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2.  Maternal current smoking: Concordance between adolescent proxy and mother’s self-report 
Nicotine & Tobacco Research  2009;11(8):1016-1019.
The purpose of this study was to examine the extent to which adolescent reports on mother’s smoking status and mother’s self-reports on smoking are concordant with one another.
Mothers self-reported on their smoking at two timepoints (first query and second query), while the adolescents reported on their mother’s smoking status at one timepoint. Kappa values and percent exact agreement as well as sensitivity and specificity were calculated to examine the degree of agreement between child and mother’s reports at the two timepoints.
Overall, the results indicated good concordance between mothers’ self-reports and adolescent reports on smoking. Specifically, higher concordance was observed for mother’s first query compared with mother’s second query (Κ = 0.69 vs. Κ = 0.51). Younger adolescents and girls provided more concordant reports than older adolescents and boys.
The results indicate that adolescent reports on mothers’ smoking behavior can be used as a proxy to obtain data if mothers’ self-report data are not available. Our results further suggest that when reports are not collected concurrently, self-report data obtained from the mothers prior to the proxy report obtained from her adolescent may be more reliable than the other way around.
PMCID: PMC2711984  PMID: 19531668
3.  Association Between Hypothyroidism and Hepatocellular Carcinoma: A Case-Control Study in the United States 
Hepatology (Baltimore, Md.)  2009;49(5):1563-1570.
Thyroid hormones play an essential role in lipid mobilization, lipid degradation, and fatty acid oxidation. Hypothyroidism has been associated with nonalcoholic steatohepatitis; however, the association between thyroid diseases and hepatocellular carcinoma (HCC) in men and women has not been well established. We investigated the association between hypothyroidism and HCC risk in men and women in a case-control study, which included 420 eligible patients with HCC and 1104 healthy controls. We used multivariate unconditional logistic regression models to control for the confounding effects of established HCC risk factors. A long-term history of hypothyroidism (> 10 years) was associated with a statistically significant high risk of HCC in women; after adjusting for demographic factors, diabetes, hepatitis, alcohol consumption, cigarette smoking, and family history of cancer, the odds ratio (OR) was 2.9 (95% confidence interval [CI], 1.3–6.3). Restricted analyses among hepatitis virus—negative subjects, nondrinkers, nondiabetics, nonsmokers, and nonobese individuals indicated a significant association between hypothyroidism and HCC, with an approximate two-fold to three-fold increased risk of HCC development. We observed risk modification among women with diabetes mellitus (OR = 9.4; 95% CI = 2.7–32.7) and chronic hepatitis virus infection (OR = 31.2; 95% CI = 6.3–153.2). A history of hyperthyroidism was not significantly related to HCC (OR = 1.7; CI = 0.6–5.1). We noted significant elevated risk association between hypothyroidism and HCC in women that was independent of established HCC risk factors. Experimental investigations are necessary for thorough assessment of the relationship between thyroid disorders and HCC.
PMCID: PMC3715879  PMID: 19399911
4.  Sociodemographic Characteristics, Health Beliefs, and the Accuracy of Cancer Knowledge 
Journal of Cancer Education  2009;24(1):58-64.
Recent studies have found that knowledge about cancer prevention and treatment differs across ethnic and socioeconomic status (SES) backgrounds, which could directly impact our decisions to engage in protective health behaviors. In this study, we examined sociodemographic-based differences in cancer knowledge and health beliefs and examined differences in the accuracy of the cancer knowledge based on health beliefs.
Cross-sectional surveys were conducted between July 1995 and March 2004 on adult, healthy, cancer-free control participants (N = 2074; 50% male) enrolled into a molecular epidemiological case-control study. Most were non-Hispanic white, 14% were African American, and 8% were Hispanic. Participants were personally interviewed on 6 items assessing health beliefs and 10 items assessing cancer knowledge.
Unadjusted differences in cancer knowledge were observed by gender, age, ethnicity, household income, educational attainment, and smoking status. After adjusting for the other sociodemographic characteristics, women had more accurate knowledge than men, the accuracy of knowledge increased with higher educational attainment and annual household income, and never smokers had more accurate knowledge than ever smokers (P < .01 for all). Moreover, accurate cancer knowledge was associated with protective health beliefs; eg, the belief that changing health habits was worthwhile was associated with more accurate knowledge.
Results emphasize the need to develop health education programs that enhance cancer knowledge among individuals of low SES and foster protective health beliefs.
PMCID: PMC3381329  PMID: 19259867
5.  Cognitive Susceptibility to Smoking: Two Paths to Experimenting among Mexican Origin Youth 
Cognitive susceptibility to smoking, defined as the lack of a firm commitment not to smoke in the future or if offered a cigarette by a friend, begins in childhood and is an early phase in the transition from never to ever smoking. Our objectives were to examine susceptibility to smoking and other psychosocial risk factors for experimentation with cigarettes among Mexican origin adolescents and to determine whether susceptibility status moderates the relationship between established risk factors for experimentation with cigarettes and future experimentation. We examined susceptibility and several psychosocial factors associated with susceptibility as baseline predictors of experimentation after 3 years of follow-up among 964 Mexican origin girls and boys between 11 and 13 years of age from the Houston metropolitan area. Participants were recruited between May 2005 and October 2006 and reported that they had never experimented with cigarettes at baseline. Baseline susceptibility and experimentation rates were 23% and 9%, respectively, whereas the follow-up experimentation rate, among those who had not experimented at baseline, was 22%. Susceptible adolescents at baseline were 2.6 times more likely to have experimented with cigarettes by follow-up. Baseline susceptibility moderated the relationship between experimentation at follow-up and the psychosocial risk factors assessed at baseline. Susceptibility is a valid and strong marker for the transition to experimentation for Mexican origin adolescents. Our results suggest that tailoring primary prevention programs by a youth’s susceptibility status may increase the efficacy of prevention efforts among Mexican origin youth.
PMCID: PMC3183967  PMID: 19959696
6.  The evolving discipline of molecular epidemiology of cancer 
Carcinogenesis  2009;31(1):127-134.
Classical epidemiologic studies have made seminal contributions to identifying the etiology of most common cancers. Molecular epidemiology was conceived of as an extension of traditional epidemiology to incorporate biomarkers with questionnaire data to further our understanding of the mechanisms of carcinogenesis. Early molecular epidemiologic studies employed functional assays. These studies were hampered by the need for sequential and/or prediagnostic samples, viable lymphocytes and the uncertainty of how well these functional data (derived from surrogate lymphocytic tissue) reflected events in the target tissue. The completion of the Human Genome Project and Hapmap Project, together with the unparalleled advances in high-throughput genotyping revolutionized the practice of molecular epidemiology. Early studies had been constrained by existing technology to use the hypothesis-driven candidate gene approach, with disappointing results. Pathway analysis addressed some of the concerns, although the study of interacting and overlapping gene networks remained a challenge. Whole-genome scanning approaches were designed as agnostic studies using a dense set of markers to capture much of the common genome variation to study germ-line genetic variation as risk factors for common complex diseases. It should be possible to exploit the wealth of these data for pharmacogenetic studies to realize the promise of personalized therapy. Going forward, the temptation for epidemiologists to be lured by high-tech ‘omics’ will be immense. Systems Epidemiology, the observational prototype of systems biology, is an extension of classical epidemiology to include powerful new platforms such as the transcriptome, proteome and metabolome. However, there will always be the need for impeccably designed and well-powered epidemiologic studies with rigorous quality control of data, specimen acquisition and statistical analysis.
PMCID: PMC2802669  PMID: 20022891
7.  Exposure to Smoking Imagery in the Movies and Experimenting with Cigarettes among Mexican Heritage Youth 
There is growing evidence that an adolescent’s decision to try cigarettes is influenced by level of exposure to movies in which smoking is portrayed. Less is known about how ethnicity affects this process. We examined whether acculturation and/or country of birth influence the relationship between exposure to smoking imagery in the movies and experimenting with cigarettes among Mexican origin youth. We prospectively followed 1,328 Mexican origin adolescents aged 11–13 at baseline. We assessed which of 50 movies (randomly selected from a pool of 250 popular contemporary movies released from 1999–2004 and content analyzed for smoking) adolescents had seen. Smoking behavior was assessed at baseline and at 6-month intervals over 24 months. 10% of the adolescents had experimented at baseline; 17% tried subsequently. Multivariate analyses revealed, as exposure to smoking imagery in the movies increased, the chances of having ever experimented (AOR=1.27; 95% CI: 1.10–1.48) and of being a new experimenter (AOR=1.19; 95% CI: 1.01–1.40) increased, equivalent to a 4.2% increased risk of ever and a 3.0% increased risk of new experimenting for each additional quartile of movie exposure. This effect was moderated by country of birth. For Mexican-born youth, exposure to smoking imagery in the movies was the strongest independent predictor of new experimentation (AOR=1.52; 95% CI: 1.14–2.05). For US-born youth, we observed a ceiling effect: the percent of experimenters increased with increasing exposure, and then flattened. Among Mexican-born youth exposure to smoking imagery in the movies may be an important part of the acculturation process associated with smoking initiation.
PMCID: PMC2791895  PMID: 19959693
Experimenting with cigarettes; exposure to smoking imagery; Mexican origin youth
8.  Genetic and Non-Genetic Covariates of Pain Severity in Patients with Adenocarcinoma of the Pancreas: Assessing the Influence of Cytokine Genes 
We previously demonstrated that select cytokine gene polymorphisms in interleukin (IL)-8 are a significant predictor for pain and analgesia in patients with lung cancer. This study explores the role of thirteen potentially functional polymorphisms in cytokine genes including IL-1β, IL-6, IL-8, IL-10, IL-18, tumor necrosis factor (TNF-α), and nuclear factor kappa-B subunit 1 (NFkappaB1) in pain severity in patients with pancreatic cancer. We evaluated a series opatients with histologically-confirmed adenocarcinoma of the pancreas (n=484) who had completed a self-administered survey of pain prior to initiating any cancer treatment. DNA (n=156) available for a subset of white patients was assayed and assessed for association with pain severity. Results showed that 26% (128/484) reported experiencing severe pain (score of > 7 on a 0–10 scale). Severe pain varied by stage of disease (odds ratio [OR] Stage II=4.02, 95% confidence interval (CI)=1.07, 15.07; Stage III=5.02, 95% CI=1.28, 19.61; Stage IV=6.90, 95% CI=1.96, 24.29), ethnicity (OR non-Hispanic blacks=3.67; 95% CI=1.44, 9.38), reports of depressed mood (OR=1.94; 95% CI=1.09, 3.43), and female sex (OR=1.78; 95% CI=1.04, 3.05). Controlling for these covariates, IL8-251T/A (OR=2.43, 95% CI=1.3, 4.7, P<0.009) significantly predicted severe pain in a subset of white patients. When we adjusted for reported analgesic use, we found that IL8-251T/A persisted as a predictor for severe pain, with carriers of TT and AT genotypes having more than a threefold risk (OR=3.23, 95% CI=1.4, 4.7) for severe pain relative to the AA genotypes. We provide preliminary evidence of the role of IL-8 in the severity of pain in pancreatic cancer patients. Additional studies are needed in larger cohorts of patients.
PMCID: PMC2795073  PMID: 19692203
Pain; genes; cytokines; epidemiology; cancer; analgesia; molecular epidemiology
9.  Novel Susceptibility Loci for Second Primary Tumors/Recurrence in Head and Neck Cancer Patients: Large Scale Evaluation of Genetic Variants 
This study was aimed to identify novel susceptibility variants for second primary tumor (SPT) or recurrence in curatively treated early stage head and neck squamous cell carcinoma (HNSCC) patients.
We constructed a custom chip containing a comprehensive panel of 9645 chromosomal and mitochondrial single nucleotide polymorphisms (SNPs) representing 998 cancer-related genes selected by a systematic prioritization schema. Using this chip, we genotyped 150 early-stage HNSCC patients with and 300 matched patients without SPT/recurrence from a prospectively conducted randomized trial and assessed the association of these SNPs with risk of SPT/recurrence.
Individually, six chromosomal SNPs and seven mitochondrial SNPs (mtSNPs) were significantly associated with risk of SPT/recurrence after adjustment for multiple comparisons. A strong gene-dosage effect was observed these SNPs were combined, as evidenced by a progressively increasing SPT/recurrence risk as the number of unfavorable genotypes increased (P for trend < 1.00×10−20). Several polygenic analyses suggest an important role of interconnected functional network and gene-gene interaction in modulating SPT/recurrence. Furthermore, incorporation of these genetic markers into a multivariate model improved significantly the discriminatory ability over the models containing only clinical and epidemiologic variables.
This is the first large scale systematic evaluation of germline genetic variants for their roles in HNSCC SPT/recurrence. The study identified several promising susceptibility loci and demonstrated the cumulative effect of multiple risk loci in HNSCC SPT/recurrence. Furthermore, this study underscores the importance of incorporating germline genetic variation data with clinical and risk factor data in constructing prediction models for clinical outcomes.
PMCID: PMC2964280  PMID: 19584075
iSelect Infinium; Single nucleotide polymorphisms; Head and neck cancer; Secondary primary tumor; recurrence
10.  The role of inflammation gene polymorphisms on pain severity in lung cancer patients 
Many of the same inflammatory factors that promote tumor growth are also hypothesized to function as pain modulators. There is substantial interindividual variation in pain severity in cancer patients. Therefore, we evaluated 59 SNPs in 37 inflammation genes in newly diagnosed non-Hispanic Caucasian lung cancer patients (n=667) and assessed their association with pain severity. Patients rated their pain “during the past week” on an 11-point numeric scale, (0= ‘no pain’ and 10= ‘pain as bad as you can imagine’) at presentation, prior to initiating cancer therapy. Reported analgesic use was abstracted from charts and converted to an equivalent dose of morphine (MEDD). Results showed that 16% of the patients reported severe pain (score ≥ 7). Advanced stage of disease (OR=2.34; 95% CI=1.50-3.65, p-value=0.001), age≤ 50 (OR=2.10; 95%CI=1.32-3.30, p-value=0.002), reports of depressed mood (OR=3.68; 95%CI=1.96-6.93, p-value=0.001); fatigue (OR=3.72; 95% CI=2.36-5.87, p-value=0.001) and MEDD (OR=1.02; 95% C.I=1.01, 1.03) were significantly correlated with severe pain. Controlling for these non-genetic covariates, we found that patients with CC genotypes for PTGS2 exon10+837T>C (rs5275) were at lower risk for severe pain (OR=0.33; 95% Confidence Interval=0.11-0.97) and an additive model for TNF α -308GA (rs1800629) (OR=1.67, 95% CI=1.08,2.58) and NFKBIA Ex6+50C>T (rs8904) was predictive of severe pain (OR=0.64, 95% CI=0.43,0.93). In a multi-gene analysis, we found a gene-dose effect, with each protective genotype reducing the risk for severe pain by as much as 38%. This study suggests the importance of inflammation gene polymorphisms in modulating pain severity. Additional studies are needed to validate our findings.
PMCID: PMC2759856  PMID: 19773451
Pain; Genes; Inflammation; Epidemiology; Cancer
11.  Deciphering the impact of common genetic variation on lung cancer risk: A genome-wide association study 
Cancer research  2009;69(16):6633-6641.
To explore the impact of common variation on the risk of developing lung cancer we conducted a two-phase genome-wide association (GWA) study. In Phase 1, we compared the genotypes of 511,919 tagging single nucleotide polymorphisms (tagSNPs) in 1,952 cases and 1,438 controls; in Phase 2, 30,568 SNPs were genotyped in 2,465 cases and 3,005 controls. SNP selection was based on best supported P-values from Phase 1 and two other GWA studies of lung cancer. In the combined analysis of Phases 1 and 2, the strongest associations identified were defined by SNPs mapping to 15q25.1 (rs12914385; P = 3.19 × 10−16), 5p15.33 (rs4975616; P = 6.66 × 10−7), and 6p21.33 (rs3117582; P = 9.13 × 10−7). Variation at 15q25.1, but not 5p15.33 or 6p21.33, was strongly associated with smoking behaviour with risk alleles correlated to higher consumption. Variation at 5p15.33 was shown to significantly influence induction of lung cancer histology. Pooling data from the four series provided 21,620 genotypes for 7,560 cases and 8,205 controls. A meta-analysis provided increased support that variation at 15q25.1 (rs8034191; P = 3.24 × 10−26), 5p15.33 (rs4975616; P = 2.99 × 10−9), and 6p21.33 (rs3117582; P = 4.46 × 10−10) influences lung cancer risk. The next best-supported associations were attained at 15q15.2 (rs748404: P = 1.08 × 10−6) and 10q23.31 (rs1926203; P = 1.28 × 10−6). These data indicate few common variants account for 1% of the excess familial risk underscoring the necessity of having additional large sample series for gene discovery.
PMCID: PMC2754318  PMID: 19654303
lung cancer; genome-wide association

Results 1-11 (11)