human
***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: Background : Little is known about the impact of knowledge of CDKN2A and MC1R genotype on melanoma prevention behaviors like sun avoidance and skin examination in the context of familial melanoma . Methods : Seventy-three adults with a family history of melanoma were r and omly assigned to be offered individualized CDKN2A and MC1R genotyping results in the context of a genetic counseling session , or the st and ard practice of not being offered counseling or disclosure of genotyping results . Mixed effects or longitudinal logistic models were used to determine whether the intervention affected change in sun protection habits , skin examinations , and perception and beliefs related to melanoma risk , prevention , and genetic counseling . Results : All participants in the intervention group who attended genetic counseling sessions chose to receive their test results . From baseline to follow-up , participants in the intervention group reported an increase in the frequency of skin self-examinations compared with a slight decrease in the control group ( P = 0.002 ) . Participants in the intervention group reported a smaller decrease in frequency of wearing a shirt with long sleeves than did participants in the control group ( P = 0.047 ) . No effect of the intervention was noted for other outcomes . Conclusions : Feedback of CDKN2A and MC1R genotype among families without known pathogenic CDKN2A mutations does not seem to decrease sun protection behaviors . Impact : While disclosure of CDKN2A and MC1R genotype did not have negative effects on prevention , the benefits of communicating this information remain unclear . The small number of families who tested positive for CDKN2A mutations in this study is a limitation . Cancer Epidemiol Biomarkers Prev ; 22(4 ) ; 607–14 . © 2013 AACR Type 2 diabetes ( T2D ) is associated with increased risk of morbidity and premature mortality . Among those at high risk , incidence can be halved through healthy changes in behaviour . Information about genetic and phenotypic risk of T2D is now widely available . Whether such information motivates behaviour change is unknown . We aim to assess the effects of communicating genetic and phenotypic risk of T2D on risk-reducing health behaviours , anxiety , and other cognitive and emotional theory-based antecedents of behaviour change . In a parallel group , open r and omised controlled trial , approximately 580 adults born between 1950 and 1975 will be recruited from the on-going population -based , observational Fenl and Study ( Cambridgeshire , UK ) . Eligible participants will have undergone clinical , anthropometric , and psychosocial measurements , been genotyped for 23 single-nucleotide polymorphisms associated with T2D , and worn a combined heart rate monitor and accelerometer ( Actiheart ® ) continuously for six days and nights to assess physical activity .  Participants are r and omised to receive either st and ard lifestyle advice alone ( control group ) , or in combination with a genetic or a phenotypic risk estimate for T2D ( intervention groups ) . The primary outcome is objective ly measured physical activity . Secondary outcomes include self-reported diet , self-reported weight , intention to be physically active and to engage in a healthy diet , anxiety , diabetes-related worry , self-rated health , and other cognitive and emotional outcomes . Follow-up occurs eight weeks post-intervention . Values at follow-up , adjusted for baseline , will be compared between r and omised groups . This study will provide much needed evidence on the effects of providing information about the genetic and phenotypic risk of T2D . Importantly , it will be among the first to examine the impact of genetic risk information using a r and omised controlled trial design , a population -based sample , and an objective ly measured behavioural outcome . Results of this trial , along with recent evidence syntheses of similar studies , should inform policy concerning the availability and use of genetic risk information . Current Controlled Trials IS RCT Background Estimates of the risk of developing Crohn 's disease ( CD ) can be made using DNA testing for mutations in the NOD2 ( CARD15 ) gene , family history , and smoking status . Smoking doubles the risk of CD , a risk that is reduced by stopping . CD therefore serves as a timely and novel paradigm within which to assess the utility of predictive genetic testing to motivate behaviour change to reduce the risk of disease . The aim of the study is to describe the impact upon stopping smoking of communicating a risk of developing CD that incorporates DNA analysis . We will test the following main hypothesis : Smokers who are first degree relatives ( FDRs ) of CD prob and s are more likely to make smoking cessation attempts following communication of risk estimates of developing CD that incorporate DNA analysis , compared with an equivalent communication that does not incorporate DNA analysis . Methods / design A parallel groups r and omised controlled trial in which smokers who are FDRs of prob and s with CD are r and omly allocated in families to undergo one of two types of assessment of risk for developing CD based on either : i . DNA analysis , family history of CD and smoking status , orii . Family history of CD and smoking statusThe primary outcome is stopping smoking for 24 hours or longer in the six months following provision of risk information . The secondary outcomes are seven-day smoking abstinence at one week and six month follow-ups . R and omisation of 470 smoking FDRs of CD prob and s , with 400 followed up ( 85 % ) , provides 80 % power to detect a difference in the primary outcome of 14 % between r and omised arms , at the 5 % significance level . Discussion This trial provides one of the strongest tests to date of the impact of communicating DNA-based risk assessment on risk-reducing behaviour change . Specific issues regarding the choice of trial design are discussed . Trial Registration IS RCT N : IS RCT There is increasing interest in health interventions that incorporate genetic risk information . Although genetic feedback has been evaluated as an adjunct to smoking cessation interventions , its efficacy for reducing alcohol-related risks is unknown . The purpose of this study was to evaluate the feasibility , acceptability , and efficacy of a web-based alcohol intervention incorporating genetic feedback and risk information specific to ALDH2 genotype . The ALDH2 * 2 variant is associated with partial protection against alcohol dependence but confers significantly increased risk for alcohol-related cancers as a function of alcohol exposure . Two hundred Asian-American young adults were r and omly assigned to receive web-based personalized genetic feedback or attention-control feedback . Genetic feedback included health risk information specific to alcohol-related cancer or alcohol dependence , depending on genotype . Outcomes included postintervention drinking behavior and theoretical correlates of behavior change . Genetic feedback and risk information result ed in significant reductions in 30-day drinking frequency and quantity among participants with the ALDH2 * 1/*2 genotype . Genetic feedback was rated highly by participants and also showed some effects on theoretical correlates of behavior change . Results provide initial evidence of the feasibility , acceptability , and brief efficacy of web-based genetic feedback for reducing alcohol-related health risks associated with ALDH2 genotype Smoking  cessation treatment is now integrated into many health-care systems and a major research effort is under way to improve current success rates . Until now results from r and omized clinical trials have been reported in many different ways , leading to problems of interpretation . We propose six st and ard criteria comprising the ' Russell St and ard ' ( RS ) . These criteria are applicable to trials of cessation aids where participants have a defined target quit date and there is face-to-face contact with research ers or clinic staff , as follows . ( 1 ) Follow-up for 6 months ( RS6 ) or 12 months ( RS12 ) from the target quit date or the end of a predefined ' grace period ' ; ( 2 ) self-report of smoking abstinence over the whole follow-up period allowing up to five cigarettes in total ; ( 3 ) biochemical verification of abstinence at least at the 6-month or 12-month follow-up point ; ( 4 ) use of an ' intention-to-treat ' approach in which data from all r and omized smokers are included in the analysis unless they have died or moved to an untraceable address ( participants who are included in the analysis are counted as smokers if their smoking status at the final follow-up can not be determined ) ; ( 5 ) following-up ' protocol violators ' and using their true smoking status in the analysis ; and ( 6 ) collecting follow-up data blind to smokers ' allocation to trial group . We believe that these criteria provide the best compromise between practicability and surrogacy for long-term cessation and will enable meaningful comparison between studies . There may be good reasons why other outcome criteria would also be reported , and studies that involve interventions with special groups or where there is no design ated target quit date or face to face contact would need to adapt these criteria accordingly Background Genetic testing for risk of weight gain is already available over the internet despite uncertain benefits and concerns about adverse emotional or behavioral effects . Few studies have assessed the effect of adding genetic test feedback to weight control advice , even though one of the proposed applications of genetic testing is to stimulate preventive action . This study will investigate the motivational effect of adding genetic test feedback to simple weight control advice in a situation where weight gain is relatively common . Methods / design First-year university students ( n = 800 ) will be r and omized to receive either 1 ) their personal genetic test result for a gene ( FTO ) related to weight gain susceptibility in addition to a leaflet with simple weight control advice ( ‘ Feedback + Advice ’ group , FA ) , or 2 )  only the leaflet containing simple weight control advice ( ‘ Advice Only ’ group , AO).Motivation to avoid weight gain and active use of weight control strategies will be assessed one month after receipt of the leaflet with or without genetic test feedback .  Weight and body fat will be measured at baseline and eight months follow-up . We will also assess short-term psychological reactions to the genetic test result . In addition , we will explore interactions between feedback condition and gene test status . Discussion We hope to provide a first indication of the clinical utility of weight-related genetic test feedback in the prevention context .Trial registration Current controlled trials IS RCT Context Genetic and environmental risk assessment ( GERA ) , in which related genetic and environmental information identifies an individual 's risk for a disease , has been suggested as a means to motivate adherence to recommended cancer screening . Contribution This r and omized trial found that providing 1 specific GERA result to persons who were previously nonadherent to screening recommendations for colorectal cancer did not alter the subsequent rate of screening . Caution The study could assess only 1 set of GERA results and 1 method of communicating these results to patients . Implication Results of GERA can not be assumed to encourage adherence to recommended screening . The Editors Genetic testing for cancer susceptibility is offered most frequently for single-gene disorders . A mutation in the adenomatous polyposis coli gene ( APC ) confers a risk for colorectal cancer ( CRC ) of approximately 90 % ( 1 ) . Identification of this mutation substantially affects clinical practice . However , cancer usually does not arise from single mutations . Instead , susceptibility results from the modest contributions of many genes , usually with environmental interaction . Identification of these genes and their modifiers is an active area of research ( 2 ) . Genetic and environmental risk assessment ( GERA ) for common diseases is anticipated to become a widespread component of health care ( 3 , 4 ) . We assessed polymorphic variants of methylenetetrahydrofolate reductase (MTHFR),an important regulator of cellular folate metabolism . Specific MTHFR polymorphisms are associated with variable susceptibility to CRC ( 58 ) . Epidemiologic data also support a link between serum folate levels and CRC risk ( 9 ) . Assessment of the genetic ( MTHFR ) and environmental ( serum folate levels ) interaction is attractive because data that allow for CRC risk stratification among average-risk persons already exist . Specific polymorphisms in combination with low serum folate levels increase risk for CRC by approximately 1.5 to 2.0 times the baseline risk in white and African American persons in the United States ( 8) . Unlike with genetic testing for high-risk persons , such as those with familial adenomatous polyposis , little is known about the impact on health behaviors or the psychological effects of providing average-risk persons with moderately predictive genetic information ( 4 , 1013 ) . Underst and ing the benefits and harms of such testing in average-risk persons is important because similar testing is marketed directly to the public in an unsupervised manner ( 14 ) . We did a prospect i ve , r and omized , controlled trial to assess the effect of GERA feedback on CRC screening among average-risk persons who did not adhere to screening recommendations at study entry . Prevention of CRC is an optimal area to study the emerging role of moderately predictive genetic testing . Colorectal cancer is the second leading cause of cancer death in the United States ( 15 ) . Screening can reduce disease incidence and mortality ( 16 ) . Our primary hypothesis was that providing personalized GERA information would increase CRC screening uptake compared with usual care . Further , we anticipated that participants characterized as having elevated risk by GERA would undergo screening more than those at average risk . Although MTHFR and serum folate level testing provided personalized risk information , our study did not intend to evaluate the specific predictive value of this combination for colorectal neoplasia . Methods Design Overview We did a r and omized , controlled trial to compare CRC screening utilization in the  GERA group  versus the  usual care ( control ) group and to detect differences in screening proportion between the average- and elevated-risk GERA groups ( 12 ) . To increase the statistical power for comparisons within the GERA group , participants were r and omly assigned in a 2:1 ratio to GERA or usual care , respectively . Participants provided survey data at baseline , 3 weeks , and 6 months and agreed to medical record review to ascertain CRC screening status . Those in the GERA group also participated in GERA counseling and disclosure sessions and had blood drawn for genotyping and measurement of serum folate levels . Setting and Participants Part 
    Output:
    
agent
***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: Background : Little is known about the impact of knowledge of CDKN2A and MC1R genotype on melanoma prevention behaviors like sun avoidance and skin examination in the context of familial melanoma . Methods : Seventy-three adults with a family history of melanoma were r and omly assigned to be offered individualized CDKN2A and MC1R genotyping results in the context of a genetic counseling session , or the st and ard practice of not being offered counseling or disclosure of genotyping results . Mixed effects or longitudinal logistic models were used to determine whether the intervention affected change in sun protection habits , skin examinations , and perception and beliefs related to melanoma risk , prevention , and genetic counseling . Results : All participants in the intervention group who attended genetic counseling sessions chose to receive their test results . From baseline to follow-up , participants in the intervention group reported an increase in the frequency of skin self-examinations compared with a slight decrease in the control group ( P = 0.002 ) . Participants in the intervention group reported a smaller decrease in frequency of wearing a shirt with long sleeves than did participants in the control group ( P = 0.047 ) . No effect of the intervention was noted for other outcomes . Conclusions : Feedback of CDKN2A and MC1R genotype among families without known pathogenic CDKN2A mutations does not seem to decrease sun protection behaviors . Impact : While disclosure of CDKN2A and MC1R genotype did not have negative effects on prevention , the benefits of communicating this information remain unclear . The small number of families who tested positive for CDKN2A mutations in this study is a limitation . Cancer Epidemiol Biomarkers Prev ; 22(4 ) ; 607–14 . © 2013 AACR Type 2 diabetes ( T2D ) is associated with increased risk of morbidity and premature mortality . Among those at high risk , incidence can be halved through healthy changes in behaviour . Information about genetic and phenotypic risk of T2D is now widely available . Whether such information motivates behaviour change is unknown . We aim to assess the effects of communicating genetic and phenotypic risk of T2D on risk-reducing health behaviours , anxiety , and other cognitive and emotional theory-based antecedents of behaviour change . In a parallel group , open r and omised controlled trial , approximately 580 adults born between 1950 and 1975 will be recruited from the on-going population -based , observational Fenl and Study ( Cambridgeshire , UK ) . Eligible participants will have undergone clinical , anthropometric , and psychosocial measurements , been genotyped for 23 single-nucleotide polymorphisms associated with T2D , and worn a combined heart rate monitor and accelerometer ( Actiheart ® ) continuously for six days and nights to assess physical activity .  Participants are r and omised to receive either st and ard lifestyle advice alone ( control group ) , or in combination with a genetic or a phenotypic risk estimate for T2D ( intervention groups ) . The primary outcome is objective ly measured physical activity . Secondary outcomes include self-reported diet , self-reported weight , intention to be physically active and to engage in a healthy diet , anxiety , diabetes-related worry , self-rated health , and other cognitive and emotional outcomes . Follow-up occurs eight weeks post-intervention . Values at follow-up , adjusted for baseline , will be compared between r and omised groups . This study will provide much needed evidence on the effects of providing information about the genetic and phenotypic risk of T2D . Importantly , it will be among the first to examine the impact of genetic risk information using a r and omised controlled trial design , a population -based sample , and an objective ly measured behavioural outcome . Results of this trial , along with recent evidence syntheses of similar studies , should inform policy concerning the availability and use of genetic risk information . Current Controlled Trials IS RCT Background Estimates of the risk of developing Crohn 's disease ( CD ) can be made using DNA testing for mutations in the NOD2 ( CARD15 ) gene , family history , and smoking status . Smoking doubles the risk of CD , a risk that is reduced by stopping . CD therefore serves as a timely and novel paradigm within which to assess the utility of predictive genetic testing to motivate behaviour change to reduce the risk of disease . The aim of the study is to describe the impact upon stopping smoking of communicating a risk of developing CD that incorporates DNA analysis . We will test the following main hypothesis : Smokers who are first degree relatives ( FDRs ) of CD prob and s are more likely to make smoking cessation attempts following communication of risk estimates of developing CD that incorporate DNA analysis , compared with an equivalent communication that does not incorporate DNA analysis . Methods / design A parallel groups r and omised controlled trial in which smokers who are FDRs of prob and s with CD are r and omly allocated in families to undergo one of two types of assessment of risk for developing CD based on either : i . DNA analysis , family history of CD and smoking status , orii . Family history of CD and smoking statusThe primary outcome is stopping smoking for 24 hours or longer in the six months following provision of risk information . The secondary outcomes are seven-day smoking abstinence at one week and six month follow-ups . R and omisation of 470 smoking FDRs of CD prob and s , with 400 followed up ( 85 % ) , provides 80 % power to detect a difference in the primary outcome of 14 % between r and omised arms , at the 5 % significance level . Discussion This trial provides one of the strongest tests to date of the impact of communicating DNA-based risk assessment on risk-reducing behaviour change . Specific issues regarding the choice of trial design are discussed . Trial Registration IS RCT N : IS RCT There is increasing interest in health interventions that incorporate genetic risk information . Although genetic feedback has been evaluated as an adjunct to smoking cessation interventions , its efficacy for reducing alcohol-related risks is unknown . The purpose of this study was to evaluate the feasibility , acceptability , and efficacy of a web-based alcohol intervention incorporating genetic feedback and risk information specific to ALDH2 genotype . The ALDH2 * 2 variant is associated with partial protection against alcohol dependence but confers significantly increased risk for alcohol-related cancers as a function of alcohol exposure . Two hundred Asian-American young adults were r and omly assigned to receive web-based personalized genetic feedback or attention-control feedback . Genetic feedback included health risk information specific to alcohol-related cancer or alcohol dependence , depending on genotype . Outcomes included postintervention drinking behavior and theoretical correlates of behavior change . Genetic feedback and risk information result ed in significant reductions in 30-day drinking frequency and quantity among participants with the ALDH2 * 1/*2 genotype . Genetic feedback was rated highly by participants and also showed some effects on theoretical correlates of behavior change . Results provide initial evidence of the feasibility , acceptability , and brief efficacy of web-based genetic feedback for reducing alcohol-related health risks associated with ALDH2 genotype Smoking  cessation treatment is now integrated into many health-care systems and a major research effort is under way to improve current success rates . Until now results from r and omized clinical trials have been reported in many different ways , leading to problems of interpretation . We propose six st and ard criteria comprising the ' Russell St and ard ' ( RS ) . These criteria are applicable to trials of cessation aids where participants have a defined target quit date and there is face-to-face contact with research ers or clinic staff , as follows . ( 1 ) Follow-up for 6 months ( RS6 ) or 12 months ( RS12 ) from the target quit date or the end of a predefined ' grace period ' ; ( 2 ) self-report of smoking abstinence over the whole follow-up period allowing up to five cigarettes in total ; ( 3 ) biochemical verification of abstinence at least at the 6-month or 12-month follow-up point ; ( 4 ) use of an ' intention-to-treat ' approach in which data from all r and omized smokers are included in the analysis unless they have died or moved to an untraceable address ( participants who are included in the analysis are counted as smokers if their smoking status at the final follow-up can not be determined ) ; ( 5 ) following-up ' protocol violators ' and using their true smoking status in the analysis ; and ( 6 ) collecting follow-up data blind to smokers ' allocation to trial group . We believe that these criteria provide the best compromise between practicability and surrogacy for long-term cessation and will enable meaningful comparison between studies . There may be good reasons why other outcome criteria would also be reported , and studies that involve interventions with special groups or where there is no design ated target quit date or face to face contact would need to adapt these criteria accordingly Background Genetic testing for risk of weight gain is already available over the internet despite uncertain benefits and concerns about adverse emotional or behavioral effects . Few studies have assessed the effect of adding genetic test feedback to weight control advice , even though one of the proposed applications of genetic testing is to stimulate preventive action . This study will investigate the motivational effect of adding genetic test feedback to simple weight control advice in a situation where weight gain is relatively common . Methods / design First-year university students ( n = 800 ) will be r and omized to receive either 1 ) their personal genetic test result for a gene ( FTO ) related to weight gain susceptibility in addition to a leaflet with simple weight control advice ( ‘ Feedback + Advice ’ group , FA ) , or 2 )  only the leaflet containing simple weight control advice ( ‘ Advice Only ’ group , AO).Motivation to avoid weight gain and active use of weight control strategies will be assessed one month after receipt of the leaflet with or without genetic test feedback .  Weight and body fat will be measured at baseline and eight months follow-up . We will also assess short-term psychological reactions to the genetic test result . In addition , we will explore interactions between feedback condition and gene test status . Discussion We hope to provide a first indication of the clinical utility of weight-related genetic test feedback in the prevention context .Trial registration Current controlled trials IS RCT Context Genetic and environmental risk assessment ( GERA ) , in which related genetic and environmental information identifies an individual 's risk for a disease , has been suggested as a means to motivate adherence to recommended cancer screening . Contribution This r and omized trial found that providing 1 specific GERA result to persons who were previously nonadherent to screening recommendations for colorectal cancer did not alter the subsequent rate of screening . Caution The study could assess only 1 set of GERA results and 1 method of communicating these results to patients . Implication Results of GERA can not be assumed to encourage adherence to recommended screening . The Editors Genetic testing for cancer susceptibility is offered most frequently for single-gene disorders . A mutation in the adenomatous polyposis coli gene ( APC ) confers a risk for colorectal cancer ( CRC ) of approximately 90 % ( 1 ) . Identification of this mutation substantially affects clinical practice . However , cancer usually does not arise from single mutations . Instead , susceptibility results from the modest contributions of many genes , usually with environmental interaction . Identification of these genes and their modifiers is an active area of research ( 2 ) . Genetic and environmental risk assessment ( GERA ) for common diseases is anticipated to become a widespread component of health care ( 3 , 4 ) . We assessed polymorphic variants of methylenetetrahydrofolate reductase (MTHFR),an important regulator of cellular folate metabolism . Specific MTHFR polymorphisms are associated with variable susceptibility to CRC ( 58 ) . Epidemiologic data also support a link between serum folate levels and CRC risk ( 9 ) . Assessment of the genetic ( MTHFR ) and environmental ( serum folate levels ) interaction is attractive because data that allow for CRC risk stratification among average-risk persons already exist . Specific polymorphisms in combination with low serum folate levels increase risk for CRC by approximately 1.5 to 2.0 times the baseline risk in white and African American persons in the United States ( 8) . Unlike with genetic testing for high-risk persons , such as those with familial adenomatous polyposis , little is known about the impact on health behaviors or the psychological effects of providing average-risk persons with moderately predictive genetic information ( 4 , 1013 ) . Underst and ing the benefits and harms of such testing in average-risk persons is important because similar testing is marketed directly to the public in an unsupervised manner ( 14 ) . We did a prospect i ve , r and omized , controlled trial to assess the effect of GERA feedback on CRC screening among average-risk persons who did not adhere to screening recommendations at study entry . Prevention of CRC is an optimal area to study the emerging role of moderately predictive genetic testing . Colorectal cancer is the second leading cause of cancer death in the United States ( 15 ) . Screening can reduce disease incidence and mortality ( 16 ) . Our primary hypothesis was that providing personalized GERA information would increase CRC screening uptake compared with usual care . Further , we anticipated that participants characterized as having elevated risk by GERA would undergo screening more than those at average risk . Although MTHFR and serum folate level testing provided personalized risk information , our study did not intend to evaluate the specific predictive value of this combination for colorectal neoplasia . Methods Design Overview We did a r and omized , controlled trial to compare CRC screening utilization in the  GERA group  versus the  usual care ( control ) group and to detect differences in screening proportion between the average- and elevated-risk GERA groups ( 12 ) . To increase the statistical power for comparisons within the GERA group , participants were r and omly assigned in a 2:1 ratio to GERA or usual care , respectively . Participants provided survey data at baseline , 3 weeks , and 6 months and agreed to medical record review to ascertain CRC screening status . Those in the GERA group also participated in GERA counseling and disclosure sessions and had blood drawn for genotyping and measurement of serum folate levels . Setting and Participants Part 
    Output:
    