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Review
. 2014 Mar 14;20(10):2634-40.
doi: 10.3748/wjg.v20.i10.2634.

Serrated pathway in colorectal carcinogenesis

Affiliations
Review

Serrated pathway in colorectal carcinogenesis

Letícia Yamane et al. World J Gastroenterol. .

Abstract

Serrated adenocarcinoma is a recently described subset of colorectal cancer (CRC), which account for about 10% of all CRCs and follows an alternative pathway in which serrated polyps replace the traditional adenoma as the precursor lesion to CRC. Serrated polyps form a heterogeneous group of colorectal lesions that includes hyperplastic polyps (HPs), sessile serrated adenoma (SSA), traditional serrated adenoma (TSA) and mixed polyps. HPs are the most common serrated polyp followed by SSA and TSA. This distinct histogenesis is believed to have a major influence in prevention strategies, patient prognosis and therapeutic impact. Genetically, serrated polyps exhibited also a distinct pattern, with KRAS and BRAF having an important contribution to its development. Two other molecular changes that have been implicated in the serrated pathway include microsatellite instability and the CpG island methylator phenotype. In the present review we will address the current knowledge of serrated polyps, clinical pathological features and will update the most recent findings of its molecular pathways. The understanding of their biology and malignancy potential is imperative to implement a surveillance approach in order to prevent colorectal cancer development.

Keywords: Colorectal carcinogenesis; CpG island methylator phenotype; Microsatellite instability; Mutation; Serrated pathway.

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Figures

Figure 1
Figure 1
Hematoxylin and eosin of representative cases of serrated lesions. A: Microvesicular hyperplastic polyp (× 100); B: Goblet cell hyperplastic polyp (× 100); C: Sessile serrated adenomas (× 100); D: Traditional serrated adenomas (× 100).
Figure 2
Figure 2
Schematic view of serrated polyps: Carcinoma sequence. MVHP: Microvesicular hyperplastic polyp; GCHP: Globet cell hyperplastic polyp; MPHP: Mucin-poor hyperplastic polyp; SSA: Sessile serrated adenoma; TSA: Traditional serrated adenoma; MP: Mixed polyp; MSI-H: High microsatellite instability; CIMP: CpG island methylator phenotype.

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References

    1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer. 2010;127:2893–2917. - PubMed
    1. Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell. 1990;61:759–767. - PubMed
    1. Pino MS, Chung DC. The chromosomal instability pathway in colon cancer. Gastroenterology. 2010;138:2059–2072. - PMC - PubMed
    1. Fred T. Bosman FC, Ralph H. Hruban, Neil D. Theise. WHO Classification of Tumors of the Digestive System. Lyon, France: Internation Agency for Research on Cancer; 2010.
    1. Jass JR, Smith M. Sialic acid and epithelial differentiation in colorectal polyps and cancer--a morphological, mucin and lectin histochemical study. Pathology. 1992;24:233–242. - PubMed

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