Thesis (M.S.)--Boston University / This study was designed to determine whether education, marital status, sex, age and religion are factors influencing the time lapse between onset of symptoms and the seeking of medical attention with cancer of the colon.

TITLE: Racial disparities associated with colon cancer screening in a nationally representative sample; A cross-sectional study AUTHOR INFO Yorandos Tafesse MD1 Manik Ahuja PhD, MA1 Author Affiliations: 1College of Public Health, East Tennessee State University, Johnson City, TN 37614, United States Colon cancer impacts nearly 2 million individuals in the U.S. each year. Early detection of colon cancer using colonoscopy can reduce the risk of mortality. The United States Preventive Services Task Force (USPSTF) recommends routine screening for colon cancer for all adults 50 to 75 years of age. Colon cancer screening behavior is different across a variety of predictor variables. Previous studies have identified older age, male gender, higher education, higher income, marriage, and the presence of chronic diseases to be associated with increased odds of colon cancer screening. However, less is known about the role of racial differences in screening. This study aims to determine if colon cancer screening rates are different between Whites and racial minorities in the United States controlling for potential confounders. This research can help bridge the existing gap on this topic and aid in identifying high-risk racial groups that could be targeted by future intervention strategies. We used cross-sectional data from the 2019 Behavioral Risk Factor Surveillance System, a nationally representative U.S. telephone-based survey of adults aged 18 years or older. We extracted data for adults age 50 or older (n=10,972). Logistic regression analyses were conducted to test the association between race and colon cancer screening. We also included chronic disease status, alcohol use, smoking, gender, and age in our model. Chronic disease status was coded as self-report 2 or more, 1 and 0 chronic diseases (referent), which included the summation of heart disease, hypertension, COPD, and diabetes. Overall, colon cancer screening is as follows among Whites (77.2%), Blacks (72.4%), Asian (60.1%), American Indian/Alaska Native (69.7%), and Hispanic (68.6%). Logistic regression results revealed that having 2 or more chronic diseases (OR=1.73; 95% CI 1.53,1.96), 1 chronic disease (OR=1.45; 95% CI 1.31,1.65), and female gender (OR=1.14; 95% CI 1.04,1.23) were associated with higher odds of screening. Race/ethnic minority status (OR=0.72; 95% CI 0.65, 0.81), low income (OR=0.64; 95% CI 0.57,0.70), and less than high school education (OR=0.71; 95% CI 0.59,0.84) were associated with lower odds of screening. Our research showed that racial minorities have lower odds of colon cancer screening after adjusting for gender, age, chronic diseases, income, and education status. Preventive practices should focus on increasing awareness on and availability of colon cancer screening means to racial minorities in the United States. Further research on the association between race and other screening modalities will help maximize the impacts of targeted interventions.

Colorectal cancer is the second most common cause of cancer deaths in the United States. Vitamin E (VE) and other antioxidants may help prevent colon cancer by decreasing the formation of mutagens arising from the free radical oxidation of fecal lipids or by "non-antioxidant" mechanisms. VE is not a single molecule, but refers to at least eight different molecules, that is, four tocopherols and four tocotrienols. Methods: Both animal models and human colon cancer cell lines were used to evaluate the chemopreventive potential of different forms of VE. Rats were fed diets deficient in tocopherols or supplemented with either α-tocopherol or γ-tocopherol. Half the rats in each of these groups received normal levels of dietary Fe and the other half Fe at eight times the normal level. In our cell experiments, we looked at the role of γ-tocopherol in upregulating peroxisome proliferator-activated receptor-γ (PPAR-γ) in the SW 480 human cell line. Results: Rats fed the diets supplemented with α-tocopherol had higher levels of VE in feces, colonocytes, plasma, and liver than did rats fed diets supplemented with γ-tocopherol. Dietary Fe levels did not influence tocopherol levels in plasma, liver, or feces. For colonocytes, high dietary Fe decreased tocopherol levels. Rats fed the γ-tocopherol-supplemented diets had lower levels of fecal lipid hydroperoxides than rats fed the α-tocopherol-supplemented diets. Ras-p21 levels were significantly lower in rats fed the γ-tocopherol-supplemented diets compared with rats fed the α-tocopherol-supplemented diets. High levels of dietary Fe were found to promote oxidative stress in feces and colonocytes. Our data with the SW480 cells suggest that both α- and γ-tocopherol upregulate PPAR-γ mRNA and protein expression, γ-tocopherol was, however, found to be a better enhancer of PPAR-γ expression than α-tocopherol at the concentrations tested.

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Final publication is available at http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=26018088 / 京都大学 / 0048 / 新制・課程博士 / 博士(医科学) / 甲第19635号 / 医科博第73号 / 新制||医科||6(附属図書館) / 32671 / 京都大学大学院医学研究科医科学専攻 / (主査)教授 妹尾 浩, 教授 渡邊 直樹, 教授 椛島 健治 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

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Sphingolipid metabolites play a role in the initiation and perpetuation of inflammatory responses. Since intestinal inflammation is a driving force in the development of colon cancer, in the present study, we investigated the suppression of dextran sodium sulfate (DSS)-induced colitis by dietary sphingomyelin in mice that lack functional peroxisome proliferator-activated receptor γ (PPAR-γ) in intestinal epithelial and immune cells. Dietary spingomyelin decreased colonic inflammation in mice of both genotypes but more efficiently in mice expressing PPAR-γ. Using a real-time polymerase chain reaction array, we detected an up-regulation in genes involved in Th1 (interferon γ) and Th17 (interleukin [IL]-17 and IL-23) responses despite the reduced inflammation. However, the genes involved in Th2 (IL-4, IL-13 and IL-13ra2) and Treg (IL-10rb) anti-inflammatory responses were up-regulated in a PPAR-γ-dependent manner. In order to direct mechanistic studies of how PPAR-γ expression is involved in SM-induced suppression of DSS colitis, we investigated the effect of dietary SM in DSS-treated mice that lack PPAR-γ in the CD4+ T-cells. While the pathogenesis of colitis was independent of PPAR-γ expression in CD4+ T-cells, dietary SM decreased disease activity and colonic inflammation in mice of both genotypes but more efficiently in mice expressing PPAR-γ, indicating both PPAR-γ dependent and independent signaling pathways. In conclusion, in contrast to endogenous sphingolipid metabolites, dietary SM modulated both pro- and anti-inflammatory responses at the early stages of the disease in a partially PPAR-γ dependent manner resulting in a suppression of inflammation that may be critical for the suppression of inflammation-driven colon cancer. / Master of Science