This study was conducted to determine the distributions of the polyp detection rate (PDR) and the adenoma detection rate (ADR) according to age by analyzing the polypectomy results.
A total of 10,098 patients who underwent a colonoscopy in 2013 were included in this study. Chi-square and logistic regression statistical analyses were performed using SPSS ver. 19.
The mean age of the patients was 52.7 years old (median, 54 ± 12.52 years; range, 14 to 92 years). A total of 6,459 adenomatous polyps (61.7%) from a total of 10,462 polyps were eliminated. The PDR was 50.9% (5,136/10,098), and the. ADR was 35.4% (3,579/10,098). The male-to-female ratio was 51.3%:48.7%, with a male-to-female ADR ratio of 42.8% : 27.7% (P < 0.001). In the age distribution, the values of the ADR were 0% for patients in their 10's, 6.3% for those in their 20's, 14.0% for those in their 30's, 28.7% for those in their 40's, 38.4% for those in their 50's, 46.2% for those in their 60's, 55.8% for those in their 70's, 56.1% for those in their 80's, and 33.3% for those in their 90's. In males, the values of the ADR were 0%, 9.1%, 17.1%, 37.8%, 48.2%, 53.6%, 61.7%, 59.1%, and 33.3% for the same age distribution, and a steep increase was found between patients in their 30's and patients in their 40's. Significant (P < 0.001) factors influencing the ADR included sex, previous colonoscopy experience, polypectomy method, and age of more than 40 years.
In considering the adenoma carcinoma sequence, 28.7% of people, especially 37.8% of males in their 40's showed adenomatous polyps. Whether an earlier first-time colonoscopy will have better results in preventing colorectal cancer should be investigated and discussed.
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Evidence that indicates bile acid is a promoter of colon cancer exists. Deoxycholic acid (DCA) modifies apoptosis or proliferation by affecting intracellular signaling and gene expression. However, because previous studies have been based on studies on colon cancer cell lines, the effect of DCA on normal colonocytes is unknown.
Normal colonocytes and Caco-2 and HCT116 cells were treated with 20 µM and 250 µM of DCA, and the effect of different concentrations of DCA was measured based on the expression of cell-cycle-related proteins by using Western blots.
The expressions of CDK2 and cyclin D1 for different concentrations of DCA in normal colonocytes and colon cancer cells were similar, but the expressions of cyclin E and A were significantly different. In HCT116 colon cancer cells, the expression of cyclin E increased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin E was not changed or decreased. In HCT116 colon cancer cells, the expression of cyclin A was not changed or decreased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin A was increased at a DCA concentration of 20 µM.
The effect of DCA on stimulating cell proliferation suggests that DNA synthesis is stimulated by an increased expression of cyclin E in colon cancer cells. Our results suggest that a low dose of DCA induces cellular proliferation through increased expression of cyclin A and that a high dose of DCA induces decreased expression of cyclin E and CDK2 in normal colonocytes.
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