***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: As genetic tests for common gene variants and multifactorial , lifestyle‐related conditions become available , it will be increasingly important to determine the psychological and behavioral impact of this emerging class of genetic tests . Our aim was to examine the potential impact of genetic testing for heart disease susceptibility on psychological predictors of smoking cessation .  Two hundred and sixty‐one smokers were asked to imagine that they had undergone a test for heart disease risk . They were r and omly assigned to a genetic test scenario ( low‐ or high‐risk result ) or an oxidative test scenario ( high‐risk result ) . Smokers in the genetic test‐high risk group reported greater intention to quit smoking than smokers in the oxidative test‐high risk group ( p = 0.009 ) ; 30 % of this was mediated by their holding stronger beliefs that quitting would reduce their heart disease risk ( outcome expectations ) ( p = 0.011 ) . The effect of genetic test‐high risk feedback on outcome expectations was greatest amongst smokers with no heart disease family history ( p = 0.038 ) . The results suggest that genetic testing for heart disease risk may enhance interventions design ed to improve health via increasing smoking cessation rates . Whether the findings hold true in studies that use real rather than hypothetical genetic tests remains to be seen Background : As genetic testing for health risk becomes increasingly available , it becomes important to study the prospect i ve impact of testing on modifiable health behavior . Purpose : This study examines the impact of genetic testing for alpha-1 antitrypsin ( AAT ) deficiency , a condition that usually results in emphysema in individuals exposed to cigarette smoke . We evaluated whether AAT testing , performed in the home and with minimal contact ( reading material s including advice on cessation ) , results in quit attempts and abstinence . Methods : Identified smokers ( N=199 ) from a larger study of genetic testing were surveyed 3 months following receipt of their AAT genotype . The primary endpoint was the incidence of quit attempts . Results : Smokers who tested severely AAT deficient were significantly more likely to report a 24-hr quit attempt ( 59 % ) than were those who tested normal ( 26 % ) . Carriers had a 34 % quit attempt rate . Severely AAT deficient smokers were more likely than both carriers and normals to seek information on treatment , use pharmacotherapy for smoking cessation , and report greater reductions in their smoking . There were no group differences in 3-month abstinence rates . Conclusions : Knowledge of severe AAT deficiency , but not carrier status , may motivate smokers toward cessation . The AAT testing experience may have consequences for outcomes of other genetic conditions with modifiable health behaviors PURPOSE Markers of genetic susceptibility to tobacco-related cancers could personalize harms of smoking and motivate cessation . Our objective was to assess whether a multicomponent intervention that included feedback about genetic susceptibility to lung cancer increased risk perceptions and rates of smoking cessation compared with a st and ard cessation intervention . EXPERIMENTAL DESIGN Our design was a two-arm trial with eligible smokers r and omized in a 1:2 ratio to Enhanced Usual Care or Biomarker Feedback ( BF ) .  Surveys were conducted at baseline , 6 , and 12 months later . The setting was an inner city community health clinic . African-American patients who were current smokers ( n = 557 ) were identified by chart abstract ion and provider referral . All smokers received a self-help manual and , if appropriate , nicotine patches . Smokers in the BF arm also were offered a blood test for genotyping the GST(3 ) gene ( GSTM1 ) , sent a test result booklet , and called up to four times by a health educator . Prevalent abstinence was assessed by self-report of having smoked no cigarettes in the prior 7 days at the 6- and 12-month follow-ups and sustained abstinence , i.e. , not smoking at either follow-up or in-between . RESULTS Smoking cessation was greater for the BF arm than the Enhanced Usual Care arm ( 19 % versus 10 % , respectively ; P < 0.006 ) at 6 months but not at 12 months . CONCLUSIONS Smokers agreed to genetic feedback as part of a multicomponent cessation program . Although the program increased short-term cessation rates compared with st and ard intervention , genetic feedback of susceptibility may not benefit smokers with high baseline risk perceptions Twin studies document substantial heritability for  successful abstinence from smoking .  A genome-wide association study has identified markers whose allele frequencies differ with nominal P<0.005 in nicotine-dependent clinical trial participants who were successful vs unsuccessful in abstaining from smoking ; many of these results are also supported by data from two additional sample s. More study is required to precisely determine the variance in quitting success that can be accounted for by the single-nucleotide polymorphisms that are currently identified and to precisely classify individuals who may display varying degrees of genetic vs environmental effects into quitters or nonquitters . However , the data at h and do allow us to model the effects of genotypic stratification in smoking cessation trials . We identify relationships between the costs of identifying and genotyping prospect i ve trial participants vs the costs of performing the clinical trials . We quantitate the increasing savings that result from genetically stratified design s as recruiting/genotyping costs go down and trial costs increase . This model helps to define the circumstances in which genetically stratified design s may enhance power and reduce costs for smoking cessation clinical trials This trial tests the hypothesis that confirming a clinical diagnosis of familial hypercholesterolemia ( FH ) by finding a genetic mutation reduces patients ' perceptions of control over the disease and adherence to risk‐reducing behaviors . Three hundred forty‐one families , comprising 341 hypercholesterolemia prob and s and 128 adult relatives , were r and omized to one of two groups : ( a ) routine clinical diagnosis ; ( b ) routine clinical diagnosis plus genetic testing ( mutation search ing in prob and s and direct gene testing in relatives ) . The main outcome measures were perceptions of control over hypercholesterolemia , adherence to cholesterol‐lowering medication , diet , physical activity , and smoking .  There was no support for the main hypothesis : finding a mutation had no impact on perceived control or adherence to risk‐reducing behavior ( all P‐values > 0.10 ) . While all groups believed that lowering cholesterol was an effective way of reducing the risk of a heart attack , participants in whom a mutation was found believed less strongly in the efficacy of diet in reducing their cholesterol level ( P = 0.02 at 6 months ) and showed a trend in believing more strongly in the efficacy of cholesterol‐lowering medication ( P = 0.06 at 6 months ) . In conclusion , finding a mutation to confirm a clinical diagnosis of FH in a previously aware population does not reduce perceptions of control or adherence to risk‐reducing behaviors . The pattern of findings leads to the new hypothesis that genetic testing does not affect the extent to which people feel they have control over a condition , but does affect their perceptions of how control is most effectively achieved . Further work is needed to determine whether similar results will be obtained in population s with little previous awareness of their risks . © 2004 Wiley‐Liss , OBJECTIVES It is well-known that smoking causes many diseases including cancers . Informing smokers of their genotypes associated with the vulnerability to the harms of smoking may be effective measures for smoking cessation . The present study examined the effects of genotype notification of an oncogene ( L-myc ) genotype to smokers on their behavior to quit smoking . METHODS Subjects were 562 employees of a bank who answered to be a smoker for a question naire used at annual health checkup at workplace from July to December 2002 . Those enrolled on August , October , and December were allocated into the genotype notification group ( intervention group ) , and the rest into the controls .  Among 286 smokers allocated into the intervention group , 257 participants ( 89.9 % ) agreed to genotype testing . One year after the enrollment , a follow-up question naire survey was conducted for all smokers including controls . RESULTS Those who stated to have quitted smoking were 22 ( 8.0 % ) among the 276 controls and 15 ( 5.8 % ) among the 257 genotype notified participants , providing that the odds ratio ( OR ) of cessation for the intervention was 0.64 ( 95 % confidence interval , 0.32 - 1.28 ) . No psychological problems associated with genotype notification were observed . CONCLUSION The present study did not show positive effects of genotype notification on smoking cessation rate . To elevate the cessation rate , methods to explain and notify genotypes should be improved This study examined the role of dopaminergic genes in prospect i ve smoking cessation and response to  bupropion treatment in a placebo-controlled clinical trial . Smokers of European ancestry ( N=418 ) provided blood sample s for genetic analysis and received either bupropion or placebo ( 10 weeks ) plus counseling . Assessment s included the dopamine D2 receptor ( DRD2 ) genotype , dopamine transporter ( SLC6A3 ) genotype , demographic factors , and nicotine dependence . Smoking status was verified at the end of treatment ( EOT ) and at 6-month follow-up . The results provided evidence for a significant DRD2 * SLC6A3 interaction effect on prolonged smoking abstinence and time to relapse at EOT , independent of treatment condition . Such effects were no longer significant at 6-month follow-up , however . These results provide the first evidence from a prospect i ve clinical trial that genes that alter dopamine function may influence smoking cessation and relapse during the treatment phase OBJECTIVE To determine the relationship between joint variation in 2 dopaminergic genes and the likelihood of  nonsmoking  following treatment with bupropion sustained release ( SR ) . DESIGN Three hundred twenty-three participants in a bupropion SR smoking cessation effectiveness trial with 12-month follow-up were genotyped for variants of dopamine receptor gene DRD2 and dopamine transporter SLC6A3 . MAIN OUTCOME MEASURES Self-reported 7-day point prevalence of nonsmoking . RESULTS Neither genotype alone was associated with 7-day point-prevalent nonsmoking at the 12-month follow-up . However , in the presence of the DRD2 A1 allele , SLC6A3 status was significantly associated with the likelihood of nonsmoking at the 12-month follow-up ( individuals with DRD2 A1 + and SLC6A3 9- were more likely to be smoking ) . In the absence of the DRD2 A1 allele , the association between SLC6A3 status and nonsmoking was nonsignificant . CONCLUSION Although these results are suggestive , a more compelling test is needed of the hypothesis that dopaminergic gene interaction underlies , in part , the likelihood of smoking following treatment with bupropion SR . Most likely this will come from larger studies involving prospect i ve r and omization to treatment based on genotype Risk information for Alzheimer disease ( AD ) may be communicated through susceptibility gene disclosure , even though this is not currently in clinical use . The REVEAL Study is the first r and omized clinical trial of risk assessment for AD with apolipoprotein E ( APOE ) genotype and numerical risk estimate disclosure . We examined whether APOE genotype and numerical risk disclosure to asymptomatic individuals at high risk for AD alters health behaviors . One hundred sixty-two participants were r and omized to either intervention ( APOE disclosure ) or control ( no genotype disclosure ) groups . Subjects in both groups received numerical lifetime risk estimates of future AD development based on sex and family history of AD . The intervention group received their APOE genotype . Subjects were informed that no proven preventive measures for AD existed and given an information sheet on preventative therapies under investigation . Participants who learned they were ϵ4 positive were significantly more likely than ϵ4 negative participants to report AD-specific health behavior change 1 year after disclosure ( adjusted odds ratio : 2.73 ; 95 % confidence interval : 1.14 , 6.54 ; P=0.02 ) . Post hoc analyses revealed similar significant associations between numerical lifetime risk estimates and self-report of AD-specific health behavior change . Despite lack of preventive measures for AD , knowledge of APOE genotype , numerical lifetime risk , or both , influences health behavior BACKGROUND To evaluate whether feedback of genetic information regarding an L-myc polymorphism , identified as impacting on tobacco-related cancer risk , has an influence on smoking cessation , an intervention study was conducted . METHODS We recruited smokers from first-visit out patients at Aichi Cancer Center Hospital . Six hundred and seventeen participated and were allocated into two groups : the biomarker feedback group ( BF ) and the follow-up smoking status group ( FS ) . The subjects were asked for their smoking status at enrolment and at 3- and 9-month follow-ups . BF subjects were notified about their L-myc genotype . RESULTS The smoking cessation rate at 9-month follow-up was essentially the same for both BF and FS cases , at 18.8 % and 17.0 % , respectively ( P = 0.798 ) . However , a difference in the rate was evident with non-cancer subjects ( 12.7 % and 8.4 % , respectively , P = 0.237 ) , especially in females ( 15.0 % and 4.2 % , respectively , P = 0.024 ) . The non-cancer subjects informed of their genotype were more likely to quit smoking than the FS patients ; particularly in those having a risky genotype 
    Output:
    
The authors observed positive short-term effects on risk perception , motivation to quit smoking and smoking cessation , but these effects fade at longer follow-ups .
Importantly , the authors did not find any evidence of adverse effect of testing negative on the risk-predisposing gene .
This systematic review does not provide solid evidence for the proposed beneficial effects of genetic testing for smoking-related diseases on smoking cessation , but does suggest the presence of an immediate motivational effect , such that genetic testing result ed in higher risk perception and more motivation to quit smoking