Serrated Polyps and Their Alternative Pathway to the Colorectal Cancer: A Systematic Review

Szylberg, Łukasz; Janiczek, Marlena; Popiel, Aneta; Marszałek, Andrzej

doi:10.1155/2015/573814

Cited by 44 publications

(33 citation statements)

References 61 publications

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“…SSA/Ps are considered the precursor lesion for many sporadic CRCs with microsatellite instability and for other CRCs characterized by hypermethylation (25–27). Initially, we evaluated TSAs and SSA/Ps as separate groups, given a presumed distinct etiology (28). While we did not identify significant differences in miRs between TSAs and HGTVs, there were several differentially expressed miRs observed between HPNMs and TSAs.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA Signatures of Colonic Polyps on Screening and Histology

Tsikitis

Potter

Mori

et al. 2016

Cancer Prevention Research

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Colorectal cancer (CRC) and adenoma adjacent to cancer exhibit distinct microRNA (miR) alterations in an apparent mucosa-to-adenocarcinoma sequence. The pattern of microRNAs in screen-detected polyps in relation to histologic features and cancer risk has not been investigated. miR expression analysis was performed on normal mucosa (NM), hyperplastic polyps (HPs), tubular adenomas (TAs), tubulovillous adenomas or high-grade dysplasia (TVHGs), and serrated polyps (sessile serrated adenoma/polyps, SSA/Ps, and traditional serrated adenomas, TSAs) in biopsy specimens from 109 patients undergoing screening/surveillance colonoscopy. Generalized linear models were used to identify differentially expressed miRs by histologic type and logistic regression to identify miR predictors of histopathology. False discovery rate (FDR) was used to control for multiple comparisons. We identified 99 miRs differing in at least one of five histopathologic groups (FDR ≤ 0.05). In a comparison of HPNM vs. TVHG, the top most up- and down-regulated miRs in HPNM included miR-145, -143, -107, -194, and -26a (upregulated), and miR-663, -1268, -320b, -1275, and -320b (down-regulated) (FDR P-value < 0.05). miR-145 and -619 showed high accuracy to discriminate low- from high-risk polyps without serrated histology (TVHG vs. HPNM+TA) (CI= 95.6%), whereas miRs-124, -143, and -30a showed high accuracy of separating high-risk polyps (TVHG+TSA) from low-risk polyps (HPNM+TA+SSA/P) (CI=96.0%). For TSAs, miRs-125b and -199a were uniquely downregulated relative to HPNMs, and miR-335, -222 and -214 discriminated between non-serrated and serrated histology. Our data support the presence of CRC-associated miR alterations in screen-detected adenomas that may be useful for risk stratification for surveillance interval planning.

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Section: Resultsmentioning

confidence: 99%

MicroRNA Signatures of Colonic Polyps on Screening and Histology

Tsikitis

Potter

Mori

et al. 2016

Cancer Prevention Research

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“…First, sporadic colorectal carcinogenesis has a diversity of pathogeneses and pathways (25)(26)(27); on the other hand, the primary and main pathogenesis of colitic cancer is chronic mucosal inflammation. Moreover, this pathogenic inflammation is diffusely distributed in the colon, which means that examining this non-neoplastic mucosa could give indications of the accumulated genetic change in UC-associated carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Increased Copy Number Variation of mtDNA in an Array-based Digital PCR Assay Predicts Ulcerative Colitis-associated Colorectal Cancer

Tanaka

Kobunai

Yamamoto

et al. 2017

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Abstract. Aim: Mitochondrial dysfunction plays a central role in carcinogenesis in numerous cancer-related diseases.We examined the copy number variation of mitochondrial DNA (mtDNA) Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD), and disease-related long-standing inflammation results in increased risk of colitic cancer. The cumulative risks of invasive adenocarcinoma have been shown to be 0.5%, 4.1%, and 6.1% at 10, 20, and 30 years, respectively (1), and colitic cancer, especially the advanced type, determines patient outcomes. Currently, in order to detect dysplastic lesions early, colonoscopy together with random and target biopsies are considered to be the most effective detection option, especially for longstanding UC; however, the characteristics of colitic cancer, such as flat mucosal lesions and widespread distribution, make early detection difficult (2). Another problem with surveillance colonoscopy is its invasiveness and cost effectiveness; therefore, we thought that another modality for the detection of colitic cancer and identification of predictors of patients at high risk was needed.As clinical indicators, the extent and severity of inflammation and the duration of disease have been observed to increase the cumulative risk of dysplasia or invasive colorectal cancer in IBD (3-6). From a molecular perspective, we studied genetic variance in non-neoplastic mucosa. We observed lower DNA copy numbers and lower expression of RUNX3 in non-neoplastic rectal mucosa in cancer-free UC patients (UC-nonCa) than in patients with colitic cancer (UC-Ca) (7). In another study, we identified 20 genes that showed differences in expressions between UC-Ca and UC-nonCa mucosae, and we introduced a prediction model that achieved a markedly high accuracy rate of 83% and negative predictive value of 100% (8). These studies contributed to a better understanding of the genetics of colitic cancer and methods of prediction.Recently, the genetic alteration of mitochondrial DNA (mtDNA) has attracted attention as a target for various diseases. The mitochondrion is a small organelle in cells that plays an important role in the production of energy 713 *These Authors contributed equally to this study.

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“…Recent published evidence, however, has indicated that there are three distinct sub-categories of SP, most commonly classified as hyperplastic polyps (HP), sessile serrated adenomas/polyps (SSA/P) and traditional serrated adenomas (TSA) 10 . SSA/P and TSA are now understood to harbour malignant potential 11 .…”

Section: Introductionmentioning

confidence: 99%