Background: Recurrent prostate cancer can be osseous, androgen independent and lethal. The purpose is to discern the efficacy of synthetic small molecule telomerase enzyme inhibitors (TEI) alone or in combination with other cytotoxic therapies in controlling metastatic osseous prostate cancer.
Methods: C4-2B was pre-treated with a match or mismatch TEI for 6 weeks and then inoculated into nude mice subcutaneously or intraosseously.
Objective: We used a population-based cancer registry to examine the association between lymph node counts and mortality to determine the minimum number of lymph nodes that should be examined as part of esophageal resection.
Methods: Using the Surveillance Epidemiology and End Results database, we identified patients who had an esophagectomy for invasive esophageal carcinoma from 1988 through 2005 and who had a known number of lymph nodes examined pathologically. After stratifying patients (0, 1-11, 12-29, and 30 or more lymph nodes examined) based on a recursive partitioning analysis, we assessed the association between lymph nodes counts and mortality using the Kaplan-Meier method.
Objectives: Describe the type-specific prevalence of anal HPV infection in women with lower genital tract intraepithelial neoplasia and cancer. Describe the prevalence of abnormal anal cytology and identify risk factors for anal HPV infection and abnormal anal cytology in this population.
Methods: We performed a cross-sectional study of women attending 2 university-based colposcopy clinics with high-grade lower genital tract intraepithelial neoplasia or cancer.
Cancer Epidemiol Biomarkers Prev
June 2008
Background: The ratio of two nicotine metabolites, cotinine and trans-3'-hydroxycotinine (3-HC), has been validated as a method of phenotyping the activity of the liver enzyme cytochrome P450 (CYP) 2A6 and, thus, the rate of nicotine metabolism. Our objective was to evaluate the correlates and stability of the 3-HC to cotinine ratio in ad libitum and reducing smokers, using nicotine replacement therapy (NRT), over a period of months.
Methods: Smokers (n = 123, 94% Caucasian) participated in a smoking reduction study, where one-third of the sample smoked ad libitum for 8 weeks (Waitlist phase), before joining the rest of the participants for 12 weeks of cigarette reduction (Reduction phase) using NRT.
Objective: To investigate if an 8- to 12-hour time delay of primary repair affects anal incontinence at 1-year follow up.
Design: Randomised controlled trial.
Setting: University hospital in Sweden.
Acetaldehyde (AA) is the major metabolite of ethanol and may be responsible for an increased gastrointestinal cancer risk associated with alcohol beverage consumption. Furthermore, AA is one of the most abundant carcinogens in tobacco smoke and induces tumors of the respiratory tract in laboratory animals. AA binding to DNA induces Schiff base adducts at the exocyclic amino group of dG, N2-ethylidene-dG, which are reversible on the nucleoside level but can be stabilized by reduction to N2-ethyl-dG.
View Article and Find Full Text PDFN'-Nitrosonornicotine (NNN) is one of the most abundant strong carcinogens in unburned tobacco and cigarette smoke and is classified by the International Agency for Research on Cancer as carcinogenic to humans. Human exposure to NNN mainly occurs upon use of tobacco products. It is also possible that additional amounts of NNN are formed endogenously.
View Article and Find Full Text PDFObjective: To compare nicotine pharmacokinetics and subjective effects of three new smokeless tobacco potential reduced exposure products (PREPs; Ariva, Revel and Stonewall) with moist snuff (Copenhagen) and medicinal nicotine (Commit lozenge).
Methods: 10 subjects completed a randomised, within-subject, crossover study. Subjects used one product for 30 min at each of the five laboratory sessions.
The hypothesis that interindividual differences among smokers in the metabolism of polycyclic aromatic hydrocarbons (PAH) are related to lung cancer risk has been extensively investigated in the literature. These studies have compared lung cancer risk in groups of smokers with or without polymorphisms in genes involved in PAH metabolism. We believe that carcinogen metabolite phenotyping, involving the actual measurement of PAH metabolites, would be a better way to investigate differences in lung cancer risk.
View Article and Find Full Text PDFThere are major interindividual differences in carcinogenic polycyclic aromatic hydrocarbon (PAH) metabolism in humans, and it has been hypothesized that these differences may be related to cancer risk in smokers and other exposed people. One important pathway of PAH metabolism involves the detoxification of the epoxide and diol epoxide metabolites by reaction with glutathione, catalyzed by glutathione-S-transferases (GSTs). Interindividual differences in these pathways have been examined by genotyping methods, investigating polymorphisms in GSTM1 and GSTP1.
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