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  • 1
    Keywords: CANCER ; POPULATION ; RISK ; PROTEIN ; INFECTION ; ASSOCIATION ; antibodies ; PLASMA ; PREVALENCE ; GASTRIC-CANCER ; RANDOMIZED-TRIAL ; FOOD FREQUENCY QUESTIONNAIRE ; ABSORPTION ; ALPHA-TOCOPHEROL ; SUPPLEMENTATION ; SOUTHERN COMMUNITY COHORT ; CAROTENE CONCENTRATIONS
    Abstract: High prevalence of Helicobacter pylori (H. pylori), the leading cause of gastric cancer, and low levels of micronutrients have been observed in many developing countries, and the question remains as to the whether an association between the 2 exists. The present study seeks to further our understanding of this potential connection in the Southern Community Cohort Study, representing a low-income population in the United States. Blood levels of antibodies to H. pylori proteins were assessed by multiplex serology for a sample of 310 African American and white participants, ages 40 to 79 years. Blood collected at baseline was also assayed for levels of carotenoids, tocopherols, retinol, and folate. Multivariate linear regression was used to calculate least-squares mean micronutrient levels within groups defined by H. pylori status. The mean serum levels of all micronutrients assayed were lower among H. pylori+ individuals than H. pylori- individuals, significantly for beta-carotene, folate, and retinol (decreases of 27.6%, 18.6%, and 9.7%, respectively). Individuals who were seropositive to the virulent CagA+ H. pylori strains had even lower mean levels of micronutrients, particularly beta-carotene, folate, total carotenoids, and retinol (decreases of 38.9%, 19.1%, 17.0%, and 11.7%, respectively, compared with H. pylori- individuals). However, dietary micronutrient levels as derived from a food frequency questionnaire did not vary between groups defined by H. pylori status. These results provide support for the hypothesis that H. pylori infection impairs nutrient absorption and suggest a need for future studies to explore the role of H. pylori infection on nutrition and gastric cancer risk in this high-risk population.
    Type of Publication: Journal article published
    PubMed ID: 21436385
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  • 2
    Keywords: POPULATION ; validation ; ASSOCIATION ; TRIAL ; DESIGN ; CIGARETTE-SMOKING ; COMPUTED-TOMOGRAPHY ; TASK-FORCE ; PREDICTION MODELS ; DECISION CURVE ANALYSIS
    Abstract: Lung cancer risk prediction models are considered more accurate than the eligibility criteria based on age and smoking in identification of high-risk individuals for screening. We externally validated four lung cancer risk prediction models (Bach, Spitz, LLP, and PLCOM2012) among 20,700 ever smokers in the EPIC-Germany cohort. High-risk subjects were identified using the eligibility criteria applied in clinical trials (NELSON/LUSI, DLCST, ITALUNG, DANTE, and NLST) and the four risk prediction models. Sensitivity, specificity, and positive predictive value (PPV) were calculated based on the lung cancers diagnosed in the first 5 years of follow-up. Decision curve analysis was performed to compare net benefits. The number of high-risk subjects identified by the eligibility criteria ranged from 3,409 (NELSON/LUSI) to 1,458 (NLST). Among the eligibility criteria, the DLCST produced the highest sensitivity (64.13%), whereas the NLST produced the highest specificity (93.13%) and PPV (2.88%). The PLCOM2012 model showed the best performance in external validation (C-index: 0.81; 95% CI, 0.76-0.86; E/O: 1.03; 95% CI, 0.87-1.23) and the highest sensitivity, specificity, and PPV, but the superiority over the Bach model and the LLP model was modest. All the models but the Spitz model showed greater net benefit over the full range of risk estimates than the eligibility criteria. We concluded that all of the lung cancer risk prediction models apart from the Spitz model have a similar accuracy to identify high-risk individuals for screening, but in general outperform the eligibility criteria used in the screening trials. Cancer Prev Res; 8(9); 777-85. (c)2015 AACR.
    Type of Publication: Journal article published
    PubMed ID: 26076698
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  • 3
    Keywords: CANCER ; RESPONSES ; antibodies ; PARTICLES ; EFFICACY ; EPITOPE ; IMMUNOGENICITY ; HUMAN-PAPILLOMAVIRUS VACCINES ; CAPSID PROTEIN L2
    Abstract: Current prophylactic virus-like particle (VLP) human papillomavirus (HPV) vaccines are based on the L1 major capsid protein and provide robust but virus type-restricted protection. Moreover, VLP vaccines have a high production cost, require cold-chain storage, and are thus not readily implementable in developing countries, which endure 85% of the cervical cancer-related death burden worldwide. In contrast with L1, immunization with minor capsid protein L2 elicits broad cross-neutralization, and we previously showed that insertion of a peptide spanning amino acids 20-38 of L2 into bacterial thioredoxin (Trx) greatly enhances its immunogenicity. Building on this finding, we use, here, four different neutralization assays to demonstrate that low doses of a trivalent Trx-L2 vaccine, incorporating L2(20-38) epitopes from HPV16, HPV31 and HPV51, and formulated in a human-compatible adjuvant, induce broadly protective responses. Specifically, we show that this vaccine, which uses a far-divergent archaebacterial thioredoxin as scaffold and is amenable to an easy one-step thermal purification, induces robust cross-neutralization against 12 of the 13 known oncogenic HPV types. Immune performance measured with two different in vitro neutralization assays was corroborated by the results of mouse cervico-vaginal challenge and passive transfer experiments indicating robust cross-protection also in vivo. Altogether, our results attest to the potential of Trx-L2 as a thermostable second-generation HPV vaccine particularly well suited for low-resource countries. Cancer Prev Res; 8(10); 932-41. (c)2015 AACR.
    Type of Publication: Journal article published
    PubMed ID: 26170394
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  • 4
    Abstract: Pharmacoepidemiologic studies provide evidence that use of metformin, a drug commonly prescribed for type II diabetes, is associated with a substantial reduction in cancer risk. Experimental models show that metformin inhibits the growth of certain neoplasms by cell autonomous mechanisms such as activation of AMP kinase with secondary inhibition of protein synthesis or by an indirect mechanism involving reduction in gluconeogenesis leading to a decline in insulin levels and reduced proliferation of insulin-responsive cancers. Here, we show that metformin attenuates paraquat-induced elevations in reactive oxygen species (ROS), and related DNA damage and mutations, but has no effect on similar changes induced by H(2)0(2), indicating a reduction in endogenous ROS production. Importantly, metformin also inhibited Ras-induced ROS production and DNA damage. Our results reveal previously unrecognized inhibitory effects of metformin on ROS production and somatic cell mutation, providing a novel mechanism for the reduction in cancer risk reported to be associated with exposure to this drug.
    Type of Publication: Journal article published
    PubMed ID: 22262811
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  • 5
    Keywords: CANCER ; EXPRESSION ; tumor ; RISK ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; RNA ; SAMPLE ; SAMPLES ; TISSUE ; INDEX ; BIOMARKERS ; BIOLOGY ; CYCLE ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; prevention ; gene expression ; HUMANS ; ASSAY ; WOMEN ; REPRODUCIBILITY ; risk factors ; NECROSIS-FACTOR-ALPHA ; cancer risk ; REGION ; FAT ; INDIVIDUALS ; BIOPSY ; TNF-ALPHA ; ADIPOSE-TISSUE ; POSTMENOPAUSAL WOMEN ; leptin ; EXTRACTION ; mRNA ; INTERLEUKIN-6 ; LEVEL ; biomarker ; methods ; ASSAYS ; OVERWEIGHT ; female ; RELEVANCE ; CANCER-RISK ; NECROSIS ; AGREEMENT ; colorectal ; SHORT-TERM ; Adiponectin ; AROMATASE ; INSIGHT ; Abdominal ; Adiponectin/biosynthesis/genetics ; Aromatase/biosynthesis/genetics ; Biopsy/methods ; Breast Neoplasms/*genetics/pathology ; Colorectal Neoplasms/*genetics/pathology ; Interleukin-6/biosynthesis/genetics ; Leptin/biosynthesis/genetics ; Obesity/*complications/genetics/pathology ; Overweight/complications/genetics/pathology ; Pilot Projects ; RNA,Messenger/analysis ; Subcutaneous Fat/metabolism/*pathology/surgery ; Tumor Markers,Biological/*analysis/genetics ; Tumor Necrosis Factor-alpha/biosynthesis/genetics
    Abstract: Examination of adipose tissue biology may provide important insight into mechanistic links for the observed association between higher body fat and risk of several types of cancer, in particular colorectal and breast cancer. We tested two different methods of obtaining adipose tissue from healthy individuals. Ten overweight or obese (body mass index, 25-40 kg/m(2)), postmenopausal women were recruited. Two subcutaneous abdominal adipose tissue samples were obtained per individual (i.e., right and left lower abdominal regions) using two distinct methods (method A: 14-gauge needle with incision, versus method B: 16-gauge needle without incision). Gene expression was examined at the mRNA level for leptin, adiponectin, aromatase, interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in flash-frozen tissue, and at the protein level for leptin, adiponectin, IL-6, and TNF-alpha following short-term culture. Participants preferred biopsy method A and few participants reported any of the usual minor side effects. Gene expression was detectable for leptin, adiponectin, and aromatase, but was below detectable limits for IL-6 and TNF-alpha. For detectable genes, relative gene expression in adipose tissue obtained by methods A and B was similar for adiponectin (r = 0.64, P = 0.06) and leptin (r = 0.80, P = 0.01), but not for aromatase (r = 0.37,P = 0.34). Protein levels in tissue culture supernatant exhibited good intra-assay agreement [coefficient of variation (CV), 1-10%], with less agreement for intraindividual agreement (CV, 17-29%) and reproducibility, following one freeze-thaw cycle (CV, 〉14%). Subcutaneous adipose tissue biopsies from healthy, overweight individuals provide adequate amounts for RNA extraction, gene expression, and other assays of relevance to cancer prevention research.
    Type of Publication: Journal article published
    PubMed ID: 19139016
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  • 6
    Keywords: CANCER ; Germany ; PROSTATE ; COHORT ; RISK ; METABOLISM ; COMPLEX ; COMPLEXES ; ASSOCIATION ; TRIAL ; prevention ; MEN ; OBESITY ; PROSTATE-CANCER ; diabetes ; DIABETES-MELLITUS ; body mass index ; ONCOLOGY ; HYPERPLASIA ; INSULIN-RESISTANCE ; PLUS ; BODY-MASS INDEX ; ANDROGEN ; SCREENING TRIAL ; FINASTERIDE ; Hormone metabolism ; HYPERINSULINEMIA ; PREVENTION TRIAL
    Abstract: This perspective on the report by Neuhouser et al. (beginning on page 279 in this issue of the journal) examines the associations that have been observed between body mass index, serum insulin, preexisting diabetes, androgen metabolism, and prostate cancer risk. Based on data of the Prostate Cancer Prevention Trial, the observations by Neuhouser et al. plus findings from other studies suggest a complex mix of higher and lower risks for high- and low-grade cancer in association with obesity and endogenous hormone metabolism. Cancer Prev Res; 3(3); 259-62. (C) 2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20179295
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  • 7
    Abstract: Cancer is the consequence of genetic and epigenetic alterations. Genetic mutations likely result in part from exposure to environmental carcinogens, giving rise to a large field of cancer-prevention study of these carcinogens and ways to develop strategies to avoid them. Our understanding of regulatory epigenetic mechanisms associated with DNA methylation, histone modifications, and microRNA production is increasing rapidly. The involvement of these processes in carcinogenesis raises the possibility that environmental exposures may promote or prevent cancer through affecting the epigenome. Modifying the epigenome to prevent cancer is particularly intriguing because epigenetic alterations are potentially reversible, unlike gene mutations, and because certain dietary factors, such as the B-vitamin folate, may affect genes' DNA methylation status (as reported by Wallace et al., beginning on page 1552 in this issue of the journal). Rapidly improving techniques for assessing epigenetic alterations promise to yield important insights for cancer prevention.
    Type of Publication: Journal article published
    PubMed ID: 21149325
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  • 8
    Keywords: CANCER ; GROWTH ; MORTALITY ; ASSOCIATION ; VALIDITY ; BRAIN-TUMORS ; WEIGHT ; HEIGHT ; PARTICIPANTS ; OVERWEIGHT ; HORMONES
    Abstract: Body fatness has been associated with increased risk of a number of hormone-dependent cancers. Recent studies suggest that body mass index (BMI) may be related to meningiomas, which are more common in women than men, and for which estrogens are believed to play a role. Using data from a large European propective cohort, 203 incident cases of meningioma and 340 cases of glioma were included in the analysis for measures of body fat, height, and physical activity among 380,775 participants. All analyses were conducted using Cox proportional hazards model and controlling for age, sex, country, and education. A 71% increase in risk of meningioma was observed among men and women in the top quartile of waist circumference (HR = 1.71, 95% CI = 1.08-2.73, P(trend) = 0.01). A positive association was also observed for BMI and meningioma (HR = 1.48, 95% CI = 0.98-2.23, for BMI 〉= 30 compared with a BMI of 20-24.9, P(trend) = 0.05). An association with height and meningioma was also suggestive (HR = 1.24, 95% 0.96-1.51, for each 10 cm increase). In contrast, no associations were observed for height and different measures of body fat and risk of glioma. Physical activity was not related to either type of brain tumors. Results from this study support an increase in risk of meningioma with higher body fatness among both men and women. No association was observed between anthropometric measures and risk of glioma.
    Type of Publication: Journal article published
    PubMed ID: 21685234
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  • 9
    Keywords: CANCER ; Germany ; DIAGNOSIS ; MORTALITY ; COMPONENTS ; COLORECTAL-CANCER ; INSULIN-RESISTANCE SYNDROME
    Abstract: Metabolic syndrome (MetS) is purportedly related to risk of developing colorectal cancer; however, the association of MetS, as defined according to recent international criteria, and colorectal cancer has not been yet evaluated. In particular, it remains unclear to what extent the MetS components individually account for such an association. We addressed these issues in a nested case-control study that included 1,093 incident cases matched (1: 1) to controls by using incidence density sampling. Conditional logistic regression was used to estimate relative risks (RR) and 95% CIs. MetS was defined according to the criteria of the National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATPIII), the International Diabetes Federation (IDF), and the 2009 harmonized definition. Among individual components, abdominal obesity (RR = 1.51; 95% CI: 1.16-1.96) was associated with colon cancer, whereas abnormal glucose metabolism was associated with both colon (RR = 2.05; 95% CI: 1.57-2.68) and rectal cancer (RR = 2.07; 95% CI: 1.45-2.96). MetS, as defined by each of the definitions, was similarly associated with colon cancer (e. g., RR = 1.91; 95% CI: 1.47-2.42 for MetS by NCEP/ATPIII), whereas MetS by NCEP/ATPIII, but not IDF or harmonized definition, was associated with rectal cancer (RR = 1.45; 95% CI: 1.02-2.06). Overall, these associations were stronger in women than in men. However, the association between MetS and colorectal cancer was accounted for by abdominal obesity and abnormal glucose metabolism such that MetS did not provide risk information beyond these components (likelihood ratio test P = 0.10 for MetS by NCEP/ATPIII). These data suggest that simple assessment of abnormal glucose metabolism and/or abdominal obesity to identify individuals at colorectal cancer risk may have higher clinical utility than applying more complex MetS definitions.
    Type of Publication: Journal article published
    PubMed ID: 21697276
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  • 10
    Keywords: cancer prevention ; NECROSIS-FACTOR-ALPHA ; POSTMENOPAUSAL WOMEN ; PHYSICAL-ACTIVITY ; INSULIN-RESISTANCE ; RANDOMIZED CONTROLLED-TRIAL ; LOW-CALORIE DIET ; OBESE WOMEN ; MACROPHAGE INFILTRATION ; HYPOCALORIC DIETS
    Abstract: Adipose tissue plays a role in obesity-related cancers via increased production of inflammatory factors, steroid hormones, and altered adipokines. The impact of weight loss on adipose-tissue gene expression may provide insights into pathways linking obesity with cancer risk. We conducted an ancillary study within a randomized trial of diet, exercise, or combined diet+exercise vs. control among overweight/obese postmenopausal women. In 45 women, subcutaneous adipose-tissue biopsies were performed at baseline and after 6 months and changes in adipose-tissue gene expression were determined by microarray with an emphasis on pre-specified candidate pathways, as well as by unsupervised clustering of 〉37,000 transcripts (Illumina). Analyses were conducted first by randomization group, and then by degree of weight change at 6-months in all women combined. At 6 months, diet, exercise and diet+exercise participants lost a mean of 8.8 kg, 2.5 kg, and 7.9 kg (all p〈0.05 vs. no change in controls). There was no significant change in candidate-gene expression by intervention group. In analysis by weight-change category, greater weight loss was associated a decrease in 17beta-hydroxysteroid dehydrogenase-1 (HSD17B1, p-trend〈0.01) and leptin (LEP, p-trend〈0.01) expression, and marginally significant increased expression of estrogen receptor-1 (ESR1, p-trend=0.08) and insulin-like growth factor binding protein-3 (IGFBP3, p-trend=0.08). Unsupervised clustering revealed 83 transcripts with statistically significant changes. Multiple gene-expression changes correlated with changes in associated serum biomarkers. Weight-loss was associated with changes in adipose-tissue gene expression after 6 months, particularly in two pathways postulated to link obesity and cancer, i.e., steroid-hormone metabolism and IGF signaling.
    Type of Publication: Journal article published
    PubMed ID: 23341572
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