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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Introducción: El SII se caracteriza por la presencia de dolor abdominal, diarrea, estreñimiento, o la alternancia de ambas, la causa de esta patología tiene que ver con muchos factores: alimentación, antecedentes de enfermedades, estilo de vida, etc. En el Hospital Guillermo Almenara Irigoyen (HGAI), se desconoce la prevalencia del SII. Objetivos: Determinar la prevalencia del SII en la consulta ambulatoria del servicio de Gastroenterología del HGAI, así como también describir los subtipos de SII que se presentan. Material y Métodos: El presente estudio es de tipo descriptivo y de corte transversal. La muestra consta de 1365 pacientes, se utilizo el muestreo por conveniencia. Se confecciono una encuesta ad hoc, con dos partes: una ficha de recolección de datos (clínicos y sociodemográficos) y otra con los criterios de ROMA II para el diagnostico de SII. Los pacientes fueron encuestados en la sala de espera de los dos (02) consultorios ambulatorios del Servicio de Gastroenterología (SG) del HGAI, del 06 de Abril del 2003 al 06 de Junio del 2003. Se realizo el análisis estadístico con el programa SPSS v11, para la descripción de los resultados. Resultados: La prevalencia del SII en el SG del HGAI fue de 38.8%. De los pacientes con SII de acuerdo a los criterios de Roma II tenemos; el 44% presento SII tipo diarrea, el 32% fue tipo estreñimiento, el 19% fue tipo mixto y el 5% no se pudo determinar. De la prevalencia general de 38.8 %, el sexo femenino aportó una prevalencia del 26.5%, y el sexo masculino aporto una prevalencia del 12.2 %. La variable Sexo fue significativa, por lo que la probabilidad de que el diagnostico de SII se relaciona mas con el sexo femenino. Por lo que existiría un riesgo de 1.8 veces en el sexo femenino de tener el SII en relación al sexo masculino. El grupo etareo de 60 a 69 años es el que presenta la mayor prevalencia en el diagnostico de SII (10.2%). El grupo de edad de 50 años hacia delante presenta una prevalencia acumulada de 28.8%. Asimismo se encontraron hallazgos secundarios con las variables que tuvieron significancia estadística las cuales fueron: Sexo, Grupo etareo, Diabetes Mellitus (DM), Antecedente de Cirugía Pélvica y Antecedente personal de Cáncer gastrointestinal. Conclusión: Existe una alta prevalencia del SII (38.8%) en la población estudiada, siendo el SII de tipo Diarrea el más frecuente. El grupo de edad de 50 años hacia delante presenta una prevalencia acumulada de 28.8%. / Tesis de segunda especialidad

No description available.

京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第17815号 / 医博第3813号 / 新制||医||999(附属図書館) / 30630 / 京都大学大学院医学研究科医学専攻 / (主査)教授 松田 道行, 教授 野田 亮, 教授 藤田 潤 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

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

La expresión de hemoxigenasa 1 (HO-1) ha demostrado estar sobre-regulada en el cáncer colorrectal (CCR), pero el papel que desempeña en este tipo de cáncer aún no se ha dilucidado. Los objetivos de este estudio han sido analizar la expresión de HO-1 en CCR invasivo humano, evaluar su correlación con parámetros clínicos -histopatológicos e investigar los mecanismos por los cuales la enzima influye en la progresión tumoral. Se confirmó que HO-1 fue sobre-expresada en CCR invasivo humano y se encontró que la expresión de la enzima se asocia con un mayor tiempo de supervivencia global de los pacientes. Además, se observó, en un modelo de CCR en ratas inducido químicamente con 1,2-dimetilhidrazina que la expresión total y nuclear de HO-1 aumenta con la progresión tumoral. El estudio de los mecanismos implicados en la acción de la HO-1 en CCR demostró que la proteína reduce la viabilidad celular a través de la inducción de la detención del ciclo celular y de la apoptosis; y que se requiere la proteína supresora de tumores p53 funcional para estos efectos. Esta reducción en la viabilidad celular se acompaña por la modulación de los niveles de p21, p27, ciclina D1, Bax, uPARP y por la modulación de las vías de caspasa-3, Akt y PKC´s. También, en modelos animales murinos, se demostró que la modulación genética y farmacológica de HO-1 reduce la tasa de crecimiento y la carga tumoral cuando p53 se encuentra en su estado salvaje. En adición, se observó que la sobre-expresión de HO-1 reduce la migración e invasión celular. En conclusión, estos resultados demuestran un papel antitumoral de HO-1 apuntando a la importancia de la condición de p53 en esta actividad antitumoral. / The expression of heme oxygenase-1 (HO-1) was shown to be up-regulated in colorectal cancer (CRC), but the its role in this type of cancer has not yet been elucidated. The objectives of this study were to analyze the expression of HO-1 in human invasive CRC, to evaluate its correlation with clinical-histopathological parameters and to investigate the mechanisms by which the enzyme affects tumor progression. It was confirmed that HO-1 was over-expressed in invasive human CRC and was found that the expression of the enzyme is associated with an increased overall survival time of patients. Furthermore, it was observed in a chemical animal model of CRC induced in rats with 1,2-dimethylhydrazine that the total and the nuclear expression of HO-1 increased with tumor progression. The study of the mechanisms involved in the action of HO-1 protein in CRC, showed that the protein reduces cell viability through induction of cell cycle arrest and apoptosis; and functional suppressor protein p53 is required for this purpose. This reduction in cell viability is accompanied by modulation of the levels of p21, p27, cyclin D1, Bax, uPARP and modulation of caspase-3, Akt and PKC's pathways. Also, in animal murine models, it was demonstrated that genetic and pharmacological modulation of HO-1 reduces the rate of growth of tumors and the tumor load when wild type p53 is present. In addition, we observed that overexpression of HO-1 decreases migration and cell invasion. Altogether, this results show an antitumor role of HO-1 pointing to the importance of p53 status with its antitumor activiy.

Deep-frying is now a popular cooking method all over the world due to its low cost and time-saving property. It also provides special and likeable flavor, helps prolong shelf lives of commercial products, and offering food products of stable quality. However, by- products formed during the frying process, such as malonaldehyde, were shown to be harmful to human health. Such compounds can be taken in when having fried foods, potentially inducing or promoting some diseases. However, there is limited research studying the direct effects of frying oil consumption on cancer. In order to have a better understanding of the effects on cancer by frying oil, we used a well-established AOM/DSS- induced colon cancer animal model to study the impact by frying oil. After 10-week treatment with diet containing deep-frying oil (3.8% in diet) or with un-oxidized oil (10% in diet), the mice showed enhanced tumorigenesis in colon, where the total tumor burden significantly increased (4.5 ± 1.9 mm2 for the treatment group, compared with 0.5 ± 0.5 mm2 for the control group, P < 0.05). Also, the expression of pro-inflammatory and pro- tumorigenic cytokines (Mcp-1, Inf-γ, Il-6, Il-1β, Myc, Axin2 and Vegf) were increased in the mice treated with frying oil diets. Together the results showed that consumption of deep-frying oil promoted the colorectal cancer in mice, providing more detailed information for health instruction.