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1.  “Drivers” of Translational Cancer Epidemiology in the 21st Century: Needs and Opportunities 
Cancer epidemiology is at the cusp of a paradigm shift--propelled by an urgent need to accelerate the pace of translating scientific discoveries into healthcare and population health benefits. As part of a strategic planning process for cancer epidemiologic research, the Epidemiology and Genomics Research Program (EGRP) at the National Cancer Institute (NCI) is leading a “longitudinal” meeting with members of the research community to engage in an on-going dialogue to help shape and invigorate the field. Here, we review a translational framework influenced by “drivers” that we believe have begun guiding cancer epidemiology towards translation in the past few years and are most likely to drive the field further in the next decade. The drivers include: (1) collaboration and team science; (2) technology; (3) multi-level analyses and interventions; and (4) knowledge integration from basic, clinical and population sciences. Using the global prevention of cervical cancer as an example of a public health endeavor to anchor the conversation, we discuss how these drivers can guide epidemiology from discovery to population health impact, along the translational research continuum.
PMCID: PMC3565029  PMID: 23322363
cancer; epidemiology; medicine; public health; translational research
2.  Dietary fiber and grain consumption in relation to head and neck cancer in the NIH-AARP Diet and Health Study 
Cancer causes & control : CCC  2011;22(10):1405-1414.
Dietary fiber and grain consumption may reduce the risk of head and neck cancer; however, the epidemiological evidence is limited. We investigated this relationship in the National Institutes of Health (NIH)-AARP Diet and Health Study.
Cox proportional hazards models were used to calculate multivariable hazard ratios (HR) and 95% confidence intervals (CI) to investigate dietary fiber and grain intake in relation to head and neck cancer.
During approximately 11 years of follow-up, 1,867 (401 women/1,466 men) cases of head and neck cancer were diagnosed. Our data indicated that the relationship between fiber and grain intake and head and neck cancer is modified by sex (p-interactions <0.001 and 0.001, respectively). Women with higher intake of total fiber and total grains had a lower risk of head and neck cancer (HR10g/day=0.77, 95% CI=0.64-0.93; HRserving/1000kcal =0.89, 95% CI=0.80-0.99, respectively); this inverse relation was consistent across subtypes of fiber and grains. Conversely in men, the inverse associations were weaker and nonsignificant.
In the largest prospective cohort study to investigate this relation to date, intake of total fiber and grain foods was inversely associated with head and neck cancer incidence among women, but not men.
PMCID: PMC3215506  PMID: 21785948
diet; fiber; grains; head and neck cancer; prospective study
4.  Evidence synthesis and guideline development in genomic medicine: current status and future prospects 
With the accelerated implementation of genomic medicine, health-care providers will depend heavily on professional guidelines and recommendations. Because genomics affects many diseases across the life span, no single professional group covers the entirety of this rapidly developing field.
To pursue a discussion of the minimal elements needed to develop evidence-based guidelines in genomics, the Centers for Disease Control and Prevention and the National Cancer Institute jointly held a workshop to engage representatives from 35 organizations with interest in genomics (13 of which make recommendations). The workshop explored methods used in evidence synthesis and guideline development and initiated a dialogue to compare these methods and to assess whether they are consistent with the Institute of Medicine report “Clinical Practice Guidelines We Can Trust.”
The participating organizations that develop guidelines or recommendations all had policies to manage guideline development and group membership, and processes to address conflicts of interests. However, there was wide variation in the reliance on external reviews, regular updating of recommendations, and use of systematic reviews to assess the strength of scientific evidence.
Ongoing efforts are required to establish criteria for guideline development in genomic medicine as proposed by the Institute of Medicine.
PMCID: PMC4272332  PMID: 24946156
evidence synthesis; genomic medicine; guideline development
5.  Heme-related gene expression signatures of meat intakes in lung cancer tissues 
Molecular carcinogenesis  2013;53(7):548-556.
Lung cancer causes more deaths worldwide than any other cancer. In addition to cigarette smoking, dietary factors may contribute to lung carcinogenesis. Epidemiologic studies, including the Environment and Genetics in Lung cancer Etiology (EAGLE), have reported increased consumption of red/processed meats to be associated with higher risk of lung cancer. Heme-iron toxicity may link meat intake with cancer. We investigated this hypothesis in meat-related lung carcinogenesis using whole genome expression.
We measured genome-wide expression (HG-U133A) in 49 tumor and 42 non-involved fresh frozen lung tissues of 64 adenocarcinoma EAGLE patients. We studied gene expression profiles by high-versus-low meat consumption, with and without adjustment by sex, age, and smoking. Threshold for significance was a False Discovery Rate (FDR) ≤0.15. We studied whether the identified genes played a role in heme-iron related processes by means of manually curated literature search and gene ontology-based pathway analysis.
We found that gene expression of 232 annotated genes in tumor tissue significantly distinguished lung adenocarcinoma cases who consumed above/below the median intake of fresh red meats (FDR=0.12). Sixty-three (~28%) of the 232 identified genes (12 expected by chance, p-value<0.001) were involved in heme binding, absorption, transport, and Wnt signaling pathway (e.g., CYPs, TPO, HPX, HFE, SLCs, WNTs). We also identified several genes involved in lipid metabolism (e.g., NCR1, TNF, UCP3) and oxidative stress (e.g., TPO, SGK2, MTHFR) that may be indirectly related to heme-toxicity.
The study’s results provide preliminary evidence that heme-iron toxicity might be one underlying mechanism linking fresh red meat intake and lung cancer.
PMCID: PMC4152901  PMID: 23681825
6.  Transforming Epidemiology for 21st Century Medicine and Public Health 
In 2012, the National Cancer Institute (NCI) engaged the scientific community to provide a vision for cancer epidemiology in the 21st century. Eight overarching thematic recommendations, with proposed corresponding actions for consideration by funding agencies, professional societies, and the research community emerged from the collective intellectual discourse. The themes are (i) extending the reach of epidemiology beyond discovery and etiologic research to include multilevel analysis, intervention evaluation, implementation, and outcomes research; (ii) transforming the practice of epidemiology by moving towards more access and sharing of protocols, data, metadata, and specimens to foster collaboration, to ensure reproducibility and replication, and accelerate translation; (iii) expanding cohort studies to collect exposure, clinical and other information across the life course and examining multiple health-related endpoints; (iv) developing and validating reliable methods and technologies to quantify exposures and outcomes on a massive scale, and to assess concomitantly the role of multiple factors in complex diseases; (v) integrating “big data” science into the practice of epidemiology; (vi) expanding knowledge integration to drive research, policy and practice; (vii) transforming training of 21st century epidemiologists to address interdisciplinary and translational research; and (viii) optimizing the use of resources and infrastructure for epidemiologic studies. These recommendations can transform cancer epidemiology and the field of epidemiology in general, by enhancing transparency, interdisciplinary collaboration, and strategic applications of new technologies. They should lay a strong scientific foundation for accelerated translation of scientific discoveries into individual and population health benefits.
PMCID: PMC3625652  PMID: 23462917
big data; clinical trials; cohort studies; epidemiology; genomics; medicine; public health; technologies; training; translational research
7.  Anthropometric Measures and Physical Activity and the Risk of Lung Cancer in Never-Smokers: A Prospective Cohort Study 
PLoS ONE  2013;8(8):e70672.
Worldwide, lung cancer in never-smokers is ranked the seventh most common cause of cancer death; however, the etiology of lung cancer in never-smokers is unclear. We investigated associations for body mass index (BMI) at various ages, waist circumference, hip circumference, and physical activity with lung cancer in 158,415 never-smokers of the NIH-AARP Diet and Health Study. Multivariable hazard ratios (HR) and 95% confidence intervals (CI) were estimated from Cox proportional hazards models. Over 11 years of follow-up, 532 lung cancer cases occurred. The risk estimate for obese (BMI≥30 kg/m2) participants at baseline was 1.21 (95%CI = 0.95–1.53) relative to those with a normal BMI between 18.5≤BMI<25.0. Overweight (25.0≤BMI<30.0) at age 18 (HRoverweight-vs-normal = 1.51;95%CI = 1.01–2.26) and time spent sitting (HR≥3 hrs-vs-<3 hrs = 1.32;95%CI = 1.00–1.73) was each associated with lung cancer after adjustment for baseline BMI, as was waist (HRQ4-vs-Q1 = 1.75;95%CI = 1.09–2.79) and hip circumference (HRQ4-vs-Q1 = 0.62;95%CI = 0.39–0.99), after mutual adjustment for each other and baseline BMI. No associations were observed for vigorous activity or television watching. In summary, using a large prospective cohort study, we found no evidence that BMI at baseline or middle age was associated with decreased lung cancer risk in never smokers. If anything, we observed some evidence for positive associations with a larger BMI or waist circumference.
PMCID: PMC3734257  PMID: 23940620
8.  The Geometric Increase in Meta-Analyses from China in the Genomic Era 
PLoS ONE  2013;8(6):e65602.
Meta-analyses are increasingly popular. It is unknown whether this popularity is driven by specific countries and specific meta-analyses types. PubMed was used to identify meta-analyses since 1995 (last update 9/1/2012) and catalogue their types and country of origin. We focused more on meta-analyses from China (the current top producer of meta-analyses) versus the USA (top producer until recently). The annual number of meta-analyses from China increased 40-fold between 2003 and 2011 versus 2.4-fold for the USA. The growth of Chinese meta-analyses was driven by genetics (110-fold increase in 2011 versus 2003). The HuGE Navigator identified 612 meta-analyses of genetic association studies published in 2012 from China versus only 109 from the USA. We compared in-depth 50 genetic association meta-analyses from China versus 50 from USA in 2012. Meta-analyses from China almost always used only literature-based data (92%), and focused on one or two genes (94%) and variants (78%) identified with candidate gene approaches (88%), while many USA meta-analyses used genome-wide approaches and raw data. Both groups usually concluded favorably for the presence of genetic associations (80% versus 74%), but nominal significance (P<0.05) typically sufficed in the China group. Meta-analyses from China typically neglected genome-wide data, and often included candidate gene studies published in Chinese-language journals. Overall, there is an impressive rise of meta-analyses from China, particularly on genetic associations. Since most claimed candidate gene associations are likely false-positives, there is an urgent global need to incorporate genome-wide data and state-of-the art statistical inferences to avoid a flood of false-positive genetic meta-analyses.
PMCID: PMC3680482  PMID: 23776510
9.  Body Mass Index and Risk of Lung Cancer Among Never, Former, and Current Smokers 
Although obesity has been directly linked to the development of many cancers, many epidemiological studies have found that body mass index (BMI)—a surrogate marker of obesity—is inversely associated with the risk of lung cancer. These studies are difficult to interpret because of potential confounding by cigarette smoking, a major risk factor for lung cancer that is associated with lower BMI.
We prospectively examined the association between BMI and the risk of lung cancer among 448 732 men and women aged 50–71 years who were recruited during 1995–1996 for the National Institutes of Health–AARP Diet and Health Study. BMI was calculated based on the participant’s self-reported height and weight on the baseline questionnaire. We identified 9437 incident lung carcinomas (including 415 in never smokers) during a mean follow-up of 9.7 years through 2006. Multivariable Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with adjustment for lung cancer risk factors, including smoking status. To address potential bias due to preexisting undiagnosed disease, we excluded potentially unhealthy participants in sensitivity analyses. All statistical tests were two-sided.
The crude incidence rate of lung cancer over the study follow-up period was 233 per 100 000 person-years among men and 192 per 100 000 person-years among women. BMI was inversely associated with the risk of lung cancer among both men and women (BMI ≥35 vs 22.5–24.99 kg/m2: HR = 0.81, 95% CI = 0.70 to 0.94 and HR = 0.73, 95% CI = 0.61 to 0.87, respectively). The inverse association was restricted to current and former smokers and was stronger after adjustment for smoking. Among smokers, the inverse association persisted even after finely stratifying on smoking status, time since quitting smoking, and number of cigarettes smoked per day. Sensitivity analyses did not support the possibility that the inverse association was due to prevalent undiagnosed disease.
Our results suggest that a higher BMI is associated with a reduced risk of lung cancer in current and former smokers. Our inability to attribute the inverse association between BMI and the risk of lung cancer to residual confounding by smoking or to bias suggests the need for considering other explanations.
PMCID: PMC3352831  PMID: 22457475
10.  Racial Differences in Chronic Immune Stimulatory Conditions and Risk of Non-Hodgkin's Lymphoma in Veterans From the United States 
Journal of Clinical Oncology  2010;29(4):378-385.
To examine underlying etiologic factors that may explain the racial disparity in non-Hodgkin's lymphoma (NHL) incidence patterns.
Patients and Methods
We assessed immune-related conditions and risk of developing NHL among more than 4 million hospitalized US veterans including 9,496 patients with NHL (7,999 white patients and 1,497 black patients) with up to 26 years of follow-up. We used time-dependent Poisson regression to estimate rate ratios (RRs) and 95% CIs for NHL risk among patients with a history of specific autoimmune diseases, infections, and allergies compared with patients without such history, adjusting for attained age, calendar year, race, number of hospital visits, and time between study entry and exit.
Patients with infectious conditions had an increased risk of developing NHL (RR, 1.2; 95% CI, 1.1 to 1.2), particularly for gastrohepatic, genital, and systemic infectious conditions. Patients with autoimmune disease were generally more likely to develop NHL than patients without autoimmune disease, especially for conditions that typically present with detectable autoantibodies with systemic involvement (RR, 2.0; 95% CI, 1.8 to 2.2). Allergies were also associated with increased risk (RR, 1.4; 95% CI, 1.3 to 1.5). Although the risk of NHL was lower for blacks than whites (RR, 0.87; 95% CI, 0.82 to 0.92), blacks had a slightly higher risk of NHL associated with infections than whites (likelihood ratio test, P = .002) and a tendency toward higher risk associated with allergies (likelihood ratio test, P = .05). Risks associated with autoimmune conditions were similar by race (likelihood ratio test, P = .5).
The observed difference in NHL risk by race supports a role for race-related differences in genes regulating immune/inflammatory response.
PMCID: PMC3058284  PMID: 21172877
11.  Cruciferous vegetable intake and lung cancer risk: a nested case-control study matched on cigarette smoking 
Due predominantly to cigarette smoking, lung cancer is the leading cancer-related cause of death worldwide. Cruciferous vegetables may reduce lung cancer risk. The association between intake of cruciferous vegetables and lung cancer risk was investigated in the CLUE II study, a community-based cohort established in 1989.
We matched 274 incident cases of lung cancer diagnosed from 1990–2005 to 1089 cancer-free controls on age, sex, and cigarette smoking. Dietary information was collected at baseline. Multivariable odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression.
Intake of cruciferous vegetables were inversely associated with lung cancer risk (highest-versus-lowest fourth: OR Q4vsQ1=0. 57; 95%CI = 0.38–0.85; p-trend=0.01). The inverse associations held true for former smokers (ORQ4vsQ1=0.49; 95%CI = 0.27–0.92; p-trend=0.05) and current smokers (ORQ4vsQ1)= 0.52; 95%CI = 0.29–0.95; p-trend=0.02).
After careful control of cigarette smoking, higher intake of cruciferous vegetable was associated with lower risk of lung cancer.
The observed inversed association coupled with the accumulating evidence suggests that cruciferous vegetables are inversely associated lung cancer risk and this association seems to hold true beyond the confounding effects of cigarette smoking.
PMCID: PMC2952042  PMID: 20841387
Cruciferous vegetables; isothiocyanates; lung cancer risk
12.  Alcohol Consumption and the Risk of Nasopharyngeal Carcinoma: A Systematic Review 
Nutrition and cancer  2009;61(1):1-15.
The evidence concerning the influence of alcohol drinking on the risk of nasopharyngeal carcinoma (NPC) has yielded intriguing findings but has lacked a clear-cut interpretation due to inconsistencies. To unify this body of evidence, we performed a systematic review. With funding and using a protocol developed by the World Cancer Research Fund (WCRF), 15 bibliographic databases were searched for epidemiological studies that reported a measure of association between alcoholic beverage consumption and NPC. Pooled odds ratios (ORs) for highest-vs.-lowest categories of total alcohol intake was obtained by using an inverse-variance weighted random-effects model. A dose-response trend was examined in models using generalized least square estimation. The search identified 14 case-control studies from 5 countries. For total alcohol intake, the pooled ORs in a comparison of the highest to the lowest category was 1.33 (95% CI: = 1.09–1.62) in 11 studies. Data from 6 studies indicated a J-shape dose-response trend, with NPC risk decreasing with up to 15 drinks/wk and increasing with higher intake. Fewer data were available to assess the associations between NPC and intake of beer, wine, and spirits. The potential J-shaped dose-response trend suggests a reduced risk of NPC related to the light alcohol drinking, an observation that warrants further study. Considered in total, the quantitative summaries of the case-control evidence suggest that heavy alcohol consumption is associated with an increased risk of NPC.
PMCID: PMC3072894  PMID: 19116871
13.  Dietary quercetin, quercetin-gene interaction, metabolic gene expression in lung tissue and lung cancer risk 
Carcinogenesis  2009;31(4):634-642.
Epidemiological and mechanistic evidence on the association of quercetin-rich food intake with lung cancer risk and carcinogenesis are inconclusive. We investigated the role of dietary quercetin and the interaction between quercetin and P450 and glutathione S-transferase (GST) polymorphisms on lung cancer risk in 1822 incident lung cancer cases and 1991 frequency-matched controls from the Environment And Genetics in Lung cancer Etiology study. In non-tumor lung tissue from 38 adenocarcinoma patients, we assessed the correlation between quercetin intake and messenger RNA expression of the same P450 and GST metabolic genes. Multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for sex-specific quintiles of intake were calculated using unconditional logistic regression adjusting for putative risk factors. Frequent intake of quercetin-rich foods was inversely associated with lung cancer risk (OR = 0.49; 95% CI: 0.37–0.67; P-trend < 0.001) and did not differ by P450 or GST genotypes, gender or histological subtypes. The association was stronger in subjects who smoked >20 cigarettes per day (OR = 0.35; 95% CI: 0.19–0.66; P-trend = 0.003). Based on a two-sample t-test, we compared gene expression and high versus low consumption of quercetin-rich foods and observed an overall upregulation of GSTM1, GSTM2, GSTT2, and GSTP1 as well as a downregulation of specific P450 genes (P-values < 0.05, adjusted for age and smoking status). In conclusion, we observed an inverse association of quercetin-rich food with lung cancer risk and identified a possible mechanism of quercetin-related changes in the expression of genes involved in the metabolism of tobacco carcinogens in humans. Our findings suggest an interplay between quercetin intake, tobacco smoking, and lung cancer risk. Further research on this relationship is warranted.
PMCID: PMC2847089  PMID: 20044584
14.  Alcohol Consumption and Lung Cancer Risk in the Environment and Genetics in Lung Cancer Etiology (EAGLE) Study 
American Journal of Epidemiology  2009;171(1):36-44.
The authors investigated the relation between alcohol consumption and lung cancer risk in the Environment and Genetics in Lung Cancer Etiology (EAGLE) Study, a population-based case-control study. Between 2002 and 2005, 2,100 patients with primary lung cancer were recruited from 13 hospitals within the Lombardy region of Italy and were frequency-matched on sex, area of residence, and age to 2,120 randomly selected controls. Alcohol consumption during adulthood was assessed in 1,855 cases and 2,065 controls. Data on lifetime tobacco smoking, diet, education, and anthropometric measures were collected. Adjusted odds ratios and 95% confidence intervals for categories of mean daily ethanol intake were calculated using unconditional logistic regression. Overall, both nondrinkers (odds ratio = 1.42, 95% confidence interval: 1.03, 2.01) and very heavy drinkers (≥60 g/day; odds ratio = 1.44, 95% confidence interval: 1.01, 2.07) were at significantly greater risk than very light drinkers (0.1–4.9 g/day). The alcohol effect was modified by smoking behavior, with no excess risk being observed in never smokers. In summary, heavy alcohol consumption was a risk factor for lung cancer among smokers in this study. Although residual confounding by tobacco smoking cannot be ruled out, this finding may reflect interplay between alcohol and smoking, emphasizing the need for preventive measures.
PMCID: PMC2800301  PMID: 19933698
alcohol drinking; case-control studies; ethanol; lung neoplasms; risk factors; smoking
15.  Copy number variants of GSTM1 and GSTT1 in relation to lung cancer risk in a prospective cohort study 
Annals of epidemiology  2009;19(8):546-552.
Previous studies did not discriminate wild-type from hemizygous genotypes of GSTM1 and GSTT1. In this study, we investigated wild-type, hemizygous deletion, and homozygous deletion genotypes of GSTM1 and GSTT1 and lung cancer risk.
We conducted a nested case-control study of 143 primary incident lung cancer cases and 447 matched to cancer-free controls Genotyped data were obtained using a real-time PCR-based assay. Conditional logistic regression models were used to estimate odds ratios (ORs) and 95% Confidence Intervals (CIs).
Compared to GSTM1 wild-type carriers, the relative odds of lung cancer increased from 1.49 (95% CI=0.66–3.40) to 1.80 (95% CI=0.81–4.02) for the hemizygous and homozygous deletion genotypes, respectively (p-trend=0.13). The strongest associations were seen among those who smoked <1 pack/day and had ≥deletion variant of GSTM1 (OR=3.25; 95% CI=0.93–11.34; p-trend=0.07) whereas the reverse was observed for smokers who smoked ≥1 pack per day (OR=0.80; 95% CI=0.24–2.67; p-interaction=0.08). No clear associations were observed for GSTT1 genotypes.
Risk of lung cancer increased as the number of deletion variants increased for GSTM1, though the associations were non-significant. Discriminating between the wild-type, hemizygous, and homozygous deletion GSTM1 genotypes permitted a more precise characterization of the associations between GSTM1 deletion variants and lung cancer.
PMCID: PMC2720160  PMID: 19394866
Glutathione S-transferase; GSTM1; GSTT1; lung carcinoma; hemizygous deletion; homozygous deletion; copy number variants; metabolic genes
16.  Intakes of red meat, processed meat, and meat-mutagens increase lung cancer risk 
Cancer research  2009;69(3):932-939.
Red and processed meat intake may increase lung cancer risk. However, the epidemiologic evidence is inconsistent and few studies have evaluated the role of meat-mutagens formed during high cooking temperatures. We investigated the association of red meat, processed meat, and meat-mutagen intake with lung cancer risk in Environment And Genetics in Lung cancer Etiology (EAGLE), a population-based case-control study. Primary lung cancer cases (n=2101) were recruited from 13 hospitals within the Lombardy region of Italy examining ~80% of the cases from the area. Non-cancer population controls (n=2120), matched to cases on gender, residence, and age, were randomly selected from the same catchment area. Diet was assessed in 1903 cases and 2073 controls, and used in conjunction with a meat-mutagen database to estimate intake of heterocyclic amines and benzo[a]pyrene. Multivariable odds ratios (ORs) and 95% confidence intervals (CIs) for sex-specific tertiles of intake were calculated using unconditional logistic regression. Red and processed meat were positively associated with lung cancer risk (highest-versus-lowest tertile: OR=1.8; 95% CI=1.5–2.2; p-trend<0.001 and OR=1.7; 95% CI=1.4–2.1; p-trend<0.001, respectively); the risks were strongest among never smokers (OR=2.4, 95% CI=1.4–4.0, p-trend=0.001 and OR=2.5, 95% CI=1.5–4.2, p-trend=0.001, respectively). Heterocyclic amines and benzo[a]pyrene were significantly associated with increased risk of lung cancer. When separated by histology, significant positive associations for both meat groups were restricted to adenocarcinoma and squamous cell carcinoma, but not small cell carcinoma of the lung. In summary, red meat, processed meat, and meat-mutagens were independently associated with increased risk of lung cancer.
PMCID: PMC2720759  PMID: 19141639
red meat; processed meat; meat-mutagens; cooking methods; lung cancer
17.  Cruciferous vegetable consumption and lung cancer risk: a systematic review 
Cruciferous vegetables, rich in isothiocyanates, may protect against lung cancer. Glutathione S-transferases are important in metabolizing isothiocyanates; hence, variants in GST genes may modify the association between cruciferous vegetable intake and lung cancer. We carried out a systematic review to characterize the association between cruciferous vegetable intake and lung cancer risk, with an emphasis on the potential interaction between cruciferous vegetables and GST gene variants.
A search of the epidemiological literature through December, 2007 was conducted using 15 bibliographic databases without language restrictions. Thirty-one studies on the association between lung cancer and either total cruciferous vegetable consumption (6 cohort and 13 case-control studies) or specific cruciferous vegetables (1 cohort and 11 case-control studies) were included.
We ascertained 31 studies of either total cruciferous vegetable consumption (6 cohort,13 case-control studies) or specific cruciferous vegetables (1 cohort, 11 case-control studies) in relation to lung cancer risk. The risk of lung cancer among those in the highest category of total cruciferous vegetable intake was 23% lower in case-control studies (random-effects pooled odds ratio 0.77; 95% CI 0.68-0.88) and 17% lower in cohort studies (pooled relative risk 0.83; 95% CI 0.62-1.08) compared to those in the lowest category of intake. The strongest inverse association of total cruciferous vegetable intake with lung cancer risk was seen among individuals with GSTM1 and GSTT1 double null genotypes (OR 0.41; 95% CI 0.26-0.65).
Epidemiologic evidence suggests that cruciferous vegetable intake may be weakly and inversely associated with lung cancer risk. Due to a gene-diet interaction, the strongest inverse association was among those with homozygous deletion for GSTM1 and GSTT1.
PMCID: PMC2735794  PMID: 19124497

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