Biomedical subjects

Susan T Mayne

Publications and source records attributed to Susan T Mayne.

33 records · Page 2Linked to original sources

PubMed2004

Nonsteroidal anti-inflammatory drug use associated with reduced incidence of adenocarcinomas of the esophagus and gastric cardia that overexpress cyclin D1: a population-based study.

This study was undertaken to determine whether selected risk factors for esophageal and gastric cancer are associated with tumors that overexpress cyclin D1. Archived tumor tissue was available for 630 esophageal and gastric cancer patients who participated in a population-based case-control study. Patients were categorized into case groups based on whether protein overexpression of the cyclin D1 gene, as assessed by immunohistochemistry, was present (cyclin D1+, n = 285) or not (cyclin D1-, n = 345) in the tumor. The distribution of risk factors in each of these case groups was then compared with the distribution among the 695 controls. Multivariate-adjusted odds ratios (OR) for esophageal adenocarcinoma were reduced in relation to use of aspirin and other nonsteroidal anti-inflammatory drug (NSAID) use but only among patients with cyclin D1+ tumors (0.45, 95% confidence interval [CI] = 0.26, 0.79) and not among those with cyclin D1- tumors (1.12, 95% CI = 0.67, 1.86). A similar pattern was observed for gastric cardia adenocarcinomas. In contrast, ORs for esophageal squamous cell carcinoma and noncardia gastric adenocarcinomas in relation to NSAID use were reduced, regardless of cyclin D1 status. ORs did not vary with cyclin D1 status in relation to alcohol, body size, or cigarette smoking, with the following exception; for noncardia gastric adenocarcinomas the cyclin D1- tumors showed a 2-fold elevation in the OR with ever smoking. These data suggest that the reduction in risk associated with NSAID use may be restricted to those esophageal and gastric cardia adenocarcinomas that overexpress cyclin D1.

Adenocarcinoma↗

PubMed2004

Supplemental beta-carotene, smoking, and urinary F2-isoprostane excretion in patients with prior early stage head and neck cancer.

Supplemental beta-carotene has been shown to increase lung cancer risk in recent chemoprevention trials, especially in current smokers. Several possible mechanisms for this effect have been suggested based upon in vitro and animal studies, but mechanistic data from human studies to explain the excess risk are lacking. beta-Carotene has both antioxidant and prooxidant effects in vitro; therefore, we evaluated whether or not high-dose supplemental beta-carotene might have prooxidant effects in vivo, especially in current smokers taking high-dose supplemental beta-carotene for several years (median 4.0 yr). Urine samples (n = 55 total) were collected from both smokers and nonsmokers participating in a multiyear randomized chemoprevention trial of supplemental beta-carotene (50 mg/day) versus placebo. Samples were analyzed by GC/MS for total isoprostanes and for 8-iso-prostaglandin F2 (8-iso-PGF2), stable end products of lipid peroxidation in vivo. Smokers had higher levels of both total isoprostanes and 8-iso-PGF2. Smokers and nonsmokers randomized to beta-carotene had nonsignificantly lower concentrations of total isoprostanes and of 8-iso-PGF2 [mean +- SD 8-iso-PGF2/ml = 2.00 +- 1.72 (placebo smoker); 1.72 +- 1.66 (beta-carotene smoker); 1.22 +- 0.68 (placebo nonsmoker); 0.97 +- 0.62 (beta-carotene nonsmoker)]. These results indicate that supplemental beta-carotene, even when given at high doses for many years, does not have prooxidant effects in either smokers or nonsmokers, as measured by urinary excretion of F2-isoprostanes.

Adult↗

PubMed2003

Population attributable risks of esophageal and gastric cancers.

BACKGROUND: Several risk factors have been identified for esophageal adenocarcinoma, gastric cardia adenocarcinoma, esophageal squamous cell carcinoma, and noncardia gastric adenocarcinoma, but no study has comprehensively examined their contributions to the cancer burden in the general population. Herein, we estimate the population attributable risks (PARs) for various risk factors observed in a multicenter population-based case-control study. METHODS: We calculated PARs by using 293 patients with esophageal adenocarcinoma, 261 with gastric cardia adenocarcinoma, 221 with esophageal squamous cell carcinoma, 368 with noncardia gastric adenocarcinoma, and 695 control subjects. We included smoking for all four tumor types and Helicobacter pylori infection for noncardia gastric adenocarcinoma as established causal risk factors as well as several other factors for which causality is under evaluation. RESULTS: Ever smoking, body mass index above the lowest quartile, history of gastroesophageal reflux, and low fruit and vegetable consumption accounted for 39.7% (95% confidence interval [CI] = 25.6% to 55.8%), 41.1% (95% CI = 23.8% to 60.9%), 29.7% (95% CI = 19.5% to 42.3%), and 15.3% (95% CI = 5.8% to 34.6%) of esophageal adenocarcinomas, respectively, with a combined PAR of 78.7% (95% CI = 66.5% to 87.3%). Ever smoking and body mass index above the lowest quartile were responsible for 45.2% (95% CI = 31.3% to 59.9%) and 19.2% (95% CI = 4.9% to 52.0%) of gastric cardia adenocarcinomas, respectively, with a combined PAR of 56.2% (95% CI = 38.1% to 72.8%). Ever smoking, alcohol consumption, and low fruit and vegetable consumption accounted for 56.9% (95% CI = 36.6% to 75.1%), 72.4% (95% CI = 53.3% to 85.8%), and 28.7% (95% CI = 11.1% to 56.5%) of esophageal squamous cell carcinomas, respectively, with a combined PAR of 89.4% (95% CI = 79.1% to 95.0%). Ever smoking, history of gastric ulcers, nitrite intake above the lowest quartile, and H. pylori infection were responsible for 18.3% (95% CI = 6.5% to 41.8%), 9.7% (95% CI = 5.4% to 16.8%), 40.7% (95% CI = 23.4% to 60.7%), and 10.4% (95% CI = 0.3% to 79.6%) of noncardia gastric adenocarcinomas, respectively, with a combined PAR of 59.0% (95% CI = 16.2% to 91.4%). CONCLUSION: In this population, a few known risk factors account for a majority of esophageal and gastric cancers. These results suggest that the incidence of these cancers may be decreased by reducing the prevalence of smoking, gastroesophageal reflux, and being overweight and by increasing the consumption of fruits and vegetables.

Adenocarcinoma↗

PubMed2003

Serum selenium and risk of prostate cancer in U.S. blacks and whites.

Prostate cancer is the fourth most common cancer in men worldwide and the most common cancer in men in the United States, with reported incidence rates for U.S. blacks being the highest in the world. The etiology of prostate cancer and an explanation for the racial disparity in incidence in the United States remain elusive. Epidemiologic studies suggest that selenium, an essential trace element, may protect against the disease. To further explore this hypothesis, we measured serum selenium in 212 cases and 233 controls participating in a multicenter, population-based case-control study that included comparable numbers of U.S. black and white men aged 40-79 years. Serum selenium was inversely associated with risk of prostate cancer (comparing highest to lowest quartiles, OR = 0.71, 95% CI 0.39-1.28; p for trend = 0.11), with similar patterns seen in both blacks and whites. Cubic regression spline analysis of continuous serum selenium indicated a reduced risk of prostate cancer above concentrations of 0.135 microg/ml (median among controls) compared to a reference value set at the median of the lowest selenium quartile. Because both the selenoenzyme GPX and vitamin E can function as antioxidants, we also explored their joint effect. Consistent with other studies, the inverse association with selenium was strongest among men with low serum alpha-tocopherol concentrations. In conclusion, our results suggest a moderately reduced risk of prostate cancer at higher serum selenium concentrations, a finding that can now be extended to include U.S. blacks. Since selenium exposure varies widely throughout the world, further research on optimal concentrations for cancer prevention is justified.

Adult↗

PubMed2003

Increased risk of noncardia gastric cancer associated with proinflammatory cytokine gene polymorphisms.

BACKGROUND & AIMS: Genetic variations in proinflammatory and anti-inflammatory cytokine genes influence individual response to carcinogenic exposures. Polymorphisms in interleukin (IL)-1 beta and its endogenous receptor antagonist are associated with risk of Helicobacter pylori-related gastric cancer. The aim of this study was to evaluate the role of proinflammatory cytokine gene polymorphisms in gastric and esophageal cancers defined by anatomic subsite. METHODS: We assessed polymorphisms of the IL-1 gene cluster and 4 other cytokine genes in a population-based case-control study of upper gastrointestinal cancers, including gastric cardia (n = 126) and noncardia adenocarcinoma (n = 188), esophageal squamous cell carcinoma (n = 53), and adenocarcinoma (n = 108), and frequency-matched controls (n = 212). ORs for the different cancers were computed from logistic regression models adjusted for potential confounding factors. RESULTS: Proinflammatory genotypes of tumor necrosis factor alpha and IL-10 were each associated with more than doubling of the risk of noncardia gastric cancer. Carriage of multiple proinflammatory polymorphisms of IL-1B(o) IL-1 receptor antagonist, tumor necrosis factor A, and IL-10 conferred greater risk, with ORs (and 95% confidence intervals) of 2.8 (1.6-5.1) for one, 5.4 (2.7-10.6) for 2, and 27.3 (7.4-99.8) for 3 or 4 high-risk genotypes. In contrast, these polymorphisms were not consistently related to the risks of esophageal or gastric cardia cancers. Polymorphisms in IL-4 and IL-6 were not associated with any of the cancers studied. CONCLUSIONS: A proinflammatory cytokine genetic profile increases the risk of noncardia gastric adenocarcinoma but not other upper gastrointestinal cancers, possibly by inducing a hypochlorhydric and atrophic response to gastric H. pylori infection.

Aged↗

PubMed2003

Dietary carotenoids, vegetables, and lung cancer risk in women: the Missouri women's health study (United States).

OBJECTIVE: To examine the effect of specific dietary carotenoids and their primary plant food sources on lung cancer risk in a population-based case-control study of women. METHODS: Data were available for 587 incident primary lung cancer cases and 624 controls frequency matched to cases based on age. A modified version of the 100-item NCI-Block food-frequency questionnaire was used to obtain information concerning usual diet 2-3 years prior to interview. RESULTS: In models adjusted for age, total calorie intake, pack-years of smoking, and education, beta-carotene, beta-cryptoxanthin, lutein + zeaxanthin, and total carotenoid intake were each associated with a significantly lower risk of lung cancer. Several vegetable groups were predictive of lower lung cancer risk, particularly the frequency of total vegetable intake. Individual and total carotenoids were no longer significantly associated with lower lung cancer risk in models adjusted for total vegetable intake. However, total vegetable intake remained significantly inversely associated with risk in models adjusted for total carotenoids. CONCLUSIONS: These results indicate that consumption of a wide variety of vegetables has a greater bearing on lung cancer risk in a population of smoking and nonsmoking women than intake of any specific carotenoid or total carotenoids.

Aged↗

PubMed2003

Classification of dental caries patterns in the primary dentition: a multidimensional scaling analysis.

OBJECTIVE: Clinical patterns of early childhood caries (ECC) encompassing specific teeth or surfaces have been previously proposed on an a priori basis and have been used as case definitions. The underlying assumption is that the patterns result from different host response and environmental conditions. Identifying caries patterns has utility in refining case definitions of ECC. Well-defined caries patterns should enhance the ability of an analysis to identify meaningful associations between suspected risk factors and ECC. The purpose of this project was to identify patterns of caries in the dentition of preschool children using multidimensional scaling without a priori pattern delineation. METHODS: Between February 1994 and September 1995, five examiners visually examined 5171 Arizona preschool children aged 5-59 months old. Multidimensional scaling (MDS) was used as a classification/taxonomy technique to identify any underlying structure of the caries data. MDS provided a classification scheme for individual tooth surfaces based on the dissimilarity measures of squared Euclidean distance and of variance using an alscal analysis. Both two- and three-dimensional solutions were pursued; s-stress, stress, R-square and residual patterns were assessed in determining the best dimensional model, with the resulting quadrant positions of the tooth surfaces suggesting potential caries patterns. RESULTS: All models demonstrated excellent fit. Two- and three-dimensional solutions suggested four caries patterns: (i) any maxillary incisor surfaces, (ii) first molar occlusal surfaces, (iii) second molar pit and fissure surfaces, and (iv) any smooth surfaces, excluding the maxillary incisor surfaces. CONCLUSIONS: This is the first delineation of primary dentition caries patterns produced by a classification analysis without a priori pattern definitions. The identified caries patterns may arise from specific risk factors and/or be a function of the timing of various risk factor exposures. Use of these patterns as case definitions should enhance the ability to identify associations between suspected risk factors and ECC.

Child, Preschool↗

PubMed2003

Antioxidant nutrients and chronic disease: use of biomarkers of exposure and oxidative stress status in epidemiologic research.

Oxidation of lipid, nucleic acids or protein has been suggested to be involved in the etiology of several chronic diseases including cancer, cardiovascular disease, cataract, age-related macular degeneration and aging in general. A large body of research has investigated the potential role of antioxidant nutrients in the prevention of these and other chronic diseases. This review concentrates on the following antioxidant nutrients: beta-carotene and other carotenoids, vitamin E, vitamin C and selenium. The first part of the review emphasizes the utility of biological markers of exposure for these nutrients and the relationship to dietary intake data. The second part considers functional assays of oxidative stress status in humans including the strengths and limitations of various assays available for use in epidemiologic research. A wide variety of functional assays both in vivo and ex vivo, are covered, including various measures of lipid oxidation (thiobarbituric acid reactive substances, exhaled pentane/ethane, low-density lipoprotein resistance to oxidation, isoprostanes), DNA oxidation (oxidized DNA bases such as 8-OHdG, autoantibodies to oxidized DNA, modified Comet assay) and protein oxidation (protein carbonyls). Studies that have examined the effects of antioxidant nutrients on these functional markers are included for illustrative purposes. The review concludes with a discussion of methodologic issues and challenges for studies involving biomarkers of exposure to antioxidant nutrients and of oxidative stress status.

Antioxidants↗

PubMed2003

Dietary (n-3)/(n-6) fatty acid ratio: possible relationship to premenopausal but not postmenopausal breast cancer risk in U.S. women.

Recent research has suggested that an increased (n-3) fatty acid intake and/or increased (n-3)/(n-6) polyunsaturated fatty acid (PUFA) ratio in the diet is associated with a lower breast cancer risk. This case-control study investigated the association between intake of (n-3) and other fatty acids and the (n-3)/(n-6) PUFA ratio and breast cancer risk. After combining data from two related case-control studies in Connecticut, we had information available on a total of 1119 women (565 cases and 554 controls). Cases were all histologically confirmed, incident breast carcinoma patients. Controls were hospital-based (Yale-New Haven Hospital study site) and population-based (Tolland County study site). Information on dietary intake was obtained through a validated food-frequency questionnaire. Standard multivariate methods were used to address the independent effects of specific fatty acids, fat classes and macronutrients on breast cancer risk. In the full study population, there were no significant trends for any macronutrient/fatty acid when comparing the highest to the lowest quartile of intake. When the analysis was restricted to premenopausal women, consumption of the highest compared with the lowest quartile of the (n-3)/(n-6) PUFA ratio was associated with a nonsignificant 41% lower risk of breast cancer [odds ratio (OR) = 0.59, 95% confidence interval (CI) 0.29, 1.19, P for trend = 0.09]. A higher (n-3)/(n-6) PUFA ratio was significantly associated with a lower risk of breast cancer when the data were restricted to the Tolland County (population-based) study site; OR = 0.50, 95% CI 0.27, 0.95, P for trend = 0.02. These results are consistent with the hypothesis that a higher (n-3)/(n-6) PUFA ratio may reduce the risk of breast cancer, especially in premenopausal women.

Adult↗

PubMed2002

Dietary carotenoids, serum beta-carotene, and retinol and risk of lung cancer in the alpha-tocopherol, beta-carotene cohort study.

Findings from several beta-carotene supplementation trials were unexpected and conflicted with most observational studies. Carotenoids other than beta-carotene are found in a variety of fruits and vegetables and may play a role in this important malignancy, but previous findings regarding the five major carotenoids are inconsistent. The authors analyzed the associations between dietary beta-carotene, beta-carotene, lutein/zeaxanthin, lycopene, beta-cryptoxanthin, vitamin A, serum beta-carotene, and serum retinol and the lung cancer risk in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of male smokers conducted in southwestern Finland between 1985 and 1993. Of the 27,084 male smokers aged 50-69 years who completed the 276-food item dietary questionnaire at baseline, 1,644 developed lung cancer during up to 14 years of follow-up. Cox proportional hazards models were used to estimate relative risks and 95% confidence intervals. Consumption of fruits and vegetables was associated with a lower lung cancer risk (relative risk = 0.73, 95% confidence interval: 0.62, 0.86, highest vs. lowest quintile). Lower risks of lung cancer were observed for the highest versus the lowest quintiles of lycopene (28%), lutein/zeaxanthin (17%), beta-cryptoxanthin (15%), total carotenoids (16%), serum beta-carotene (19%), and serum retinol (27%). These findings suggest that high fruit and vegetable consumption, particularly a diet rich in carotenoids, tomatoes, and tomato-based products, may reduce the risk of lung cancer.

Aged↗

PubMed2002

Maximum likelihood estimation in the joint analysis of time-to-event and multiple longitudinal variables.

Joint modelling of longitudinal and survival data has received much attention in recent years. Most have concentrated on a single longitudinal variable. This paper considers joint modelling in the presence of multiple longitudinal variables. We explore direct association of time-to-event and multiple longitudinal processes through a frailty model and use a mixed effects model for each of the longitudinal variables. Correlations among the longitudinal variables are induced through correlated random effects. We allow effects of categorical and continuous covariates on both longitudinal and time-to-event responses and explore interactions between the longitudinal variables and other covariates on time-to-event. Estimates of the parameters are obtained by maximizing the joint likelihood for the longitudinal variable processes and the event process. We use a one-step-late EM algorithm to handle the direct dependence of the event process on the modelled longitudinal variables along with the presence of other fixed covariates in both processes. We argue that such a joint analysis with multiple longitudinal variables is advantageous to one with only a single longitudinal variable in revealing interplay among multiple longitudinal variables and the time-to-event.

Head and Neck Neoplasms↗

PubMed2002

Occupation and risk of esophageal and gastric cardia adenocarcinoma.

BACKGROUND: Adenocarcinomas of the esophagus and gastric cardia have risen dramatically in incidence over the past few decades, however, little research has been conducted on the occupational risk factors for these cancers. METHODS: In this population-based case-control study, lifetime job histories were compared between cases of esophageal adenocarcinoma (n = 283), gastric cardia adenocarcinoma (n = 259), and population controls (n = 689). Odds ratios (OR) and 95% confidence intervals (CI) for ever employment and by duration in various occupational and industrial categories were calculated using unconditional logistic regression. RESULTS: The risk of esophageal adenocarcinoma was elevated for persons ever employed in administrative support (OR = 1.5; 95%CI = 1.0-2.1); financial, insurance, and real estate (OR = 1.6; 95%CI = 1.0-2.4); and health services (OR = 2.2; 95%CI = 1.2-3.9). The risk of gastric cardia adenocarcinoma was increased among transportation workers (OR = 1.7; 95%CI = 1.1-2.6), as well as among carpenters (OR = 1.8; 95%CI = 0.9-3.9) and workers in the furniture manufacturing industry (OR = 2.4; 95%CI = 0.9-6.3). However, we observed few duration-response relations between length of employment in any category and cancer risk. CONCLUSIONS: This study revealed associations of esophageal adenocarcinoma with employment in administrative support, health services, and a category of financial, insurance, and real estate industries, and of gastric cardia adenocarcinoma with transportation and certain woodworking occupations. Some of these findings may be due to the play of chance associated with the multiple comparisons made in this study. Our results suggest that, overall, workplace exposures play a minor role in the etiology and upward trend of esophageal and gastric cardia adenocarcinomas.

Adenocarcinoma↗

PubMed2002

Diet, obesity and reflux in the etiology of adenocarcinomas of the esophagus and gastric cardia in humans.

Incidence rates for esophageal adenocarcinoma have increased >350% since the mid-1970s. Rates for gastric cardia adenocarcinoma have also increased, although less steeply. This led to the initiation of large population-based case-control studies, particularly in the United States and Sweden, aimed at identifying risk factors for these cancers. Results have been emerging from these studies, with the consistent finding that obesity and gastroesophageal reflux disease are important risk factors for these cancers. Analyses of dietary factors are also available and indicate that diets high in total fat, saturated fat and cholesterol are associated with an increased risk of these cancers, whereas several nutrients, particularly those found in plant foods (fiber, vitamin C, beta-carotene, folate), are associated with a reduced risk. Considering the incidence trends of these cancers and the trends in the prevalence of risk factors, the increasing prevalence of obesity in the United States likely accounts for some of the increased incidence. However, other contributors to the increasing trends have been suggested and will be discussed. Because diet, obesity and gastroesophageal reflux disease may not act independently in contributing to these cancers, current research is attempting to identify associations between the three risk factors and potential mechanisms of action to better understand the etiology of these cancers.

Adenocarcinoma↗

PubMedDate not supplied

Median ages of eruption of the primary teeth in white and Hispanic children from Arizona.

PURPOSE: The purpose of this project was to establish median eruption ages of primary teeth and evaluate eruption differences between contralateral teeth by gender, ethnicity, and household income. Data was derived from a caries study of preschool children. METHODS: A total of 4,277 white (non-Hispanic) and Hispanic preschool children from Arizona were visually examined for caries and tooth eruption status by 5 examiners between February 1994 and September 1995. Analyses of eruption status were conducted using logistic regression to produce an eruption probability distribution from which median eruption ages for the primary teeth were determined. Possible differences in eruption timing between contralateral teeth by gender, ethnicity, and household income were examined. RESULTS: Eruption status of 1 tooth was significantly predictive of the pair-matched tooth for all pairs. Differences were found for the maxillary central incisor (gender) and the mandibular second molar (ethnicity). Eruption ages did not vary by household income. Median eruption ages for each of the 10 primary teeth are presented. CONCLUSIONS: This study provides contemporary median eruption ages for primary teeth.

Age Factors↗

PubMedDate not supplied

Historical evolution of primary dentition caries pattern definitions.

A variety of dental caries patterns encompassing differing teeth have been proposed, and their use may have utility in Early Childhood Caries (ECC) investigations by minimizing case misclassification. Recent reports have proposed multiple pattern schemes. The purpose of this paper was to review the historical evolution of ECC patterns to assist the clinician and researcher in understanding the strengths and limitations of contemporary caries pattern definition(s).

Dental Caries↗