect adenomas and early cancers include fecal tests (occult blood and DNA testing), endoscopic tests (flexible sigmoidoscopy and colonoscopy), and radiologic tests (barium enema and CT colonography [“virtual colonoscopy”]). Consideration of size, morphology, anatomic distribution, and pathologic and

Endoscopic Management of Hyperplastic Polyps and Sessile Serrated Adenomas

Small and diminutive hyperplastic polyps can be dealt with by standard polypectomy techniques used for adenomas; however a single large (≥10-mm) hyperplastic polyp requires careful consideration of the available management strategies. The colonoscopist needs to weigh the risks and benefits of immediate polypectomy versus observation with biopsy to confirm SSA and/or resection at a later date. There are almost no data on therapy for large hyperplastic polyps or SSAs, as opposed to conventional

Management of Hyperplastic Polyposis Syndrome

Management of HPS involves the removal of premalignant lesions, subsequent surveillance, and counseling of the patient and other family members regarding genetic risk. If the initial presenting lesion is a carcinoma, then, as in the management of colon cancer associated with hereditary nonpolyposis colorectal cancer or attenuated familial adenomatous polyposis, an ileorectal anastomosis is the operation of choice to remove the at-risk colon together with the cancer [82]. This therapy eliminates

Surveillance of Sessile Serrated Adenomas and Hyperplastic Polyposis Syndrome

There are limited data on the natural history and rate of progression of hyperplastic polyps and SSAs to advanced lesions. SSAs that are too few or too small to qualify as HPS may be treated like adenomas in terms of their premalignant risk and as predictors of future colorectal cancer risk. Thus, removal of an SSA 10 mm or larger would trigger colonoscopy at 3 years, as would an adenoma of similar size [84], [85]. Whether the risk of SSA and adenomas are additive, so that two SSAs smaller than

Preventive Strategies

If 20% of colorectal cancer arises from hyperplastic polyps and SSAs, colonoscopic surveillance and removal of these lesions is likely to help prevent colon cancer. Hyperplastic polyp prevention may be particularly important because these lesions are not detected well by any screening strategy except colonoscopy, and even detection by colonoscopy is challenging.

Case-control studies provide evidence that the same lifestyle factors associated with adenomas and colorectal cancer also are

Summary

This article describes evidence underlying an alternative pathway to colorectal cancer implicating hyperplastic polyps and allied lesions. The genetic, molecular, and morphologic features of hyperplastic polyps and two types of serrated adenomas (traditional and sessile) are presented. The importance of BRAF mutations is discussed. Pathologists are incorporating these evolving concepts clinically. There is a need for improved diagnostic criteria and an internationally agreed classification for

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An increasing burden on health care resources has resulted in a backlog of individuals requiring colonoscopy, with delays in surveillance possibly detrimental for individuals at increased risk of colorectal cancer (CRC). This study investigated the use of a 2-sample fecal immunochemical test (FIT) to establish those most likely to have advanced neoplasia (AN) and in need of prioritized surveillance colonoscopy.
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Association between use of low-dose aspirin and detection of colorectal polyps and cancer in a screening setting
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The possible protective effect of aspirin on risk of colorectal cancer (CRC) is still highly debated.
We used data from Bowel Cancer Screening in Norway, a trial randomizing individuals from general population, aged 50-74 years, to flexible sigmoidoscopy or faecal immunochemical test (FIT), to study the association between aspirin use and detection of CRC and two CRC precursors: adenomas and advanced serrated lesions (ASL). Prescriptions of low-dose aspirin were obtained from Norwegian prescription database. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).
Among 64,889 screening participants (24,159 sigmoidoscopy, 40,730 FIT), 314 (0.5%) had CRC, 6,208 (9.6%) adenoma and 659 (1.0%) ASL. Overall and short-term use (<3 years) of low-dose aspirin, versus no use, were not associated with any colorectal lesion. Long-term use (≥3 years) was associated with lower detection of CRC (overall OR 0.66, 95%CI 0.46-0.93; sigmoidoscopy: 0.56, 0.33-0.97; FIT: 0.72, 0.45-1.15), adenomas in sigmoidoscopy arm (overall OR 0.95, 95%CI 0.87-1.03; sigmoidoscopy: 0.89, 0.80-0.99; FIT: 1.03, 0.89-1.18), but not ASLs. We did not observe significant differences in the effect of aspirin according to the location of colorectal lesions.
Our results suggest that long-term use of aspirin might have a protective effect against adenomas and colorectal cancer, but not ASLs.
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Colorectal cancer (CRC) is a complex disease, in which at least three distinct molecular pathways to carcinogenesis and four consensus molecular subtypes have been described. There has, therefore, been an increasing role for molecular testing in the diagnosis and clinical management of CRC and a rapid expansion in the molecular technologies available for use in the clinical laboratory. Current clinical recommendations for molecular testing in CRCs are aimed at identification of hereditary colon cancer syndromes, predicting response to targeted therapeutics, and testing of microsatellite instability (MSI) status in individual tumors. Molecular biomarkers with predictive or prognostic significance in CRC are increasingly utilized in the clinical management of these patients, with a particular focus on the EGFR signaling pathway and immunotherapies. In addition, high-throughput molecular testing of CRCs in cancer-specific mutation panels by next-generation sequencing have become increasingly utilized as diagnostic assays in the clinical laboratory. The standard-of-care recommendations for molecular testing of CRCs will likely continue to evolve as we advance in our understanding of the molecular mechanisms of disease and rapidly develop new targeted therapeutics for the treatment of CRC.
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«Pólipos serrados» es el término utilizado para describir lesiones epiteliales del colon y recto que demuestran un patrón de «dientes de sierra» de la superficie y epitelio de las criptas. La llamada vía serrada describe la progresión de adenomas serrados sésiles y adenomas serrados tradicionales a cáncer colorrectal. Esta vía está bien reconocida como un mecanismo de carcinogénesis alternativo, el cual representa el 15-30% de los casos de cáncer colorrectal, explicando además una proporción significativa de los casos de cáncer colorrectal de intervalo. Por tal motivo, debido a su comportamiento incierto y usualmente agresivo, los pólipos serrados son un tema de suma relevancia en el cribado de cáncer colorrectal. Nuestro objetivo fue revisar la historia, nomenclatura actual, fisiopatología, características morfológicas, tratamiento y vigilancia de los pólipos serrados.
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Red and processed meat, recognized carcinogens, are risk factors for colorectal neoplasia, including polyps, the precursor for colorectal cancer. The mechanism is unclear. One possible explanation is the mutagenic activity of these foods, perhaps due to generation during cooking [e.g., heterocyclic amine (HCA) intake]. Few studies have evaluated meat intake and sessile serrated lesion (SSL) risk, a recently recognized precursor, and no study has evaluated meat cooking methods and meat-derived mutagens with SSL risk.
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Sporadic and Syndromic Hyperplastic Polyps and Serrated Adenomas of the Colon: Classification, Molecular Genetics, Natural History, and Clinical Management

Section snippets

Colorectal Cancer: More Than One Disease

Hyperplastic Polyps, Serrated Adenomas, and the Serrated Pathway to Colorectal Cancer

Hyperplastic Polyposis and the Sessile Serrated Adenoma

Multiple Serrated Pathways to Colorectal Cancer

Diagnosis of Sessile Serrated Adenoma: Recognition and Nomenclature

Sessile Serrated Adenoma and Risk of Colorectal Cancer

Detection of Hyperplastic Polyps and Sessile Serrated Adenomas

Endoscopic Management of Hyperplastic Polyps and Sessile Serrated Adenomas

Management of Hyperplastic Polyposis Syndrome

Surveillance of Sessile Serrated Adenomas and Hyperplastic Polyposis Syndrome

Preventive Strategies

Summary

Cell

Gastroenterology

Gastrointest Endosc

Am J Pathol

Gastroenterology

Gastroenterology

Gastroenterology

Clin Gastroenterol Hepatol

Gastroenterology

Gastroenterology

Hum Pathol

Gastroenterology

Lancet

Gastrointest Endosc

Gastrointest Endosc

Gastrointest Endosc

Clin Gastroenterol Hepatol

Gastrointest Endosc

Gastrointest Endosc

Gastrointest Endosc

Gastroenterology

Gastroenterology

Gastroenterology

Identification of FAP locus genes from chromosome 5q21

Science

APC, signal transduction and genetic instability in colorectal cancer

Nat Rev Cancer

Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis

Nature

Microsatellite instability in cancer of the proximal colon

Science

Microsatellite marker analysis in screening for hereditary nonpolyposis colorectal cancer (HNPCC)

Cancer Res

Mutation of the type ii transforming growth factor-beta receptor is coincident with the transformation of human colon adenomas to malignant carcinomas

Cancer Res

APC mutations in colorectal tumors with mismatch repair deficiency

Proc Natl Acad Sci U S A

Alternative genetic pathways in colorectal carcinogenesis

Proc Natl Acad Sci U S A

Colorectal cancer with and without microsatellite instability involves different genes

Genes Chromosomes Cancer

BRAF mutation is associated with DNA methylation in serrated polyps and cancers of the colorectum

Gut

CpG island methylator phenotype underlies sporadic microsatellite instability and is tightly associated with BRAF mutation in colorectal cancer

Nat Genet

Methylation of the hMLH1 promoter correlates with lack of expression of hMLH1 in sporadic colon tumors and mismatch repair-defective human tumor cell lines

Cancer Res

Mixed hyperplastic adenomatous polyps/serrated adenomas: a distinct form of colorectal neoplasia

Am J Surg Pathol

DNA microsatellite instability in hyperplastic polyps, serrated adenomas, and mixed polyps: a mild mutator pathway for colorectal cancer?

J Clin Pathol

Metaplastic polyps and polyposis of the colorectum

Histopathology

Adenomatous and carcinomatous changes within hyperplastic colonic epithelium

Dis Colon Rectum

Neoplastic progression occurs through mutator pathways in hyperplastic polyposis of the colorectum

Gut

Morphologic reappraisal of serrated colorectal polyps

Am J Surg Pathol

Clinicopathologic differences among subtypes of serrated adenomas of the colorectum

Hepatogastroenterology

BRAF and KRAS Mutations in hyperplastic polyps and serrated adenomas of the colorectum: relationship to histology and CpG island methylation status

Am J Surg Pathol

Hyperplastic polyps and DNA microsatellite unstable cancers of the colorectum

Histopathology

Advanced colorectal polyps with the molecular and morphological features of serrated polyps and adenomas: concept of a ‘fusion’ pathway to colorectal cancer