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1.
Microbiome ; 6(1): 210, 2018 Nov 26.
Artigo em Inglês | MEDLINE | ID: mdl-30477563

RESUMO

The National Cancer Institute (NCI) sponsored a 2-day workshop, "Next Steps in Studying the Human Microbiome and Health in Prospective Studies," in Bethesda, Maryland, May 16-17, 2017. The workshop brought together researchers in the field to discuss the challenges of conducting microbiome studies, including study design, collection and processing of samples, bioinformatics and statistical methods, publishing results, and ensuring reproducibility of published results. The presenters emphasized the great potential of microbiome research in understanding the etiology of cancer. This report summarizes the workshop and presents practical suggestions for conducting microbiome studies, from workshop presenters, moderators, and participants.

2.
Paediatr Perinat Epidemiol ; 32(6): 568-583, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30466188

RESUMO

BACKGROUND: Childhood cancer is a rare but leading cause of morbidity and mortality. Established risk factors, accounting for <10% of incidence, have been identified primarily from case-control studies. However, recall, selection and other potential biases impact interpretations particularly, for modest associations. A consortium of pregnancy and birth cohorts (I4C) was established to utilise prospective, pre-diagnostic exposure assessments and biological samples. METHODS: Eligibility criteria, follow-up methods and identification of paediatric cancer cases are described for cohorts currently participating or planning future participation. Also described are exposure assessments, harmonisation methods, biological samples potentially available for I4C research, the role of the I4C data and biospecimen coordinating centres and statistical approaches used in the pooled analyses. RESULTS: Currently, six cohorts recruited over six decades (1950s-2000s) contribute data on 388 120 mother-child pairs. Nine new cohorts from seven countries are anticipated to contribute data on 627 500 additional projected mother-child pairs within 5 years. Harmonised data currently includes over 20 "core" variables, with notable variability in mother/child characteristics within and across cohorts, reflecting in part, secular changes in pregnancy and birth characteristics over the decades. CONCLUSIONS: The I4C is the first cohort consortium to have published findings on paediatric cancer using harmonised variables across six pregnancy/birth cohorts. Projected increases in sample size, expanding sources of exposure data (eg, linkages to environmental and administrative databases), incorporation of biological measures to clarify exposures and underlying molecular mechanisms and forthcoming joint efforts to complement case-control studies offer the potential for breakthroughs in paediatric cancer aetiologic research.

3.
Cancer Epidemiol Biomarkers Prev ; 27(3): 233-244, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-29254934

RESUMO

Very large international and ethnic differences in cancer rates exist, are minimally explained by genetic factors, and show the huge potential for cancer prevention. A substantial portion of the differences in cancer rates can be explained by modifiable factors, and many important relationships have been documented between diet, physical activity, and obesity, and incidence of important cancers. Other related factors, such as the microbiome and the metabolome, are emerging as important intermediary components in cancer prevention. It is possible with the incorporation of newer technologies and studies including long follow-up and evaluation of effects across the life cycle, additional convincing results will be produced. However, several challenges exist for cancer researchers; for example, measurement of diet and physical activity, and lack of standardization of samples for microbiome collection, and validation of metabolomic studies. The United States National Cancer Institute convened the Research Strategies for Nutritional and Physical Activity Epidemiology and Cancer Prevention Workshop on June 28-29, 2016, in Rockville, Maryland, during which the experts addressed the state of the science and areas of emphasis. This current paper reflects the state of the science and priorities for future research. Cancer Epidemiol Biomarkers Prev; 27(3); 233-44. ©2017 AACR.

4.
Cancer Med ; 6(10): 2419-2423, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28879665

RESUMO

Heavy alcohol drinking is associated with increased breast cancer risk, but associations with low-to-moderate alcohol consumption are less clear and the biological mechanisms are not well defined. The objective of this study was to evaluate the effects of 8 weeks of low (15 g/d) and moderate (30 g/d) alcohol ingestion on concentrations of 15 urinary estrogen metabolites (EMs) in postmenopausal women (n = 51) in a controlled feeding study with a randomized crossover design. Compared to no alcohol, 15 g/day for 8 weeks had no effect on urinary EMs. However, compared to no alcohol, 30 g/day for 8 weeks decreased urinary 2-hydroestrone (2-OHE1) by 3.3% (P = 0.055) and increased 16-epiestriol (16-EpiE3) by 26.6% (P = 0.037). Trends for reduced urinary 2-OHE1 (P = 0.045), reduced ratio of 2-OH:16OH pathways (P = 0.008), and increased 16-EpiE3 (P = 0.035) were observed as alcohol ingestion increased from 0 g to 15 g to 30 g/d. Moderate alcohol consumption for 8 weeks had modest effects on urinary concentrations of 2-OHE1 and 16-EpiE3 among postmenopausal women in a carefully controlled feeding study.


Assuntos
Consumo de Bebidas Alcoólicas , Estrogênios/metabolismo , Metaboloma , Metabolômica , Pós-Menopausa , Vigilância em Saúde Pública , Idoso , Cromatografia Líquida , Estrogênios/urina , Comportamento Alimentar , Feminino , Humanos , Metabolômica/métodos , Pessoa de Meia-Idade , Vigilância em Saúde Pública/métodos , Espectrometria de Massas em Tandem
6.
Cancer Med ; 4(12): 1908-22, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26377256

RESUMO

There is a growing understanding that several infectious agents are acquired in early life and this is the reason why available vaccines target the new born, infants, and adolescents. Infectious agents are associated with cancer development and it is estimated that about 20% of the world's cancer burden is attributed to infectious agents. There is a growing evidence that certain infectious agents acquired in early life can give rise to cancer development, but estimates of the cancer burden from this early-life acquisition is unknown. In this article, we have selected five cancers (cervical, liver, Burkitt's lymphoma-leukemia, nasopharyngeal carcinoma, and adult T-cell leukemia-lymphoma) and examine their links to infectious agents (HPV, HBV, HCV, EBV, and HTLV-1) acquired in early life. For these agents, the acquisition in early life is from mother-to-child transmission, perinatal contact (with genital tract secretions, amniotic fluids, blood, and breast milk), saliva, sexual intercourse, and blood transfusion. We also discuss prevention strategies, address future directions, and propose mechanisms of action after a long latency period from the time of acquisition of the infectious agent in early life to cancer development.


Assuntos
Transformação Celular Neoplásica , Exposição Ambiental , Interações Hospedeiro-Patógeno , Neoplasias/epidemiologia , Neoplasias/etiologia , Fatores Etários , Feminino , Humanos , Infecção/complicações , Controle de Infecções , Masculino , Neoplasias/diagnóstico , Neoplasias/prevenção & controle
7.
J Adolesc Health ; 52(5 Suppl): S30-5, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-23298994

RESUMO

It is increasingly evident that diet during preadolescence and adolescence has important consequences for breast cancer during adulthood. However, only a few epidemiologic studies have been conducted on the relationship between diet during preadolescence and adolescence, and cancer during adulthood. This situation is partly because of methodological challenges such as the long latency period, the complexity of breast cancer, the lack of validated diet assessment tools, and the large number of subjects that must be followed, all of which increase costs. In addition, funding opportunities are few for such studies. Results from the small number of epidemiologic studies are inconsistent, but evidence is emerging that specific aspects of the diet during preadolescence and adolescence are important. For example, during preadolescence and adolescence, severe calorie restriction with poor food quality, high total fat intake, and alcohol intake tend to increase risk, whereas high soy intake decreases risk. Research on preadolescent and adolescent diet is a paradigm shift in breast cancer investigations. This research paradigm has the potential to produce transformative knowledge to inform breast cancer prevention strategies through dietary intervention during preadolescence and adolescence, rather than later in life, as is current practice, when it is perhaps less effective. Methodological challenges that have plagued the field might now be overcome by leveraging several existing large-scale cohort studies in the U.S. and around the world to investigate the role of diet during preadolescence and adolescence in risk for adult breast cancer.


Assuntos
Neoplasias da Mama/etiologia , Dieta , Adolescente , Consumo de Bebidas Alcoólicas/efeitos adversos , Neoplasias da Mama/epidemiologia , Neoplasias da Mama/prevenção & controle , Restrição Calórica , Criança , Gorduras na Dieta , Ingestão de Energia , Feminino , Humanos , Risco
8.
Cancer Causes Control ; 23(6): 983-90, 2012 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-22527169

RESUMO

It is becoming increasingly evident that early-life events and exposures have important consequences for cancer development later in life. However, epidemiological studies of early-life factors and cancer development later in life have had significant methodological challenges such as the long latency period, the distinctiveness of each cancer, and large number of subjects that must be studied, all likely to increase costs. These traditional hurdles might be mitigated by leveraging several existing large-scale prospective studies in the United States (US) and globally, as well as birth databases and birth cohorts, in order to launch both association and mechanistic studies of early-life exposures and cancer development later in life. Dedicated research funding will be needed to advance this paradigm shift in cancer research, and it seems justified by its potential to produce transformative understanding of how cancer develops over the life-course. This in turn has the potential to transform cancer prevention strategies through interventions in early-life rather than later in life, as is the current practice, where it is perhaps less effective.


Assuntos
Exposição Ambiental/estatística & dados numéricos , Neoplasias/epidemiologia , Fatores Etários , Animais , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Estudos Epidemiológicos , Humanos , Acontecimentos que Mudam a Vida , Neoplasias/etiologia , Estudos Prospectivos , Fatores de Risco
9.
Front Genet ; 2: 91, 2011.
Artigo em Inglês | MEDLINE | ID: mdl-22303385

RESUMO

Epigenetics is the study of heritable changes in gene expression that occur without a change in DNA sequence. Cancer is a multistep process derived from combinational crosstalk between genetic alterations and epigenetic influences through various environmental factors. The observation that epigenetic changes are reversible makes them an attractive target for cancer prevention. Until recently, there have been difficulties studying epigenetic mechanisms in interactions between dietary factors and environmental toxicants. The development of the field of cancer epigenetics during the past decade has been advanced rapidly by genome-wide technologies - which initially employed microarrays but increasingly are using high-throughput sequencing - which helped to improve the quality of the analysis, increase the capacity of sample throughput, and reduce the cost of assays. It is particularly true for applications of cancer epigenetics in epidemiologic studies that examine the relationship among diet, epigenetics, and cancer because of the issues of tissue heterogeneity, the often limiting amount of DNA samples, and the significant cost of the analyses. This review offers an overview of the state of the science in nutrition, environmental toxicants, epigenetics, and cancer to stimulate further exploration of this important and developing area of science. Additional epidemiologic research is needed to clarify the relationship between these complex epigenetic mechanisms and cancer.

10.
Cancer Epidemiol Biomarkers Prev ; 19(8): 1976-83, 2010 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-20696660

RESUMO

BACKGROUND: Using data from a case-control study, we previously reported that low dietary intakes of magnesium (Mg), iron (Fe), zinc (Zn), copper (Cu), but not selenium (Se) and calcium (Ca), were associated with increased lung cancer risk. Due to dietary recall bias in case-control studies, our objective was to assess whether these findings hold in a prospective cohort study. METHODS: We analyzed data from the NIH-American Association of Retired Persons Diet and Health study of 482,875 subjects (288,257 men and 194,618 women) who were cancer-free and completed a food frequency questionnaire at enrollment between 1995 and 2003. Cox proportional hazards models were computed to estimate the relative risk adjusted for potential confounders. RESULTS: During a mean follow-up of 7 years, 7,052 lung cancer cases were identified. For all subjects, we observed no significant associations between total (diet + supplement) Ca, Mg, Fe, Cu, Se, and Zn intakes and lung cancer risk. Total Ca intake was protective (P trend < 0.05) for current smokers and subjects with adenocarcinomas. Total Mg intake increased risk (P trend < 0.05) in men and current smokers. Total Fe intake was inversely associated with risk in women (P trend < 0.01). For dietary minerals, Mg increased risk (P trend < 0.05) in all subjects, among men and current smokers. Increased dietary Ca intake reduced risk in women (P trend = 0.05). Dietary Fe decreased risk in all subjects and among women (P trend < 0.05). Mineral intake from supplements did not affect lung cancer risk. CONCLUSIONS: Dietary minerals are risk factors for lung cancer. IMPACT: Dietary mineral consumption may influence lung cancer risk, but the associations differ by type of mineral and population subgroups.


Assuntos
Dieta , Neoplasias Pulmonares/etiologia , Minerais/efeitos adversos , Idoso , Suplementos Nutricionais/efeitos adversos , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , National Institutes of Health (U.S.) , Estudos Prospectivos , Medição de Risco , Inquéritos e Questionários , Estados Unidos
11.
Am J Epidemiol ; 171(6): 682-90, 2010 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-20139126

RESUMO

In the current era of diet-gene analyses, large sample sizes are required to uncover the etiology of complex diseases. As such, consortia form and often combine available data. Food frequency questionnaires, which commonly use 2 different types of responses about the frequency of intake (predefined responses and open-ended responses), may be pooled to achieve the desired sample size. The common practice is to categorize open-ended responses into the predefined response categories. A problem arises when the predefined categories are noncontiguous: possible open-ended responses may fall in gaps between the predefined categories. Using simulated data modeled from frequency of intake among 1,664 controls in a lung cancer case-control study at The University of Texas M. D. Anderson Cancer Center (Houston, Texas, 2000-2005), the authors describe the effect of different categories of open-ended responses that fall in between noncontiguous, predefined response sets on estimates of the mean difference in intake and the odds ratios. A significant inflation of false positives appears when comparing mean differences of intake, while the bias in estimating odds ratios may be acceptably small. Therefore, if pooling data cannot be restricted to the same type of response, inferences should focus on odds ratio estimation to minimize bias.


Assuntos
Interpretação Estatística de Dados , Inquéritos sobre Dietas , Inquéritos e Questionários , Adulto , Idoso , Viés , Estudos de Casos e Controles , Simulação por Computador , Humanos , Modelos Logísticos , Neoplasias Pulmonares , Pessoa de Meia-Idade , Razão de Chances , Projetos Piloto , Reprodutibilidade dos Testes , Inquéritos e Questionários/normas , Texas
12.
J Clin Oncol ; 26(25): 4072-7, 2008 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-18757321

RESUMO

PURPOSE: To understand the mechanism through which obesity in breast cancer patients is associated with poorer outcome, we evaluated body mass index (BMI) and response to neoadjuvant chemotherapy (NC) in women with operable breast cancer. PATIENTS AND METHODS: From May 1990 to July 2004, 1,169 patients were diagnosed with invasive breast cancer at M. D. Anderson Cancer Center and received NC before surgery. Patients were categorized as obese (BMI >or= 30 kg/m(2)), overweight (BMI of 25 to < 30 kg/m(2)), or normal/underweight (BMI < 25 kg/m(2)). Logistic regression was used to examine associations between BMI and pathologic complete response (pCR). Breast cancer-specific, progression-free, and overall survival times were examined using the Kaplan-Meier method and Cox proportional hazards regression analysis. All statistical tests were two-sided. RESULTS: Median age was 50 years; 30% of patients were obese, 32% were overweight, and 38% were normal or underweight. In multivariate analysis, there was no significant difference in pCR for obese compared with normal weight patients (odds ratio [OR] = 0.78; 95% CI, 0.49 to 1.26). Overweight and the combination of overweight and obese patients were significantly less likely to have a pCR (OR = 0.59; 95% CI, 0.37 to 0.95; and OR = 0.67; 95% CI, 0.45 to 0.99, respectively). Obese patients were more likely to have hormone-negative tumors (P < .01), stage III tumors (P < .01), and worse overall survival (P = .006) at a median follow-up time of 4.1 years. CONCLUSION: Higher BMI was associated with worse pCR to NC. In addition, its association with worse overall survival suggests that greater attention should be focused on this risk factor to optimize the care of breast cancer patients.


Assuntos
Neoplasias da Mama/complicações , Neoplasias da Mama/metabolismo , Obesidade/complicações , Obesidade/terapia , Adulto , Idoso , Idoso de 80 Anos ou mais , Índice de Massa Corporal , Peso Corporal , Neoplasias da Mama/tratamento farmacológico , Estudos de Coortes , Feminino , Humanos , Oncologia/métodos , Pessoa de Meia-Idade , Terapia Neoadjuvante , Fatores de Tempo , Resultado do Tratamento
13.
Int J Cancer ; 123(5): 1173-80, 2008 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-18546288

RESUMO

Studies of vitamin E and cancer have focused on the alpha-tocopherol form of the vitamin. However, other forms of vitamin E, in particular gamma-tocopherol may have unique mechanistic characteristics relevant to lung cancer prevention. In an ongoing study of 1,088 incident lung cancer cases and 1,414 healthy matched controls, we studied the associations between 4 tocopherols (alpha-, beta-, gamma-, and delta-tocopherol) in the diet and lung cancer risk. Using multiple logistic regression analysis, the adjusted odds ratios (OR) and 95% confidence intervals (CI) of lung cancer for increasing quartiles of dietary alpha-tocopherol intake were 1.0, 0.63 (0.50-0.79), 0.58 (0.44-0.76) and 0.39 (0.28-0.53), respectively (p-trend < 0.0001). For dietary intake of beta-tocopherol, the OR and 95% CI for all subjects were: 1.0, 0.79 (0.63-0.98), 0.59 (0.45-0.78) and 0.56 (0.42-0.74), respectively (p-trend < 0.0001). Similar results for dietary gamma-tocopherol intake were observed: 1.0, 0.84 (0.67-1.06), 0.76 (0.59-0.97) and 0.56 (0.42-0.75), respectively (p- trend = 0.0002). No significant association between delta-tocopherol intake and lung cancer risk was detected. When the 4 tocopherols were summed as total tocopherol intake, a monotonic risk reduction was also observed. When we entered the other tocopherols in our model, only the association with dietary alpha-tocopherol intake remained significant; i.e., increasing intake of dietary alpha-tocopherol accounted for 34-53% reductions in lung cancer risk. To the best of our knowledge, this is the first report of the independent associations of the 4 forms of dietary tocopherol (alpha-, beta-, gamma- and delta-tocohperol) on lung cancer risk. Given the limitations with case-control studies, these findings need to be confirmed in further investigations.


Assuntos
Antioxidantes/administração & dosagem , Suplementos Nutricionais , Neoplasias Pulmonares/prevenção & controle , Tocoferóis/administração & dosagem , Adenocarcinoma/prevenção & controle , Adulto , Idoso , Carcinoma Pulmonar de Células não Pequenas/prevenção & controle , Carcinoma de Células Pequenas/prevenção & controle , Carcinoma de Células Escamosas/prevenção & controle , Estudos de Casos e Controles , Feminino , Humanos , Modelos Logísticos , Neoplasias Pulmonares/epidemiologia , Masculino , Pessoa de Meia-Idade , Razão de Chances , Medição de Risco , Fatores de Risco , Estados Unidos/epidemiologia , alfa-Tocoferol/administração & dosagem , beta-Tocoferol/administração & dosagem , gama-Tocoferol/administração & dosagem
14.
Carcinogenesis ; 29(5): 949-56, 2008 May.
Artigo em Inglês | MEDLINE | ID: mdl-18448487

RESUMO

Magnesium (Mg) is required for maintenance of genomic stability; however, data on the relationship between dietary Mg intake and lung cancer are lacking. In an ongoing lung cancer case-control study, we identified 1139 cases and 1210 matched healthy controls with data on both diet and DNA repair capacity (DRC). Dietary intake was assessed using a modified Block-NCI food frequency questionnaire and DRC was measured using the host-cell reactivation assay to assess repair in lymphocyte cultures. After adjustment for potential confounding factors including DRC, the odds ratios (ORs) and 95% confidence intervals (CIs) for lung cancer with increasing quartiles of dietary Mg intake were 1.0, 0.83 (0.66-1.05), 0.64 (0.50-0.83) and 0.47 (0.36-0.61), respectively, for all subjects (P-trend < 0.0001). Similar results were observed by histology and clinical stage of lung cancer. Low dietary Mg intake was associated with poorer DRC and increased risk of lung cancer. In joint effects analyses, compared with those with high dietary Mg intake and proficient DRC, the OR (95% CI) for lung cancer in the presence of both low dietary Mg and suboptimal DRC was 2.36 (1.83-3.04). Similar results were observed for men and women. The effects were more pronounced among older subjects (>60 years), current or heavier smokers, drinkers, those with a family history of cancer in first-degree relatives, small cell lung cancer and late-stage disease. These intriguing results need to be confirmed in prospective studies.


Assuntos
Reparo do DNA , Neoplasias Pulmonares/epidemiologia , Magnésio/farmacologia , Idoso , Estudos de Casos e Controles , Grupos de Populações Continentais , Dieta , Feminino , Humanos , Entrevistas como Assunto , Neoplasias Pulmonares/genética , Masculino , Pessoa de Meia-Idade , Razão de Chances , Valores de Referência , Fatores de Risco , Fumar/epidemiologia
15.
Cancer Epidemiol Biomarkers Prev ; 16(12): 2756-62, 2007 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-18086784

RESUMO

In a large case-control study, we previously reported that dietary intakes of zinc (Zn) and copper (Cu), but not selenium (Se), were inversely associated with lung cancer risk. Because Zn, Cu, Se, iron (Fe), and calcium (Ca) are important for maintaining DNA stability, we examined their associations with DNA repair capacity (DRC) measured by the lymphocyte host-cell reactivation assay in 1,139 cases and 1,210 of the controls. Dietary intake was reported in a food frequency questionnaire. In multivariate analyses, compared to those with high dietary Cu + proficient DRC, the odds ratio (95% confidence interval) [OR (95% CI)] for lung cancer for low Cu + suboptimal DRC was 2.54 (1.97-3.27). Similar results were observed for men and women. These effects were more pronounced in older and lean subjects, those with late-stage disease, and those with a family history of cancer in first-degree relatives. Compared to subjects with high Zn + proficient DRC, the OR for lung cancer for low Zn + suboptimal DRC was 1.82 (95% CI, 1.41-2.34), with pronounced effects in men, current smokers, subjects with longer duration of smoking, those with late-stage disease, or those with a family history of cancer. An OR of 1.94 (95% CI, 1.51-2.48) was observed for low Fe + suboptimal DRC compared with high Fe + proficient DRC, and pronounced effects appeared in older, lean subjects, those with longer duration of smoking, are heavier smokers, those with a late-stage disease, and those with a family history of cancer. No significant joint associations were seen for Se or Ca and DRC. Our joint associations between Cu-DRC, Zn-DRC and Fe-DRC and lung cancer risk require confirmation in prospective studies.


Assuntos
Reparo do DNA , Dieta , Neoplasias Pulmonares/genética , Oligoelementos/administração & dosagem , Cálcio/administração & dosagem , Estudos de Casos e Controles , Cobre/administração & dosagem , Feminino , Humanos , Ferro/administração & dosagem , Masculino , Fatores de Risco , Selênio/administração & dosagem , Fumar , Zinco/administração & dosagem
16.
Curr Cancer Drug Targets ; 7(5): 484-91, 2007 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-17691908

RESUMO

The prevalence of obesity, an established epidemiologic risk factor for many cancers, has risen steadily for the past several decades in the U.S. Particularly alarming are the increasing rates of obesity among children, portending continuing increases in the rates of obesity and obesity-related cancers for many years to come. Unfortunately, the mechanisms underlying the association between obesity and cancer are not well understood. In particular, the effects and mechanistic targets of interventions that modulate energy balance, such as reduced calorie diets and physical activity, on the carcinogenesis process have not been well characterized. The purpose of this review is to provide a strong foundation for future mechanistic-based research in this area by describing key animal and human studies of energy balance modulations involving diet, exercise, or pharmaceutical agents and by focusing on the interrelated pathways affected by alterations in energy balance. Particular attention in this review is placed on the components of the insulin/IGF-1/Akt pathway, which has emerged as a predominant target for disrupting the obesity-cancer link. Also discussed is the promise of global approaches, including genomics, proteomics, and metabolomics, for the elucidation of energy balance-responsive pathways. The ultimate goal of this work is to provide the missing mechanistic information necessary to identify targets for the prevention and control of cancers related to or caused by excess body weight.


Assuntos
Metabolismo Energético/fisiologia , Neoplasias/metabolismo , Neoplasias/prevenção & controle , Transdução de Sinais/fisiologia , Animais , Humanos , Neoplasias/dietoterapia , Fitoterapia , Extratos Vegetais/uso terapêutico
17.
J Epidemiol Community Health ; 61(8): 737-41, 2007 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-17630376

RESUMO

BACKGROUND: Stroke is the leading cause of death in Linxian, China. Although there is evidence of DNA damage in experimental stroke, no data exist on DNA repair and stroke in human populations. AIM: To assess the risk of stroke conferred by polymorphisms in the DNA repair genes, XRCC1, XPD23 and APE/ref-1 in a cohort of individuals originally assembled as subjects in two cancer prevention trials in Linxian, China. METHODS: The subjects for this prospective study were sampled from a cohort of 4,005 eligible subjects who were alive and cancer free in 1991 and had blood samples available for DNA extraction. Using real-time Taqman analyses, all incident cases of stroke (n = 118) that developed from May 1996, and an age- and a sex-stratified random sample (n = 454) drawn from all eligible subjects were genotyped. Cox proportional hazards models were used to estimate relative risks (RRs) and 95% CIs. RESULTS: No association was observed between polymorphisms in APE/ref-1 codon 148 and XRCC16 codon 194, and stroke. Polymorphisms in XRCC110 codon 399 were associated with a significantly reduced risk of stroke (RR 0.59, 95% CI 0.36 to 0.96, p = 0.033), whereas XPD23 codon 312 was associated with a significantly increased risk of stroke (RR 2.18, 95% CI 1.14 to 4.17, p = 0.010). CONCLUSIONS: Polymorphisms in DNA repair genes may be important in the aetiology of stroke. These data should stimulate research on DNA damage and repair in stroke.


Assuntos
Reparo do DNA/genética , DNA Liase (Sítios Apurínicos ou Apirimidínicos)/genética , Proteínas de Ligação a DNA/genética , Polimorfismo Genético/genética , Acidente Vascular Cerebral/genética , Proteína Grupo D do Xeroderma Pigmentoso/genética , China/epidemiologia , Códon/genética , Feminino , Frequência do Gene/genética , Genótipo , Humanos , Desequilíbrio de Ligação/genética , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Fatores de Risco , Acidente Vascular Cerebral/epidemiologia , Proteína 1 Complementadora Cruzada de Reparo de Raio-X
18.
Obesity (Silver Spring) ; 15(4): 1043-52, 2007 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-17426341

RESUMO

OBJECTIVE: To evaluate the association between birthplace (Mexico or U.S.) and obesity in men and women and to analyze the relationship between duration of U.S. residency and prevalence of obesity in Mexican immigrants. RESEARCH METHODS AND PROCEDURES: We used cross-sectional data from 7503 adults of Mexican descent residing in Harris County, TX, to evaluate the relationships among BMI, birthplace, and years of residency in the U.S., controlling for demographic characteristics, physical activity level, and acculturation level. RESULTS: U.S.-born adults had an increased risk (between 34% and 65%) of obesity compared with their Mexican-born counterparts. After controlling for recognized confounders and risk factors, this association was maintained in the highly acculturated only. Among highly acculturated obese U.S.-born men, 6% of the cases were attributable to the joint effect of birthplace and acculturation; in women, this proportion was 25%. Among Mexican-born women, there was an increasing trend in mean BMI with increasing duration of residency in the U.S.. Compared with immigrants who had lived in the U.S. for <5 years, Mexican-born women who had resided in the U.S. for >or=15 years had an adjusted BMI mean difference of 2.12 kg/m2 (95% confidence interval, 1.53-2.72). DISCUSSION: Mexican-born men and women have a lower risk of obesity than their U.S.-born counterparts, but length of U.S. residency among immigrants, especially in women, is directly associated with risk of obesity. Development of culturally specific interventions to prevent obesity in recent immigrants may have an important public health effect in this population.


Assuntos
Obesidade/diagnóstico , Obesidade/epidemiologia , Aculturação , Adulto , Índice de Massa Corporal , Estudos de Coortes , Emigração e Imigração , Feminino , Humanos , Masculino , Americanos Mexicanos , Pessoa de Meia-Idade , Características de Residência , Texas , Fatores de Tempo , Ganho de Peso
19.
Nutr J ; 6: 3, 2007 Jan 17.
Artigo em Inglês | MEDLINE | ID: mdl-17229323

RESUMO

BACKGROUND: The relationship between BMI and leptin has been studied extensively in the past, but previous reports in postmenopausal women have not been conducted under carefully controlled dietary conditions of weight maintenance using precise measures of body fat distribution. The aim of the present study was to examine the association between serum leptin concentration and adiposity as estimated by BMI and dual energy x-ray absorptiometry (DEXA) measures (percent body fat, central and peripheral fat, and lean mass) in postmenopausal women. METHODS: This study was conducted as a cross-sectional analysis within the control segment of a randomized, crossover trial in which postmenopausal women (n = 51) consumed 0 (control), 15 (one drink), and 30 (two drinks) g alcohol (ethanol)/d for 8 weeks as part of a controlled diet. BMIs were determined and DEXA scans were administered to the women during the 0 g alcohol treatment, and a blood sample was collected at baseline and week 8 of each study period for leptin analysis. RESULTS AND DISCUSSION: In multivariate analysis, women who were overweight (BMI > 25 to < or = 30 kg/m2) had a 2-fold increase, and obese women (BMI > 30 kg/m2) had more than a 3-fold increase in serum leptin concentrations compared to normal weight (BMI < or =25 kg/m2) women. When the models for the different measures of adiposity were assessed by multiple R2, models which included percent body fat explained the highest proportion (approximately 80%) of the serum leptin variance. CONCLUSION: Under carefully controlled dietary conditions, we confirm that higher levels of adiposity were associated with higher concentrations of serum leptin. It appears that percent body fat in postmenopausal women may be the best adiposity-related predictor of serum leptin.


Assuntos
Distribuição da Gordura Corporal , Índice de Massa Corporal , Leptina/sangue , Pós-Menopausa/fisiologia , Absorciometria de Fóton , Idoso , Estudos Cross-Over , Feminino , Humanos , Pessoa de Meia-Idade , Obesidade/sangue , Fumar
20.
Int J Cancer ; 120(5): 1108-15, 2007 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-17131334

RESUMO

Zinc, copper and selenium are important cofactors for several enzymes that play a role in maintaining DNA integrity. However, limited epidemiologic research on these dietary trace metals and lung cancer risk is available. In an ongoing study of 1,676 incident lung cancer cases and 1,676 matched healthy controls, we studied the associations between dietary zinc, copper and selenium and lung cancer risk. Using multiple logistic regression analysis, the odds ratios (OR) and 95% confidence intervals (CI) of lung cancer for all subjects by increasing quartiles of dietary zinc intake were 1.0, 0.80 (0.65-0.99), 0.64 (0.51-0.81), 0.57 (0.42-0.75), respectively (p trend = 0.0004); similar results were found for men. For dietary copper, the ORs and 95% CI for all subjects were 1.0, 0.59 (0.49-0.73), 0.51 (0.41-0.64), 0.34 (0.26-0.45), respectively (p trend < 0.0001); similar reductions in risk and trend were observed by gender. Dietary selenium intake was not associated with risk, except for a significant inverse trend (p = 0.04) in men. Protective trends (p < 0.05) against lung cancer with increased dietary zinc intake were also found for all ages, BMI > 25, current smokers, pack-years < or =30, light drinkers and participants without emphysema. Increased dietary copper intake was associated with protective trends (p < 0.05) across all ages, BMI, smoking and vitamin/mineral supplement categories, pack-years < or =30 and 30.1-51.75 and participants without emphysema. Our results suggest that dietary zinc and copper intakes are associated with reduced risk of lung cancer. Given the known limitations of case-control studies, these findings must be interpreted with caution and warrant further investigation.


Assuntos
Cobre/administração & dosagem , Dieta , Neoplasias Pulmonares/epidemiologia , Selênio/administração & dosagem , Zinco/administração & dosagem , Idoso , Índice de Massa Corporal , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Risco
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