Inflammatory bowel disease and colon cancer

Levin, Bernard

doi:10.1002/1097-0142(19920901)70:3+<1313::aid-cncr2820701518>3.0.co;2-b

Cited by 61 publications

(38 citation statements)

References 22 publications

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“…[1][2][3] Recent studies suggest a cumulative incidence of carcinoma of about 5-10% at 20 years and 12-20% at 30 years from the onset of UC. 4) UC-associated neoplasia (UCAN) consists of dysplasia limited to the mucosal layer and invasive carcinomas. Dysplasia is subdivided into high-grade dysplasia (HGD), low-grade dysplasia (LGD), and indefinite dysplasia (IND) according to the histological grade.…”

supporting

confidence: 63%

Genetic Alterations in Ulcerative Colitis‐associated Neoplasia Focusing on APC, K‐ras Gene and Microsatellite Instability

Umetani

Sasaki

Watanabe

et al. 1999

Japanese Journal of Cancer Research

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The status of genetic alterations in ulcerative colitis (UC)-associated neoplasia (UCAN) was investigated focusing on microsatellite instability (MSI) which is seen in a certain fraction of colorectal carcinomas, and adenomatous polyposis coli (APC) gene and K-ras gene, in which mutations occur in the early stage of sporadic colorectal tumorigenesis. Thirty-one UCAN from 15 UC patients who had undergone colorectal resection at our institution were investigated. There were 8 lesions of invasive carcinoma, 15 high-grade dysplasia (HGD) and 8 low-grade dysplasia (LGD). DNA was extracted from each neoplastic lesion and corresponding non-neoplastic tissue by a microdissection method. MSI status at 9 microsatellite loci, loss of heterozygosity (LOH) at the APC locus, and Kras codon 12 point mutation were examined. As for MSI, 4/31 (13%) UCAN (carcinoma: 1/8 (13%), HGD: 2/15 (13%), LGD: 1/8 (13%)) were MSI-high (3 or more unstable loci) and 12/31 (39%) UCAN (carcinoma: 3/8 (38%), HGD: 6/15 (40%), LGD: 3/8 (38%)) were MSI-low (1 or 2 unstable loci). LOH at the APC locus was not found in 9 UCAN from 6 informative (heterozygous) cases. The K-ras mutation rate of UCAN was 3/31 (9.7%) (carcinoma: 2/8 (25%), HGD: 1/15 (7%) and LGD: 0/8). MSI is relatively common in UCAN and is present at the early stage of tumorigenesis of UCAN, while the involvement of genetic alterations of the APC gene and K-ras gene is small. MSI may be one of the mechanisms of the increased neoplastic risk in UC, and UCAN may develop through a different carcinogenic pathway from sporadic carcinomas.

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supporting

confidence: 63%

Genetic Alterations in Ulcerative Colitis‐associated Neoplasia Focusing on APC, K‐ras Gene and Microsatellite Instability

Umetani

Sasaki

Watanabe

et al. 1999

Japanese Journal of Cancer Research

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“…We first fit a model (model 1) adjusted for age (41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60), and >60 years) only. For multivariable analyses (model 2), we additionally included sociodemographic factors, including gender, race-ethnicity (non-Hispanic white, non-Hispanic black, Mexican-American, other), level of education (less than high school, high school or more), annual family income (<$20,000, $20,000), and lifestyle-related variables, including body mass index (BMI; <25, 25-29.9, and 30 kg/m 2 ), pack-years of smoking, serum cotinine levels, alcohol consumption (g/day), and physical activity (more active, less active or about the same compared with others of same age).…”

Section: Discussionmentioning

confidence: 99%

C-Reactive Protein and Colorectal Cancer Mortality in U.S. Adults

Goyal¹,

Terry

Jin

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Chronic inflammation has been associated with colorectal cancer. Prediagnostic levels of C-reactive protein (CRP), a highly sensitive marker of inflammation, have been weakly associated with increased colorectal cancer incidence, but few data are available examining its relationship with colorectal cancer mortality.Methods: In the Third National Health and Nutrition Examination Survey (NHANES III), 65% of the 15,924 adult participants had CRP levels 0.21 mg/dL. Using this as the reference group, we calculated hazard ratios (HR) for higher CRP categories and colorectal cancer mortality, and compared them with HRs for other mortality causes.Results: Over a median follow-up period of 14.2 years, there were 92 deaths from colorectal cancer. Compared with the reference group, multivariable adjusted HRs for colorectal cancer mortality were 2.66 [95% confidence interval (CI), 1.36-5.20] for CRP levels 0.22-0.50 mg/dL; 3.40 (95% CI, 1.48-7.77) for levels 0.51-1.00 mg/dL; and 3.96 (95% CI, 1.64-9.52) for levels >1.00 mg/dL. Estimates for colorectal cancer mortality did not change appreciably after excluding deaths within the first 3 years or by limiting follow-up to 5 or 10 years.Conclusions: In a large representative study of U.S. adults, we observed strong dose-response associations between CRP levels and colorectal cancer mortality.Impact: Further evaluation of CRP may help identify high-risk groups for colorectal cancer screening and those who might benefit most from prophylactic anti-inflammatory therapy. Cancer Epidemiol Biomarkers Prev; 23(8); 1609-18. Ó2014 AACR.

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“…It was revealed that IBD patients with proctitis and proctosigmoiditis are at the lowest risk of CACRC and the higher risk is combined with left-sided colitis and pan-colitis [15,16].…”

Section: Risk Factors In Cacrcmentioning

confidence: 99%