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1.  Bridging the clinical gaps: genetic, epigenetic and transcriptomic biomarkers for the early detection of lung cancer in the post-National Lung Screening Trial era 
BMC Medicine  2013;11:168.
Lung cancer is the leading cause of cancer death worldwide in part due to our inability to identify which smokers are at highest risk and the lack of effective tools to detect the disease at its earliest and potentially curable stage. Recent results from the National Lung Screening Trial have shown that annual screening of high-risk smokers with low-dose helical computed tomography of the chest can reduce lung cancer mortality. However, molecular biomarkers are needed to identify which current and former smokers would benefit most from annual computed tomography scan screening in order to reduce the costs and morbidity associated with this procedure. Additionally, there is an urgent clinical need to develop biomarkers that can distinguish benign from malignant lesions found on computed tomography of the chest given its very high false positive rate. This review highlights recent genetic, transcriptomic and epigenomic biomarkers that are emerging as tools for the early detection of lung cancer both in the diagnostic and screening setting.
doi:10.1186/1741-7015-11-168
PMCID: PMC3717087  PMID: 23870182
Biomarker; Diagnostics; Early detection; Epigenetics; Genetics; Lung cancer; Screening; Transcriptomics
2.  A case-control study of a sex-specific association between a 15q25 variant and lung cancer risk 
Background
Genetic variants located at 15q25, including those in the cholinergic receptor nicotinic cluster (CHRNA5) have been implicated in both lung cancer risk and nicotine dependence in recent genome-wide association studies. Among these variants, a 22 base pair insertion/deletion, rs3841324 showed the strongest association with CHRNA5 mRNA expression levels. However the influence of rs3841324 on lung cancer risk has not been studied in depth.
Methods
We have therefore evaluated the association of rs3841324 genotypes with lung cancer risk in a case-control study of 624 Caucasian subjects with lung cancer and 766 age- and sex-matched cancer-free Caucasian controls. We also evaluated the joint effects of rs3841324 with single-nucleotide polymorphisms (SNPs) rs16969968 and rs8034191 in the 15q25 region that have been consistently implicated in lung cancer risk.
Results
We found that the homozygous genotype with both short alleles (SS) of rs3841324 was associated with a decreased lung cancer risk in female ever smokers relative to the homozygous wild-type (LL) and heterozygous (LS) genotypes combined in a recessive model (OR adjusted = 0.55, 95% CI = 0.31–0.89, P = 0.0168). There was no evidence for a sex difference in the association between this variant and cigarettes smoked per day (CPD). Diplotype analysis of rs3841324 with either rs16969968 or rs8034191 showed that these polymorphisms influenced the lung cancer risk independently.
Conclusions and impact
This study has shown a sex difference in the association between the 15q25 variant rs3841324 and lung cancers. Further research is warranted to elucidate the mechanisms underlying these observations.
doi:10.1158/1055-9965.EPI-11-0749
PMCID: PMC3277830  PMID: 22028403
lung cancer; CHRNA5; Chromosome 15q25; rs3841324; sex-specific association
3.  Gender differences in sociodemographic and behavioral influences of physical activity in Mexican-origin adolescents 
Background
Understanding the factors that contribute to physical activity (PA) in Mexican-origin adolescents is essential to the design of effective efforts to enhance PA participation in this population.
Methods
Multivariable logistic regression was used to identify sociodemographic and behavioral correlates of self-reported PA in school and community settings in 1,154 Mexican-origin adolescents aged 12–17 years in Houston, TX.
Results
The majority of adolescents were born in the US (74%), approximately half (51%) were overweight or obese, and nearly three-quarters (73%) watched more than 2 hours of weekday television. Similarities and differences by setting and gender were observed in the relationships between sociodemographic and behavioral characteristics and PA. In boys, parental education and attending physical education (PE) were positively associated with PA across multiple PA outcomes. Adolescent linguistic acculturation was inversely associated with participation in community sports, whereas parental linguistic acculturation was positively associated with PA at school. In girls, PA in school and community settings was inversely associated with TV viewing and positively associated with PE participation.
Conclusions
These findings highlight similarities and differences in correlates of PA among boys and girls, and point towards potential sources of opportunities as well as disparities for PA behaviors in Mexican-origin adolescents.
PMCID: PMC3250565  PMID: 21952224
Mexican American; acculturation; physical education
4.  Automated detection of genetic abnormalities combined with cytology in sputum is a sensitive predictor of lung cancer 
Modern Pathology  2008;21(8):950-960.
Detection of lung cancer by sputum cytology has low sensitivity but is noninvasive and, if improved, could be a powerful tool for early lung cancer detection. To evaluate whether the accuracy of diagnosing lung cancer by evaluating sputa for cytologic atypia and genetic abnormalities is greater than that of conventional cytology alone, automated scoring of genetic abnormalities for 3p22.1 and 10q22.3 (SP-A) by fluorescence in situ hybridization (FISH) and conventional cytology was done on sputa from 35 subjects with lung cancer, 25 high-risk smokers, and 6 healthy control subjects. Multivariate analysis was performed to select variables that most accurately predicted lung cancer. A model of probability for the presence of lung cancer was derived for each subject. Cells exfoliated from patients with lung cancer contained genetic aberrations and cytologic atypias at significantly higher levels than in those from control subjects. When combined with cytologic atypia, a model of risk for lung cancer was derived that had 74% sensitivity and 82% specificity to predict the presence of lung cancer, whereas conventional cytology achieved only 37% sensitivity and 87% specificity. For diagnosing lung cancer in sputum, a combination of molecular and cytologic variables was superior to using conventional cytology alone.
doi:10.1038/modpathol.2008.71
PMCID: PMC3377448  PMID: 18500269
surfactant protein A gene; 3p22.1; FISH; cytology; field cancerization effect; sputum
5.  Genetic variants and risk of lung cancer in never smokers: a genome-wide association study 
The lancet oncology  2010;11(4):321-330.
Summary
Background
Lung cancer in individuals who have never smoked tobacco products is an increasing medical and public-health issue. We aimed to unravel the genetic basis of lung cancer in never smokers.
Methods
We did a four-stage investigation. First, a genome-wide association study of single nucleotide polymorphisms (SNPs) was done with 754 never smokers (377 matched case-control pairs at Mayo Clinic, Rochester, MN, USA). Second, the top candidate SNPs from the first study were validated in two independent studies among 735 (MD Anderson Cancer Center, Houston, TX, USA) and 253 (Harvard University, Boston, MA, USA) never smokers. Third, further replication of the top SNP was done in 530 never smokers (UCLA, Los Angeles, CA, USA). Fourth, expression quantitative trait loci (eQTL) and gene-expression differences were analysed to further elucidate the causal relation between the validated SNPs and the risk of lung cancer in never smokers.
Findings
44 top candidate SNPs were identified that might alter the risk of lung cancer in never smokers. rs2352028 at chromosome 13q31.3 was subsequently replicated with an additive genetic model in the four independent studies, with a combined odds ratio of 1·46 (95% CI 1·26–1·70, p=5·94×10−6). A cis eQTL analysis showed there was a strong correlation between genotypes of the replicated SNPs and the transcription level of the gene GPC5 in normal lung tissues (p=1·96×10−4), with the high-risk allele linked with lower expression. Additionally, the transcription level of GPC5 in normal lung tissue was twice that detected in matched lung adenocarcinoma tissue (p=6·75×10−11).
Interpretation
Genetic variants at 13q31.3 alter the expression of GPC5, and are associated with susceptibility to lung cancer in never smokers. Downregulation of GPC5 might contribute to the development of lung cancer in never smokers.
doi:10.1016/S1470-2045(10)70042-5
PMCID: PMC2945218  PMID: 20304703
6.  Rapid method for determination of DNA repair capacity in human peripheral blood lymphocytes amongst smokers 
BMC Cancer  2010;10:439.
Background
DNA repair capacity is an important determinant of susceptibility to cancer. The hOGG1 enzyme is crucial for repairing the 8-oxoguanine lesion that occurs either as a byproduct of oxidative metabolism or as a result of exogenous sources such as exposure to cigarette smoke. It has been previously reported that smokers with low hOGG1 activity had significantly higher risk of developing lung cancer as compared to smokers with high hOGG1 activity.
Methods
In the current study we elucidate the association between plasma levels of 8-OHdG and the OGG1 repair capacity. We used the commercially available 8-OHdG ELISA (enzyme-linked immunosorbent assay), the Comet assay/FLARE hOGG1 (Fragment Length Analysis by Repair Enzymes) assay for quantification of the levels of 8-OHdG and measured the constitutive, induced and unrepaired residual damage, respectively. We compared the DNA repair capacity in peripheral blood lymphocytes following H2O2 exposure in 30 lung cancer patients, 30 non-, 30 former and 30 current smoker controls matched by age and gender.
Results
Our results show that lung cancer cases and current smoker controls have similar levels of 8-OHdG lesions that are significantly higher compared to the non-smokers controls. However, lung cancer cases showed significantly poorer repair capacity compared to all controls tested, including the current smokers controls. After adjustment for age, gender and family history of smoking-related cancer using linear regression, we observed a 5-fold increase in risk of lung cancer associated with high levels of residual damage/reduced repair capacity. Reduced OGG1 activity could be expected to be a risk factor in other smoking-related cancers.
Conclusion
Our study shows that the Comet/FLARE assay is a relatively rapid and useful method for determination of DNA repair capacity. Using this assay we could identify individuals with high levels of residual damage and hence poor repair capacity who would be good candidates for intensive follow-up and screening.
doi:10.1186/1471-2407-10-439
PMCID: PMC2933626  PMID: 20718982
7.  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.
doi:10.1158/0008-5472.CAN-09-0680
PMCID: PMC2754318  PMID: 19654303
lung cancer; genome-wide association
8.  Common 5p15.33 and 6p21.33 variants influence lung cancer risk 
Nature genetics  2008;40(12):1407-1409.
We conducted a genome-wide association (GWA) study of lung cancer comparing 511,919 SNP genotypes in 1,952 cases and 1,438 controls. The most significant association was attained at 15q25.1 (rs8042374; P = 7.75 × 10−12), confirming recent observations. Pooling data with two other GWA studies (5,095 cases, 5,200 controls) and with replication in an additional 2,484 cases and 3,036 controls, we identified two newly associated risk loci mapping to 6p21.33 (rs3117582, BAT3-MSH5; Pcombined = 4.97 × 10−10) and 5p15.33 (rs401681, CLPTM1L; Pcombined = 7.90 × 10−9).
doi:10.1038/ng.273
PMCID: PMC2695928  PMID: 18978787
9.  Genome-wide association scan of tag SNPs identifies a susceptibility locus for lung cancer at 15q25.1 
Nature genetics  2008;40(5):616-622.
To identify risk variants for lung cancer, we conducted a multistage genome-wide association study. In the discovery phase, we analyzed 315,450 tagging SNPs in 1,154 current and former (ever) smoking cases of European ancestry and 1,137 frequency-matched, ever-smoking controls from Houston, Texas. For replication, we evaluated the ten SNPs most significantly associated with lung cancer in an additional 711 cases and 632 controls from Texas and 2,013 cases and 3,062 controls from the UK. Two SNPs, rs1051730 and rs8034191, mapping to a region of strong linkage disequilibrium within 15q25.1 containing PSMA4 and the nicotinic acetylcholine receptor subunit genes CHRNA3 and CHRNA5, were significantly associated with risk in both replication sets. Combined analysis yielded odds ratios of 1.32 (P < 1 × 10−17) for both SNPs. Haplotype analysis was consistent with there being a single risk variant in this region. We conclude that variation in a region of 15q25.1 containing nicotinic acetylcholine receptors genes contributes to lung cancer risk.
doi:10.1038/ng.109
PMCID: PMC2713680  PMID: 18385676
10.  Polymorphisms of cytosolic serine hydroxymethyltransferase and risk of lung cancer: a case–control analysis 
Summary
The suboptimal DNA repair capacity is a risk factor for cancer that may be modulated by dietary nutrient intake, and the serine hydroxymethyltransferase (SHMT) participates in folate metabolism and synthesis of purine and pyrimidine needed for DNA repair. Therefore, we tested our hypothesis that genetic variants of the cytosolic SHMT (SHMT1) gene are associated with lung cancer risk. In a hospital-based case-control study of 1032 non-Hispanic white lung cancer patients and 1145 matched cancer-free controls, we genotyped five common SHMT1 polymorphisms either in the promoter, exons, or 3′-untranslated regions. Although the genotype and allele frequency distribution of each SNP did not differ between cases and controls statistically significantly in the single-locus analysis, the rs638416 polymorphism in the promoter alone and the combined putative risk variant genotypes containing rs643333C, rs638416G, rs1979277T, rs3738G, and rs1979276C were associated with altered risk. Those carrying the combined 3+ risk variant genotypes had an increased risk of lung cancer (adjusted OR = 1.65, 95% CI = 1.05–2.57, compared with those having 0–1 risk genotypes; and OR = 1.21, 95% CI = 1.01–1.45, compared with those having 0–2 risk genotypes). The risk was more pronounced among older individuals (>61 years) or those having a low total folate intake or a high methionine intake. No evidence of interactions between the putative SHMT risk variant genotypes and the selected variables was found. These results suggest that SHMT1 variants may play a role in the etiology of lung cancer, and our findings need to be verified in larger prospective studies.
doi:10.1016/j.lungcan.2007.03.002
PMCID: PMC2693017  PMID: 17420066
DNA repair; genetic susceptibility; lung cancer; serine hydroxymethyltransferase; tetrahydrofolate metabolism
11.  Correlates of susceptibility to smoking among Mexican origin youth residing in Houston, Texas: A cross-sectional analysis 
BMC Public Health  2008;8:337.
Background
Survey data suggest that in Texas Latino youth exhibit higher rates of susceptibility to smoking than youth from other ethnic groups. In this analysis we examined the relationship between susceptibility to smoking and well-known risk factors associated with smoking initiation among a cohort of 11 to 13 year old Mexican origin youth residing in Houston, Texas.
Methods
We analyzed cross-sectional survey data from 1,187 participants who reported they had never smoked, even a puff of a cigarette. The survey assessed peer and family social influence, school and neighborhood characteristics, level of family acculturation and socioeconomic status, and attitudes toward smoking. Bivariate associations, Student's t-tests, and logistic regression analysis were used to examine predictors of susceptibility.
Results
Overall, 22.1% of the never-smokers were susceptible to smoking. Boys were more likely to be susceptible than girls (25.6% vs. 18.9%), and susceptible children were slightly older than non-susceptible children (12.1 vs. 11.8 years). In addition, multivariate analyses revealed that positive expectations about smoking exerted the strongest influence on susceptibility status (odds ratio = 4.85). Multivariate analyses further revealed that compared to non-susceptible participants, susceptibles were more likely to report peer influences supportive of smoking, lower subjective social status and more detentions at school, more temptations to try smoking and to have a mother and a brother who smokes.
Conclusion
Our findings suggest that interventions that target positive expectations about smoking may be useful in this population. Furthermore, because youth encounter smoking-initiation risk factors in different social environments, our results underscore the continued need for both family- and school-based primary prevention programs to adequately combat their influence. The results also can be used to inform the development of culturally sensitive programs for Mexican origin youth.
doi:10.1186/1471-2458-8-337
PMCID: PMC2569937  PMID: 18822130
12.  Polymorphisms, Mutations, and Amplification of the EGFR Gene in Non-Small Cell Lung Cancers 
PLoS Medicine  2007;4(4):e125.
Background
The epidermal growth factor receptor (EGFR) gene is the prototype member of the type I receptor tyrosine kinase (TK) family and plays a pivotal role in cell proliferation and differentiation. There are three well described polymorphisms that are associated with increased protein production in experimental systems: a polymorphic dinucleotide repeat (CA simple sequence repeat 1 [CA-SSR1]) in intron one (lower number of repeats) and two single nucleotide polymorphisms (SNPs) in the promoter region, −216 (G/T or T/T) and −191 (C/A or A/A). The objective of this study was to examine distributions of these three polymorphisms and their relationships to each other and to EGFR gene mutations and allelic imbalance (AI) in non-small cell lung cancers.
Methods and Findings
We examined the frequencies of the three polymorphisms of EGFR in 556 resected lung cancers and corresponding non-malignant lung tissues from 336 East Asians, 213 individuals of Northern European descent, and seven of other ethnicities. We also studied the EGFR gene in 93 corresponding non-malignant lung tissue samples from European-descent patients from Italy and in peripheral blood mononuclear cells from 250 normal healthy US individuals enrolled in epidemiological studies including individuals of European descent, African–Americans, and Mexican–Americans. We sequenced the four exons (18–21) of the TK domain known to harbor activating mutations in tumors and examined the status of the CA-SSR1 alleles (presence of heterozygosity, repeat number of the alleles, and relative amplification of one allele) and allele-specific amplification of mutant tumors as determined by a standardized semiautomated method of microsatellite analysis. Variant forms of SNP −216 (G/T or T/T) and SNP −191 (C/A or A/A) (associated with higher protein production in experimental systems) were less frequent in East Asians than in individuals of other ethnicities (p < 0.001). Both alleles of CA-SSR1 were significantly longer in East Asians than in individuals of other ethnicities (p < 0.001). Expression studies using bronchial epithelial cultures demonstrated a trend towards increased mRNA expression in cultures having the variant SNP −216 G/T or T/T genotypes. Monoallelic amplification of the CA-SSR1 locus was present in 30.6% of the informative cases and occurred more often in individuals of East Asian ethnicity. AI was present in 44.4% (95% confidence interval: 34.1%–54.7%) of mutant tumors compared with 25.9% (20.6%–31.2%) of wild-type tumors (p = 0.002). The shorter allele in tumors with AI in East Asian individuals was selectively amplified (shorter allele dominant) more often in mutant tumors (75.0%, 61.6%–88.4%) than in wild-type tumors (43.5%, 31.8%–55.2%, p = 0.003). In addition, there was a strong positive association between AI ratios of CA-SSR1 alleles and AI of mutant alleles.
Conclusions
The three polymorphisms associated with increased EGFR protein production (shorter CA-SSR1 length and variant forms of SNPs −216 and −191) were found to be rare in East Asians as compared to other ethnicities, suggesting that the cells of East Asians may make relatively less intrinsic EGFR protein. Interestingly, especially in tumors from patients of East Asian ethnicity, EGFR mutations were found to favor the shorter allele of CA-SSR1, and selective amplification of the shorter allele of CA-SSR1 occurred frequently in tumors harboring a mutation. These distinct molecular events targeting the same allele would both be predicted to result in greater EGFR protein production and/or activity. Our findings may help explain to some of the ethnic differences observed in mutational frequencies and responses to TK inhibitors.
Masaharu Nomura and colleagues examine the distribution ofEGFR polymorphisms in different populations and find differences that might explain different responses to tyrosine kinase inhibitors in lung cancer patients.
Editors' Summary
Background.
Most cases of lung cancer—the leading cause of cancer deaths worldwide—are “non-small cell lung cancer” (NSCLC), which has a very low cure rate. Recently, however, “targeted” therapies have brought new hope to patients with NSCLC. Like all cancers, NSCLC occurs when cells begin to divide uncontrollably because of changes (mutations) in their genetic material. Chemotherapy drugs treat cancer by killing these rapidly dividing cells, but, because some normal tissues are sensitive to these agents, it is hard to kill the cancer completely without causing serious side effects. Targeted therapies specifically attack the changes in cancer cells that allow them to divide uncontrollably, so it might be possible to kill the cancer cells selectively without damaging normal tissues. Epidermal growth factor receptor (EGRF) was one of the first molecules for which a targeted therapy was developed. In normal cells, messenger proteins bind to EGFR and activate its “tyrosine kinase,” an enzyme that sticks phosphate groups on tyrosine (an amino acid) in other proteins. These proteins then tell the cell to divide. Alterations to this signaling system drive the uncontrolled growth of some cancers, including NSCLC.
Why Was This Study Done?
Molecules that inhibit the tyrosine kinase activity of EGFR (for example, gefitinib) dramatically shrink some NSCLCs, particularly those in East Asian patients. Tumors shrunk by tyrosine kinase inhibitors (TKIs) often (but not always) have mutations in EGFR's tyrosine kinase. However, not all tumors with these mutations respond to TKIs, and other genetic changes—for example, amplification (multiple copies) of the EGFR gene—also affect tumor responses to TKIs. It would be useful to know which genetic changes predict these responses when planning treatments for NSCLC and to understand why the frequency of these changes varies between ethnic groups. In this study, the researchers have examined three polymorphisms—differences in DNA sequences that occur between individuals—in the EGFR gene in people with and without NSCLC. In addition, they have looked for associations between these polymorphisms, which are present in every cell of the body, and the EGFR gene mutations and allelic imbalances (genes occur in pairs but amplification or loss of one copy, or allele, often causes allelic imbalance in tumors) that occur in NSCLCs.
What Did the Researchers Do and Find?
The researchers measured how often three EGFR polymorphisms (the length of a repeat sequence called CA-SSR1, and two single nucleotide variations [SNPs])—all of which probably affect how much protein is made from the EGFR gene—occurred in normal tissue and NSCLC tissue from East Asians and individuals of European descent. They also looked for mutations in the EGFR tyrosine kinase and allelic imbalance in the tumors, and then determined which genetic variations and alterations tended to occur together in people with the same ethnicity. Among many associations, the researchers found that shorter alleles of CA-SSR1 and the minor forms of the two SNPs occurred less often in East Asians than in individuals of European descent. They also confirmed that EGFR kinase mutations were more common in NSCLCs in East Asians than in European-descent individuals. Furthermore, mutations occurred more often in tumors with allelic imbalance, and in tumors where there was allelic imbalance and an EGFR mutation, the mutant allele was amplified more often than the wild-type allele.
What Do These Findings Mean?
The researchers use these associations between gene variants and tumor-associated alterations to propose a model to explain the ethnic differences in mutational frequencies and responses to TKIs seen in NSCLC. They suggest that because of the polymorphisms in the EGFR gene commonly seen in East Asians, people from this ethnic group make less EGFR protein than people from other ethnic groups. This would explain why, if a threshold level of EGFR is needed to drive cells towards malignancy, East Asians have a high frequency of amplified EGFR tyrosine kinase mutations in their tumors—mutation followed by amplification would be needed to activate EGFR signaling. This model, though speculative, helps to explain some clinical findings, such as the frequency of EGFR mutations and of TKI sensitivity in NSCLCs in East Asians. Further studies of this type in different ethnic groups and in different tumors, as well as with other genes for which targeted therapies are available, should help oncologists provide personalized cancer therapies for their patients.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0040125.
US National Cancer Institute information on lung cancer and on cancer treatment for patients and professionals
MedlinePlus encyclopedia entries on NSCLC
Cancer Research UK information for patients about all aspects of lung cancer, including treatment with TKIs
Wikipedia pages on lung cancer, EGFR, and gefitinib (note that Wikipedia is a free online encyclopedia that anyone can edit)
doi:10.1371/journal.pmed.0040125
PMCID: PMC1876407  PMID: 17455987
13.  Experimenting with cigarettes and physical activity among Mexican origin youth: a cross sectional analysis of the interdependent associations among sensation seeking, acculturation, and gender 
BMC Public Health  2012;12:332.
Background
Sensation seeking tendencies tend to manifest during adolescence and are associated with both health-compromising behaviors and health-enhancing behaviors. The purpose of this study is to evaluate the relationship between sensation seeking and physical activity, a health-enhancing behavior, and between sensation seeking and experimenting with cigarettes, a health compromising-behavior, among a cohort of Mexican origin adolescents residing in the United States with different levels of acculturation.
Methods
In 2009, 1,154 Mexican origin youth (50.5% girls, mean age 14.3 years (SD = 1.04)) provided data on smoking behavior, physical activity, linguistic acculturation, and sensation seeking. We conducted Pearson’s χ2 tests to examine the associations between categorical demographic characteristics (i.e. gender, age, country of birth and parental educational attainment) and both cigarette experimentation and physical activity and Student’s t-tests to examine mean differences on the continuous variables (i.e. sensation seeking subscale) by the behaviors. We examined mean differences in the demographic characteristics, acculturation, and both behaviors for each of the sensation seeking subscales using analysis of variance (ANOVA). To examine relationships between the sensation seeking subscales, gender, and both behaviors, at different levels of acculturation we completed unconditional logistic regression analyses stratified by level of acculturation.
Results
Overall, 23.3% had experimented with cigarettes and 29.0% reported being physically active for at least 60 minutes/day on at least 5 days/week. Experimenting with cigarettes and being physically active were more prevalent among boys than girls. Among girls, higher levels of sensation seeking tendencies were associated with higher levels of acculturation and experimentation with cigarettes, but not with physical activity. Among boys, higher levels of sensation seeking tendencies were associated with higher levels of acculturation, experimenting with cigarettes and being physically active.
Conclusions
Our results suggest that interventions designed to prevent smoking among Mexican origin youth may need to address social aspects associated with acculturation, paying close attention to gendered manifestations of sensation seeking.
doi:10.1186/1471-2458-12-332
PMCID: PMC3441442  PMID: 22559717
Smoking behavior; Physical activity; Acculturation; Sensation seeking; Gender; Mexican origin youth

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