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      Cytochrome P450 monooxygenase/soluble epoxide hydrolase-mediated eicosanoid pathway in colorectal cancer and obesity-associated colorectal cancer

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          Abstract

          Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related deaths in the United States. Furthermore, it is well established that obese individuals have high risks of developing CRC, and obesity-associated CRC represents an unmet medical problem in the United States. Using a metabolomics approach, our recent research supports that the cytochrome P450 (CYP) monooxygenase/soluble epoxide hydrolase (sEH)-mediated eicosanoid pathway could play critical roles in the pathogenesis of CRC and obesity-associated CRC. Here in this review, we discuss recent studies about the roles of the CYP/sEH eicosanoid pathway in the pathogenesis of these diseases.

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          Most cited references 34

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          Wnt signalling and its impact on development and cancer.

          The Wnt signalling pathway is an ancient system that has been highly conserved during evolution. It has a crucial role in the embryonic development of all animal species, in the regeneration of tissues in adult organisms and in many other processes. Mutations or deregulated expression of components of the Wnt pathway can induce disease, most importantly cancer. The first gene to be identified that encodes a Wnt signalling component, Int1 (integration 1), was molecularly characterized from mouse tumour cells 25 years ago. In parallel, the homologous gene Wingless in Drosophila melanogaster, which produces developmental defects in embryos, was characterized. Since then, further components of the Wnt pathway have been identified and their epistatic relationships have been defined. This article is a Timeline of crucial discoveries about the components and functions of this essential pathway.
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            Celecoxib for the prevention of sporadic colorectal adenomas.

            Studies showing that drugs that inhibit cyclooxygenase-2 (COX-2) reduce the number of colorectal adenomas in animals and patients with familial adenomatous polyposis suggest that COX-2 inhibitors may also prevent sporadic colorectal neoplasia. We randomly assigned patients who had adenomas removed before study entry to receive placebo (679 patients) or 200 mg (685 patients) or 400 mg (671 patients) of celecoxib twice daily. Randomization was stratified for the use of low-dose aspirin. Follow-up colonoscopies were performed at one and three years after randomization. The occurrence of newly detected colorectal adenomas was compared among the groups with the life-table extension of the Mantel-Haenszel test. Follow-up colonoscopies were completed at year 1 in 89.5 percent of randomized patients, and at year 3 in 75.7 percent. The estimated cumulative incidence of the detection of one or more adenomas by year 3 was 60.7 percent for patients receiving placebo, as compared with 43.2 percent for those receiving 200 mg of celecoxib twice a day (risk ratio, 0.67; 95 percent confidence interval, 0.59 to 0.77; P<0.001) and 37.5 percent for those receiving 400 mg of celecoxib twice a day (risk ratio, 0.55; 95 percent confidence interval, 0.48 to 0.64; P<0.001). Serious adverse events occurred in 18.8 percent of patients in the placebo group, as compared with 20.4 percent of those in the low-dose celecoxib group (risk ratio, 1.1; 95 percent confidence interval, 0.9 to 1.3; P=0.5) and 23.0 percent of those in the high-dose group (risk ratio, 1.2; 95 percent confidence interval, 1.0 to 1.5; P=0.06). As compared with placebo, celecoxib was associated with an increased risk of cardiovascular events (risk ratio for the low dose, 2.6; 95 percent confidence interval, 1.1 to 6.1; and risk ratio for the high dose, 3.4; 95 percent confidence interval, 1.5 to 7.9). These findings indicate that celecoxib is an effective agent for the prevention of colorectal adenomas but, because of potential cardiovascular events, cannot be routinely recommended for this indication. (ClinicalTrials.gov number, NCT00005094 [ClinicalTrials.gov].). Copyright 2006 Massachusetts Medical Society.
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              Obesity and risk of colorectal cancer: a meta-analysis of 31 studies with 70,000 events.

              Colorectal cancer is the second most common cause of death and illness in developed countries. Previous reviews have suggested that obesity may be associated with 30% to 60% greater risk of colorectal cancer, but little consideration was given to the possible effect of publication bias on the reported association. Relevant studies were identified through EMBASE and MEDLINE. Studies were included if they had published quantitative estimates of the association between general obesity [defined here as body mass index (BMI) > or = 30 kg/m(2)] and central obesity (measured using waist circumference) and colorectal cancer. Random-effects meta-analyses were done, involving 70,000 cases of incident colorectal cancer from 31 studies, of which 23 were cohort studies and 8 were case-control studies. After pooling and correcting for publication bias, the estimated relative risk of colorectal cancer was 1.19 [95% confidence interval (95% CI), 1.11-1.29], comparing obese (BMI > or = 30 kg/m(2)) with normal weight (BMI <25 kg/m(2)) people; and 1.45 (95% CI, 1.31-1.61), comparing those with the highest, to the lowest, level of central obesity. After correcting for publication bias, the risk of colorectal cancer was 1.41 (95% CI, 1.30-1.54) in men compared with 1.08 (95% CI, 0.98-1.18) for women (P(heterogeneity) <0.001). There was evidence of a dose-response relationship between BMI and colorectal cancer: for a 2 kg/m(2) increase in BMI, the risk of colorectal cancer increased by 7% (4-10%). For a 2-cm increase in waist circumference, the risk increased by 4% (2-5%). Obesity has a direct and independent relationship with colorectal cancer, although the strength of the association with general obesity is smaller than previously reported.
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                Author and article information

                Journal
                Oncoscience
                Oncoscience
                Oncoscience
                ImpactJ
                Oncoscience
                Impact Journals LLC
                2331-4737
                September 2019
                23 August 2019
                : 6
                : 9-10
                : 371-375
                Affiliations
                1 Department of Food Science, University of Massachusetts, Amherst, MA, USA
                2 Molecular and Cellular Biology Program, University of Massachusetts, Amherst, MA, USA
                Author notes
                Correspondence to: Guodong Zhang, guodongzhang@ 123456umass.edu
                Article
                488
                10.18632/oncoscience.488
                6855364
                © 2019 Zhang et al.

                This article is distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.

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