Carcinogenesis in Ulcerative Colitis

Humphries, Adam; Jawad, Noor; Ignjatovic, Ana; East, James; Leedham, Simon J.

doi:10.5772/25306

Cited by 3 publications

(3 citation statements)

References 105 publications

(117 reference statements)

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“…From a histological perspective, sporadic tumors tend to follow the adenoma-carcinoma-sequence with the stepwise accumulation of genetic mutations in onco and tumor suppressor genes [ 44 ]. However, colitis-associated colorectal cancer progress through the pathway of low- (LGD) and high-grade dysplasia (HGD) to carcinoma and is less well explored with significant differences in the requirement and timing of genetic and epigenetic alterations [ 45 ]. Profound differences of UCC and SCC carcinogenesis were supported just recently by Yaeger et al, who found different genomic variances in UCCs compared to SCCs by next-generation-sequencing [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

EB1 protein alteration characterizes sporadic but not ulcerative colitis associated colorectal cancer

et al. 2017

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BackgroundWhile carcinogenesis in Sporadic Colorectal Cancer (SCC) has been thoroughly studied, less is known about Ulcerative Colitis associated Colorectal Cancer (UCC). This study aimed to identify and validate differentially expressed proteins between clinical samples of SCC and UCC to elucidate new insights of UCC/SCC carcinogenesis and progression.ResultsMultiplex-fluorescence two-dimensional gel electrophoresis (2-D DIGE) and mass spectrometry identified 67 proteoforms representing 43 distinct proteins. After analysis by Ingenuity Pathway Analysis® (IPA), subsequent Western blot validation proofed the differential expression of Heat shock 27 kDA protein 1 (HSPB1) and Microtubule-associated protein R/EB family, member 1 (EB1) while the latter one showed also expression differences by immunohistochemistry.Materials and MethodsFresh frozen tissue of UCC (n = 10) matched with SCC (n = 10) was investigated. Proteins of cancerous intestinal mucosal cells were obtained by Laser Capture Microdissection (LCM) and compared by 2-D DIGE. Significant spots were identified by mass spectrometry. After IPA, three proteins [EB1, HSPB1, and Annexin 5 (ANXA5)] were chosen for further validation by Western blotting and tissue microarray-based immunohistochemistry.ConclusionsThis study identified significant differences in protein expression of colorectal carcinoma cells from UCC patients compared to patients with SCC. Particularly, EB1 was validated in an independent clinical cohort.

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Section: Discussionmentioning

confidence: 99%

EB1 protein alteration characterizes sporadic but not ulcerative colitis associated colorectal cancer

et al. 2017

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“…Carcinogenesis in UC is inflammation-driven and has a different pathway than usual colorectal carcinogenesis. Epithelial cells are acquiring early mutations of TP53 and KRAS genes and no mutations of APC genes, while in non-inflammatory carcinogenesis of colon, APC mutation is the earliest event [33].…”

Section: Dysplasiamentioning

confidence: 99%

Histologic Features with Predictive Value for Outcome of Patients with Ulcerative Colitis

Popp¹,

Mateescu²

2018

New Concepts in Inflammatory Bowel Disease

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Ulcerative colitis is an inflammatory bowel disease with variable evolution, in which is difficult to establish patient's outcome. Histology is an important part of diagnosis of ulcerative colitis and has an increasing role in patients' management, since increasingly more histologic features with predictive value are being identified and validated. This chapter presents the most important histologic prognostic factors that should be included in histologic reports of patients with ulcerative colitis. Basal plasmacytosis and histologic healing are the most significant validated factors of prognosis in ulcerative colitis, while dysplasia is important since colorectal carcinoma is a severe complication of the disease.

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“…The overproduction of ROS and NOS by immune cells increases the oxidative damage of the DNA and together with the epithelial injury, causes a continuous cycle of regeneration which increases the risk of mutations. Moreover, the high proliferation rate could also lead to chromosomal instability and the accumulation of chromosomal aberrations (Humphries et al, 2012;Sobczak et al, 2014). The continuous stem cells proliferation in the crypts could also compromise Wnt signaling, which has a role in IECs homeostasis and regeneration.…”

Section: Colitis-associated Colorectal Cancermentioning

confidence: 99%

The role of the Glucocorticoid Receptor in intestinal inflammation and tumorigenesis in a murine model of colitis and colitis-associated colorectal cancer

Muzzi¹

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Carcinogenesis in Ulcerative Colitis

Cited by 3 publications

References 105 publications

EB1 protein alteration characterizes sporadic but not ulcerative colitis associated colorectal cancer

EB1 protein alteration characterizes sporadic but not ulcerative colitis associated colorectal cancer

Histologic Features with Predictive Value for Outcome of Patients with Ulcerative Colitis

The role of the Glucocorticoid Receptor in intestinal inflammation and tumorigenesis in a murine model of colitis and colitis-associated colorectal cancer

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