Immunohistochemical expression of CDX2, β-catenin, and TP53 in inflammatory bowel disease-associated colorectal cancer

Laurent, Césari; Svrcek, Magali; Fléjou, Jean‐François; Chenard, Marie–Pierre; Duclos, Bernard; Freund, Jean–Noël; Reimund, Jean‐Marie

doi:10.1002/ibd.21451

Cited by 25 publications

(19 citation statements)

References 55 publications

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“…By IHC staining of colon cancer tissue, it has been shown that CDX2, APC, and b-catenin expression were correlated [52,65]. Especially at the invasive front, loss of CDX2 expression seems to inversely correlate with nuclear b-catenin [65].…”

Section: Cdx2 In Wnt/b-catenin Signaling and Proliferationmentioning

confidence: 96%

“…One study reported that CDX2 expression was inversely correlated to cytoplasmic b-catenin at the invasive front in sporadic (but not inflammatory bowel disease (IBD)-associated) tumors [52]. CDX2 expression was also inversely correlated to claudin-18 (CLDN18) expression À a component of tight junctions and a proposed oncogene [41].…”

Section: Right Versus Left Sided Tumorsmentioning

confidence: 98%

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The clinical perspectives of CDX2 expression in colorectal cancer: A qualitative systematic review

et al. 2014

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Section: Cdx2 In Wnt/b-catenin Signaling and Proliferationmentioning

confidence: 96%

Section: Right Versus Left Sided Tumorsmentioning

confidence: 98%

The clinical perspectives of CDX2 expression in colorectal cancer: A qualitative systematic review

et al. 2014

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“…Increase in mucosal pro-inflammatory cytokine or other inflammatory mediators such as reactive oxygen and nitrogen species, or cyclooxygenase-2 (COX-2)-derived prostaglandins production results in alterations of a large number of molecules such as DNA, RNA, proteins or lipids. For example, they induce the formation of adducts to DNA, generating point mutations in genes like the p53 tumour suppressor gene, which is early mutated in IBD inflamed mucosa (even before neoplastic transformation) (Laurent et al, 2011), and in CpG islands involved in DNA methylation. In addition, the increase in local tissue pro-inflammatory cytokines and prostaglandins inhibits apoptosis and favours cell proliferation, thereby facilitating carcinogenesis.…”

Section: Chronic Inflammationmentioning

confidence: 99%

“…Mesalamine has been reported to decrease the activity of the wingless and integration site growth factor (Wnt)/β-catenin pathway [which is constitutively activated in up to 80% of sporadic colorectal cancers due to somatic mutation of the Apc tumour suppressor gene, although lesser in CAC (Viennot et al, 2009;Laurent et al, 2011)], by inhibiting protein phosphatase A2 (which results in a enhancement of β-catenin phosphorylation, and induces activation of carcinogenetic genes such as cyclin D1, c-met and c-myc) (Bos et al, 2006). 5-aminosalicylic acid has also been reported to inhibit epidermal growth factor receptor (EGFR) pathway.…”

Section: Effects On the Wnt/β-catenin And The Epidermal Growth Factormentioning

confidence: 99%

Ulcerative Colitis-Associated Colorectal Cancer Prevention by 5-Aminosalicylates: Current Status and Perspectives

Reimund¹,

Tavernier²,

Viennot³

et al. 2012

Ulcerative Colitis From Genetics to Complications

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Ulcerative Colitis from Genetics to Complications 150 hypothesis have emerged, resulting from fundamental research in molecular biology and pharmacology. This increased understanding of the putative pathway(s) by which 5-ASA may interfere with CAC development appears also as the starting point for optimising 5-ASA derivatives or identifying new compounds acting more specifically and/or being more efficient in preventing neoplastic transformation of the colonic epithelium in UC patients. These different points will be addressed more precisely in the three next parts. Frequency of colorectal cancer risk in ulcerative colitis and risk factors

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“…For example, abnormal p53 expression was noted in a majority of IBD-associated tumors, whereas MSI-high (MSI-H) was found only in a minority of IBD-associated dysplasias and adenocarcinomas. [9][10][11] However, similar molecular studies in pouch adenocarcinoma after pouch are lacking. The aims of the study were to characterize the clinical and histomorphologic features of pouch adenocarcinoma in patients after pouch, compare them with UC-associated adenocarcinoma, examine the intactness of MMR proteins, overexpression of p53, and nuclear immunoreactivity in b-catenin (2 markers involved in the chromosomal instability pathway in colorectal cancer), and determine the cell lineage of pouch and peripouch adenocarcinoma.…”

mentioning

confidence: 99%

Histomorphologic and Molecular Features of Pouch and Peripouch Adenocarcinoma

Jiang¹,

Shadrach²,

Carver³

et al. 2012

American Journal of Surgical Pathology

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The occurrence of adenocarcinoma after ileal pouch-anal anastomosis for ulcerative colitis (UC) is an infrequent but potentially lethal complication. Neither histomorphologic nor molecular features of pouch adenocarcinoma after ileal pouch-anal anastomosis have been fully investigated. We report the largest series of 12 pouch and peripouch adenocarcinomas and compared them with 58 randomly selected UC-associated adenocarcinomas. The mean age of patients with pouch/peripouch adenocarcinoma was 55.2 years (SD 14.8), which was not significantly different from that of controls (P=0.52). Pouch/peripouch adenocarcinoma and UC-associated adenocarcinoma had a comparable frequency of tumor-infiltrating lymphocytes, lack of dirty necrosis, mucin differentiation, signet ring cell differentiation, heterogeneity, and well differentiation (P>0.05 for all). Pouch/peripouch adenocarcinoma was more likely to show Crohn-like reaction compared with UC-associated adenocarcinoma (P=0.047). Loss of at least 1 mismatch repair protein was noted in 9% of pouch/peripouch adenocarcinomas and 9.6% of UC-related adenocarcinomas (P=1.0). There was no significant difference in the frequency of p53 overexpression (36.4% vs. 61.1%, P=0.184) or nuclear immunoreactivity for β-catenin (9% vs. 7.4%, P=0.99) in pouch/peripouch versus UC-associated adenocarcinomas, respectively. Pouch/peripouch and UC-associated adenocarcinoma had a comparable positive rate for CK7 (54.5% vs. 55.5%, P=0.99), CK20 (100% vs. 98.1%, P=0.99), and CDX2 (72.8% vs. 72.2%, P=0.99) by immunohistochemistry. In summary, pouch and peripouch adenocarcinoma can occur in patients without colorectal neoplasia and in those with idiopathic inflammatory bowel disease, can be potentially lethal, and has histomorphologic and molecular features similar to those of UC-associated adenocarcinoma.

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Immunohistochemical expression of CDX2, β-catenin, and TP53 in inflammatory bowel disease-associated colorectal cancer

Abstract: In i-CRC and CD-associated SBA, carcinogenesis is associated early with p53 mutations and to inflammation intensity.

Cited by 25 publications

References 55 publications

The clinical perspectives of CDX2 expression in colorectal cancer: A qualitative systematic review

The clinical perspectives of CDX2 expression in colorectal cancer: A qualitative systematic review

Ulcerative Colitis-Associated Colorectal Cancer Prevention by 5-Aminosalicylates: Current Status and Perspectives

Histomorphologic and Molecular Features of Pouch and Peripouch Adenocarcinoma

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