Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-IA25
B. Kramer
Advances in the understanding of risk factors have transformed oncology, providing leads for prevention and, in particular, screening. Part of this transformation has been fueled by studies of molecular changes and genetic mutations that are inherited or that precede cancer by years, potentially leading the way to a new era of precision screening and prevention. However, these new leads bring important challenges that demand caution. As Sean Carroll has pointed out, it turns out that life from the molecular scale all the way up to the ecological scale is usually governed by longer chains of interactions than we first imagine, with more links in between (Serengeti Rules: The Quest to Discover How Life Works and Why It Matters, 2016). Rather than screening for existing asymptomatic disease, we have entered the era of screening for risk factors, or even screening for risk factors for risk factors (disease risk predisposition). This is a double-edged endeavor, because genes may influence fate, but not in a linear or straightforward manner. Therefore, prediction of outcome is far less precise than measurement of the predisposing genetic and molecular alterations. Many people may be labeled as carriers of risk factors that will never develop the clinical forms of the disease predicted by the genetic changes, a form of genetic overdiagnosis. So the new era of risk prediction can bring both benefits and harms. A critical tool in determining the balance of benefits and harms of increasingly sensitive omics technologies is the use of a formal analytic framework, to be discussed in the presentation. Citation Format: Barnett S. Kramer. Implementation of risk prediction to improve health: The promises and challenges of precision. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr IA25.
对危险因素的理解的进步已经改变了肿瘤学,为预防,特别是筛查提供了线索。这种转变的部分动力来自于对分子变化和基因突变的研究,这些变化和基因突变是遗传的,或者是在癌症发生多年之前发生的,可能会引领人们进入一个精确筛查和预防的新时代。然而,这些新的线索带来了需要谨慎对待的重大挑战。正如肖恩·卡罗尔所指出的那样,事实证明,从分子尺度一直到生态尺度的生命通常是由比我们最初想象的更长的相互作用链所控制的,它们之间有更多的联系(塞伦盖蒂规则:探索生命如何运作以及为什么它很重要,2016)。而不是筛查现有的无症状疾病,我们已经进入了筛查危险因素的时代,甚至是筛查危险因素的危险因素(疾病风险倾向)。这是一把双刃剑,因为基因可能影响命运,但不是以线性或直接的方式。因此,对结果的预测远不如对易感基因和分子改变的测量精确。许多人可能被贴上风险因素携带者的标签,这些人永远不会发展成由基因变化预测的疾病的临床形式,这是一种基因过度诊断。因此,风险预测的新时代既可以带来好处,也可以带来坏处。确定日益敏感的组学技术的利弊平衡的一个关键工具是使用正式的分析框架,将在演讲中讨论。引文格式:Barnett S. Kramer。实施风险预测以改善健康:精确度的承诺和挑战。[摘要]。摘自:AACR特别会议论文集:改进癌症风险预测以预防和早期发现;2016年11月16日至19日;费城(PA): AACR;Cancer epidemiology Biomarkers pre2017;26(5增刊):摘要nr IA25。
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Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-B06
R. MacInnis, M. Jenkins, J. Hopper, L. Cannon-Albright
Background: Family history is an important risk factor for CRC, but there is still confusion about the appropriate guidelines councilors should recommend to people depending on the specifics of their family history. Most previous studies that have estimated familial relative risk (FRR) of CRC have based this on first-degree relatives (FDRs), whereas information on second- or third-degree relatives (SDRs or TDRs) has been of poor quality or non-existent. The most notable exception to this is a publication by Taylor et al that utilized the Utah Population Database (UPDB), a population-based resource with a computerized genealogy linked to statewide cancer registry records.[1] They reported FRRs of CRC for probands by selected combinations of affected relatives, extending to third-degree. The aim of this study was to extend this work by developing a simple and clinically-useful model of familial CRC risk. Methods: We restricted the analysis to people aged 30 years or older born between 1930 and 1985 (probands) from the UPDB. Data were collected on the proband9s age, sex and history of CRC for FDRs, SDRs and TDRs. Unconditional multiple linear logistic regression was used to model the familial CRC risk for probands as a function of their family history measures. Various combinations of CRC status of relatives were considered, including categorizations by ages at diagnoses ( Results: A total of 591,535 probands were extracted of whom 2,115 probands were identified as having a primary diagnosis of CRC. The best-fitting model for CRC was FRR = exp(SUM/5)*0.8, where SUM equals: 4 points for each parent diagnosed with CRC 6 points for each sibling diagnosed with CRC 12 points for each child diagnosed with CRC 2 points for each SDR diagnosed with CRC 1 point for each TDR diagnosed with CRC. Therefore, a doubling of risk would be 5 points, a tripling of risk would be 7 points, while a 5-fold increased risk would be 10 points. The model had good internal consistency. Additional information on ages at diagnoses of affected FDRs, SDRs or TDRs or whether diagnoses were confined to a particular side of the family did not improve the model fit. Conclusions: This simple algorithm shows that knowing the total number of affected parents, siblings, children, SDRs and TDRs, irrespective of the age at diagnosis, is sufficient for accurate estimation of FRR. This model could be useful in the clinical and genetic counseling setting. 1. Taylor DP, et al. Population-based family history-specific risks for colorectal cancer: a constellation approach. Gastroenterology. 2010 Mar;138(3):877-85. This abstract is also being presented as PosterB06. Citation Format: Robert J. MacInnis, Mark A. Jenkins, John L. Hopper, Lisa A. Cannon-Albright. Utah familial colorectal cancer risk model. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemi
背景:家族史是结直肠癌的一个重要危险因素,但对于咨询师应根据其家族史的具体情况向人们推荐适当的指导方针仍然存在困惑。先前大多数估计结直肠癌家族相对风险(FRR)的研究都是基于一级亲属(FDRs),而关于二度或三度亲属(SDRs或TDRs)的信息质量较差或不存在。最值得注意的例外是Taylor等人利用犹他州人口数据库(UPDB)发表的一篇文章,UPDB是一种基于人口的资源,具有与全州癌症登记记录相关联的计算机家谱他们通过选择受影响亲属的组合报告了先证者的CRC frr,延伸到三度。本研究的目的是通过建立一种简单且临床有用的家族性结直肠癌风险模型来扩展这项工作。方法:我们将分析限制在1930年至1985年出生的30岁或以上的人(先证者)。收集fdr、sdr和tdr的年龄、性别和结直肠癌病史。使用无条件多元线性逻辑回归对先证者的家族性CRC风险作为其家族史测量的函数进行建模。考虑了亲属结直肠癌状况的各种组合,包括诊断时年龄的分类(结果:共提取了591,535个先证者,其中2,115个先证者被确定为初步诊断为结直肠癌。CRC的最佳拟合模型为FRR = exp(SUM/5)*0.8,其中SUM等于:诊断为CRC的父母每名4分诊断为CRC的兄弟姐妹每名6分诊断为CRC的儿童每名12分诊断为CRC的SDR每名2分诊断为CRC的TDR每名1分。因此,风险增加一倍为5分,风险增加三倍为7分,而风险增加五倍为10分。模型具有良好的内部一致性。关于诊断受影响的fdr、sdr或tdr的年龄或诊断是否局限于家庭的某一方的额外信息并没有改善模型拟合。结论:这一简单的算法表明,无论诊断年龄如何,只要知道患病父母、兄弟姐妹、子女、sdr和tdr的总数,就足以准确估计FRR。该模型可用于临床和遗传咨询设置。1. Taylor DP,等。以人群为基础的结直肠癌家族史特异性风险:星座方法胃肠病学杂志,2010;38(3):877-85。此摘要也以PosterB06的形式呈现。引文格式:Robert J. MacInnis, Mark A. Jenkins, John L. Hopper, Lisa A. Cannon-Albright。犹他州家族性结直肠癌风险模型。[摘要]。摘自:AACR特别会议论文集:改进癌症风险预测以预防和早期发现;2016年11月16日至19日;费城(PA): AACR;Cancer epidemiology Biomarkers pre2017;26(5增刊):摘要nr PR11。
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Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-IA07
D. Ransohoff
How can genetic information be effectively used in screening and prevention? The conceptual framework and rules of evidence for answering this question - widely used by clinicians, policy-makers, and payors - has been developed over decades in the field of Evidence-Based Medicine, exemplified by the approach of the USPSTF (US Preventive Services Task Force) and EGAPP (Evaluation of Genomic Applications in Practice and Prevention). The framework9s principles include using the best evidence (clinical trials where available, and observational data where necessary) assessed in systematic searches that consider quality of each study using specific rules of evidence. Outcomes are projected quantitatively to assess net benefit (benefits vs harms) of prevention and screening strategies. In this framework, genetic data may provide information about the magnitude of lifetime risk of developing a specific cancer, while other data (including genomic data) may provide information about the current risk that a cancer is present. Risks of appropriate magnitude may direct interventions that can prevent cancer (for example chemoprevention or preventive surgery) or that can detect the presence of early curable cancer or an important precursor. This talk will describe the quantitative conceptual framework and its rationale, along with the implications, challenges, and opportunities for the use of genetic and genomic information for cancer prevention and screening. Citation Format: David F. Ransohoff. Using genetic information in screening and prevention: Perspective of clinicians and policy-makers. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr IA07.
如何将遗传信息有效地用于筛查和预防?回答这个问题的概念框架和证据规则——被临床医生、政策制定者和付款人广泛使用——已经在循证医学领域发展了几十年,以USPSTF(美国预防服务工作组)和EGAPP(基因组在实践和预防中的应用评估)的方法为例。该框架的原则包括使用在系统检索中评估的最佳证据(可用的临床试验和必要的观察性数据),使用特定的证据规则考虑每个研究的质量。定量预测结果以评估预防和筛查策略的净收益(收益与危害)。在这一框架下,遗传数据可以提供有关患某种特定癌症的终生风险大小的信息,而其他数据(包括基因组数据)可以提供有关癌症存在的当前风险的信息。适当程度的风险可以指导可以预防癌症的干预措施(例如化学预防或预防性手术)或可以检测早期可治愈的癌症或重要前兆的存在。本讲座将描述定量概念框架及其基本原理,以及在癌症预防和筛查中使用遗传和基因组信息的含义、挑战和机遇。引文格式:David F. Ransohoff。利用遗传信息筛查和预防:临床医生和决策者的观点。[摘要]。摘自:AACR特别会议论文集:改进癌症风险预测以预防和早期发现;2016年11月16日至19日;费城(PA): AACR;Cancer epidemiology Biomarkers pre2017;26(5增刊):摘要nr IA07。
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Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-A13
Baiyu Yang, J. Petrick, C. Abnet, B. Graubard, S. Weinstein, S. Männistö, D. Albanes, K. McGlynn
Background: Periodontal disease, a common disorder of the tissue surrounding and supporting the teeth, is a major cause of tooth loss in adults. Periodontal infection by oral microorganisms may have systemic effects and has been associated with several types of cancer. However, its association with liver cancer has only been examined in two prospective studies, both of which had very small number of liver cancer cases (n Methods: We examined the association of tooth loss, as a proxy measure of periodontal infection, with primary liver cancer incidence and chronic liver disease mortality in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) study, a prospective cohort of male Finnish smokers (n = 29,096). Number of permanent teeth lost was assessed at study baseline (1985-1988). We used Cox proportional hazards models to calculate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). As a sensitivity analysis, we conducted a nested case-control study to assess confounding by hepatitis B or C virus (HBV or HCV) infection and seropositivity of Helicobacter pylori. Results: A total of 213 incident primary liver cancers occurred during a mean follow-up of 17 years. Having 11-31 permanent teeth lost was associated with a 42% higher risk of liver cancer (HR=1.42, 95% CI: 1.01-1.98), and having all 32 teeth lost was associated with a 45% higher risk of liver cancer (HR=1.45, 95% CI: 1.00-2.10), compared to having 0-10 teeth lost. In the sensitivity analysis, adjusting for Helicobacter pylori seropositivity yielded a modest attenuation of the effect estimate, whereas adjustment for HBV or HCV did not materially change the results. No consistent pattern was observed for liver disease mortality (n = 250 deaths). Conclusions: In this study, greater number of teeth lost was associated with higher risk of primary liver cancer. Further investigations are warranted to clarify the role of periodontal infection in hepatocarcinogenesis and to determine the utility of tooth loss as a predictor of liver cancer development. Citation Format: Baiyu Yang, Jessica L. Petrick, Christian C. Abnet, Barry I. Graubard, Stephanie J. Weinstein, Satu Mannisto, Demetrius Albanes, Katherine A. McGlynn. Tooth loss, liver cancer incidence, and chronic liver disease mortality in the ATBC study. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr A13.
背景:牙周病是牙齿周围和支撑组织的一种常见疾病,是成年人牙齿脱落的主要原因。口腔微生物引起的牙周感染可能具有全身性影响,并与几种癌症有关。然而,其与肝癌的相关性仅在两项前瞻性研究中得到了检验,这两项研究都有非常少的肝癌病例(n方法:我们在α -生育酚,β -胡萝卜素癌症预防(ATBC)研究中研究了牙齿脱落与原发性肝癌发病率和慢性肝病死亡率的关系,该研究是一项前瞻性芬兰男性吸烟者队列(n = 29,096)。在研究基线(1985-1988)评估恒牙脱落数量。我们使用Cox比例风险模型计算多变量调整风险比(hr)和95%置信区间(ci)。作为敏感性分析,我们进行了一项巢式病例对照研究,以评估乙型或丙型肝炎病毒(HBV或HCV)感染和幽门螺杆菌血清阳性的混杂性。结果:在平均17年的随访期间,共发生了213例原发性肝癌。失去11-31颗恒牙的人患肝癌的风险增加42% (HR=1.42, 95% CI: 1.01-1.98),与失去0-10颗恒牙的人相比,失去全部32颗恒牙的人患肝癌的风险增加45% (HR=1.45, 95% CI: 1.00-2.10)。在敏感性分析中,调整幽门螺杆菌的血清阳性产生了适度的效应估计衰减,而调整HBV或HCV并没有实质性地改变结果。没有观察到肝病死亡率的一致模式(n = 250例死亡)。结论:在本研究中,牙齿脱落越多,患原发性肝癌的风险越高。需要进一步的研究来阐明牙周感染在肝癌发生中的作用,并确定牙齿脱落作为肝癌发展预测因子的效用。引文格式:杨白宇,Jessica L. Petrick, Christian C. Abnet, Barry I. Graubard, Stephanie J. Weinstein, Satu Mannisto, Demetrius Albanes, Katherine A. McGlynn。ATBC研究中的牙齿脱落、肝癌发病率和慢性肝病死亡率[摘要]。摘自:AACR特别会议论文集:改进癌症风险预测以预防和早期发现;2016年11月16日至19日;费城(PA): AACR;Cancer epidemiology Biomarkers pre2017;26(5增刊):摘要nr A13。
{"title":"Abstract A13: Tooth loss, liver cancer incidence, and chronic liver disease mortality in the ATBC study","authors":"Baiyu Yang, J. Petrick, C. Abnet, B. Graubard, S. Weinstein, S. Männistö, D. Albanes, K. McGlynn","doi":"10.1158/1538-7755.CARISK16-A13","DOIUrl":"https://doi.org/10.1158/1538-7755.CARISK16-A13","url":null,"abstract":"Background: Periodontal disease, a common disorder of the tissue surrounding and supporting the teeth, is a major cause of tooth loss in adults. Periodontal infection by oral microorganisms may have systemic effects and has been associated with several types of cancer. However, its association with liver cancer has only been examined in two prospective studies, both of which had very small number of liver cancer cases (n Methods: We examined the association of tooth loss, as a proxy measure of periodontal infection, with primary liver cancer incidence and chronic liver disease mortality in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) study, a prospective cohort of male Finnish smokers (n = 29,096). Number of permanent teeth lost was assessed at study baseline (1985-1988). We used Cox proportional hazards models to calculate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). As a sensitivity analysis, we conducted a nested case-control study to assess confounding by hepatitis B or C virus (HBV or HCV) infection and seropositivity of Helicobacter pylori. Results: A total of 213 incident primary liver cancers occurred during a mean follow-up of 17 years. Having 11-31 permanent teeth lost was associated with a 42% higher risk of liver cancer (HR=1.42, 95% CI: 1.01-1.98), and having all 32 teeth lost was associated with a 45% higher risk of liver cancer (HR=1.45, 95% CI: 1.00-2.10), compared to having 0-10 teeth lost. In the sensitivity analysis, adjusting for Helicobacter pylori seropositivity yielded a modest attenuation of the effect estimate, whereas adjustment for HBV or HCV did not materially change the results. No consistent pattern was observed for liver disease mortality (n = 250 deaths). Conclusions: In this study, greater number of teeth lost was associated with higher risk of primary liver cancer. Further investigations are warranted to clarify the role of periodontal infection in hepatocarcinogenesis and to determine the utility of tooth loss as a predictor of liver cancer development. Citation Format: Baiyu Yang, Jessica L. Petrick, Christian C. Abnet, Barry I. Graubard, Stephanie J. Weinstein, Satu Mannisto, Demetrius Albanes, Katherine A. McGlynn. Tooth loss, liver cancer incidence, and chronic liver disease mortality in the ATBC study. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr A13.","PeriodicalId":9487,"journal":{"name":"Cancer Epidemiology and Prevention Biomarkers","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91269653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-IA12
R. Herrero
Cervical cancer screening is rapidly evolving to incorporate highly accurate molecular methods that are able to categorize women9s risk of cervical cancer and allow recommendations for follow-up or treatment. HPV nucleic acid testing provides highly sensitive and reproducible detection of HPV infection, a necessary cause of cervical cancer. Thus, virtually all women who have a cervical cancer precursor or who will develop one in the following years are HPV positive. On the other hand, the vast majority of HPV positive women have transient infections that will disappear in a few months. In this context, further evaluation of HPV positive women using triage methods allows further risk stratification that avoids unnecessary evaluations and overtreatment. Women positive for the triage test are referred for immediate colposcopic evaluation and follow-up (or, in some contexts, immediate treatment) as needed, while those who test negative usually receive another screening test in a year (or more). Triage with cytology or co-testing with HPV and cytology selects a group at clearly higher risk and generally above the recommended threshold for immediate colposcopy referral based on current consensus guidelines. For HPV positive women, genotyping for HPV 16 and 18 allows further risk stratification, but the additional benefit of other HPV genotypes is unclear. Ideally, triage methods are performed on the same specimen where the HPV test was carried out, to avoid additional visits. Risk stratification is different in different populations and age groups as HPV prevalence and type distribution, as well as screening histories are highly variable around the world. The programmatic decisions need to take into account the feasibility and logistics of different approaches and their respective burden on health services. Further research, particularly in low and middle income countries and in vaccinated cohorts is required. Citation Format: Rolando Herrero. Risk-assessment in HPV-based cervical cancer screening. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr IA12.
{"title":"Abstract IA12: Risk-assessment in HPV-based cervical cancer screening","authors":"R. Herrero","doi":"10.1158/1538-7755.CARISK16-IA12","DOIUrl":"https://doi.org/10.1158/1538-7755.CARISK16-IA12","url":null,"abstract":"Cervical cancer screening is rapidly evolving to incorporate highly accurate molecular methods that are able to categorize women9s risk of cervical cancer and allow recommendations for follow-up or treatment. HPV nucleic acid testing provides highly sensitive and reproducible detection of HPV infection, a necessary cause of cervical cancer. Thus, virtually all women who have a cervical cancer precursor or who will develop one in the following years are HPV positive. On the other hand, the vast majority of HPV positive women have transient infections that will disappear in a few months. In this context, further evaluation of HPV positive women using triage methods allows further risk stratification that avoids unnecessary evaluations and overtreatment. Women positive for the triage test are referred for immediate colposcopic evaluation and follow-up (or, in some contexts, immediate treatment) as needed, while those who test negative usually receive another screening test in a year (or more). Triage with cytology or co-testing with HPV and cytology selects a group at clearly higher risk and generally above the recommended threshold for immediate colposcopy referral based on current consensus guidelines. For HPV positive women, genotyping for HPV 16 and 18 allows further risk stratification, but the additional benefit of other HPV genotypes is unclear. Ideally, triage methods are performed on the same specimen where the HPV test was carried out, to avoid additional visits. Risk stratification is different in different populations and age groups as HPV prevalence and type distribution, as well as screening histories are highly variable around the world. The programmatic decisions need to take into account the feasibility and logistics of different approaches and their respective burden on health services. Further research, particularly in low and middle income countries and in vaccinated cohorts is required. Citation Format: Rolando Herrero. Risk-assessment in HPV-based cervical cancer screening. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr IA12.","PeriodicalId":9487,"journal":{"name":"Cancer Epidemiology and Prevention Biomarkers","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90508120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-A29
F. Schnabel, J. Chun, S. Schwartz, A. Guth, D. Axelrod, R. Shapiro, K. Hiotis, Julia A Smith
Purpose: Well-established risk factors for breast cancer include family history (FH), BRCA mutations and biopsies with atypical hyperplasia (AH) or lobular carcinoma in situ (LCIS). Several mathematical models, including the Gail and Tyrer-Cuzick models, have been developed to quantify a patient9s risk for developing breast cancer. These models all differ in the list of variables and risk factors that are included in risk calculations. As a result, there is no single model that best estimates the risk for all high risk patients. The purpose of this study is to examine the application of the Gail and Tyrer-Cuzick models in a contemporary cohort of women who are enrolled in a comprehensive high-risk breast cancer database. Methods: The institutional High Risk Breast Cancer Consortium (HRBCC) was established in January 2011. Patients who were at high risk for developing breast cancer based on family history (maternal and paternal), BRCA mutations, AH and LCIS were eligible to enroll in the database. The following variables were included in this analysis: age, family history, genetic testing results, reproductive history, AH, LCIS, Gail and Tyrer-Cuzick scores, risk reduction strategies, and outcomes. All clinical data are obtained from detailed questionnaires filled out by patients who consent to the database studies and from a review of electronic medical records. Descriptive statistics were performed. Results: A total of 604 women were enrolled between 1/2011-2/2016. The median age was 51 years (range 20-87). The majority of women were Caucasian (83%). 52% had a strong FH, 13% were BRCA1 and 2 positive, 48% had AH, and 22% had LCIS. 47% of patients in our high risk program were not eligible for Gail model analysis (age 84 years. For patients who were eligible for Gail model analysis, 26 (8%) women did not meet criteria (5-year risk ≥1.7%) for being designated as high risk for breast cancer. 34 (6%) of our patients did not have Tyrer-Cuzick scores over 20% (criterion for high risk). Notably, majority of the patients (69%) who were not defined as high-risk based on Gail scores ≥1.7% or Tyrer-Cuzick scores ≥20%, had a strong family history of breast cancer. Only 14 (2%) patients developed breast cancer during our study period, and the majority (93%) of the cancers were early stage (stage 0,I). Conclusions: Our institutional high-risk database includes women who are at high risk based on well-established risk factors for developing breast cancer (FH, BRCA mutations, AH, LCIS). Current mathematical models including the Gail and Tyrer-Cuzick models did not capture the increased risk of breast cancer in 8% of our population. While the models are helpful, in clinical practice they are not necessarily the be-all and end-all. Using heuristic risk factors is more time efficient and comprehensive risk assessment allows the clinicians and patients to better understand risk. Identifying patients as high risk and enrolling them in a high-risk database and progra
目的:确定乳腺癌的危险因素包括家族史(FH), BRCA突变和活检不典型增生(AH)或小叶原位癌(LCIS)。包括Gail和Tyrer-Cuzick模型在内的几个数学模型已经被开发出来,用来量化患者患乳腺癌的风险。这些模型在风险计算中包含的变量和风险因素列表上都有所不同。因此,没有一个单一的模型可以最好地估计所有高风险患者的风险。本研究的目的是检查Gail和Tyrer-Cuzick模型在一个综合性高风险乳腺癌数据库中登记的当代女性队列中的应用。方法:2011年1月成立机构性高危乳腺癌联盟(HRBCC)。基于家族史(母系和父系)、BRCA突变、AH和LCIS的高风险乳腺癌患者有资格进入数据库。以下变量包括在本分析中:年龄,家族史,基因检测结果,生殖史,AH, LCIS, Gail和Tyrer-Cuzick评分,风险降低策略和结果。所有临床数据均来自同意数据库研究的患者填写的详细问卷和对电子医疗记录的审查。进行描述性统计。结果:在2011年1月至2016年2月期间,共有604名女性入组。中位年龄为51岁(范围20-87岁)。大多数女性是白种人(83%)。52%有强烈的FH, 13%有BRCA1和2阳性,48%有AH, 22%有LCIS。在我们的高风险项目中,有47%的患者不符合Gail模型分析(年龄84岁)。在符合Gail模型分析的患者中,26名(8%)女性不符合被指定为乳腺癌高风险的标准(5年风险≥1.7%)。34例(6%)患者的Tyrer-Cuzick评分未超过20%(高危标准)。值得注意的是,根据Gail评分≥1.7%或Tyrer-Cuzick评分≥20%,大多数未被定义为高风险的患者(69%)具有强烈的乳腺癌家族史。在我们的研究期间,只有14例(2%)患者发生了乳腺癌,大多数(93%)的癌症是早期(0期,I期)。结论:我们的机构高风险数据库包括基于确定的乳腺癌危险因素(FH、BRCA突变、AH、LCIS)的高风险妇女。目前的数学模型,包括Gail和Tyrer-Cuzick模型,并没有捕捉到8%的人患乳腺癌的风险增加。虽然这些模型是有帮助的,但在临床实践中,它们不一定是最重要的。使用启发式风险因素更省时,全面的风险评估使临床医生和患者更好地了解风险。确定高风险患者并将其纳入高风险数据库和项目,使我们能够进行长期随访,推荐早期发现的监测,并更好地了解针对这一人群的不同风险降低和管理策略的有效性。引文格式:Freya Schnabel, Jennifer Chun, Shira Schwartz, Amber Guth, Deborah Axelrod, Richard Shapiro, Karen Hiotis, Julia Smith。数学模型并不是乳腺癌风险评估的全部和最终目的。[摘要]。摘自:AACR特别会议论文集:改进癌症风险预测以预防和早期发现;2016年11月16日至19日;费城(PA): AACR;Cancer epidemiology Biomarkers pre2017;26(5增刊):摘要nr A29。
{"title":"Abstract A29: Mathematical models are not the be-all and end-all for breast cancer risk assessment","authors":"F. Schnabel, J. Chun, S. Schwartz, A. Guth, D. Axelrod, R. Shapiro, K. Hiotis, Julia A Smith","doi":"10.1158/1538-7755.CARISK16-A29","DOIUrl":"https://doi.org/10.1158/1538-7755.CARISK16-A29","url":null,"abstract":"Purpose: Well-established risk factors for breast cancer include family history (FH), BRCA mutations and biopsies with atypical hyperplasia (AH) or lobular carcinoma in situ (LCIS). Several mathematical models, including the Gail and Tyrer-Cuzick models, have been developed to quantify a patient9s risk for developing breast cancer. These models all differ in the list of variables and risk factors that are included in risk calculations. As a result, there is no single model that best estimates the risk for all high risk patients. The purpose of this study is to examine the application of the Gail and Tyrer-Cuzick models in a contemporary cohort of women who are enrolled in a comprehensive high-risk breast cancer database. Methods: The institutional High Risk Breast Cancer Consortium (HRBCC) was established in January 2011. Patients who were at high risk for developing breast cancer based on family history (maternal and paternal), BRCA mutations, AH and LCIS were eligible to enroll in the database. The following variables were included in this analysis: age, family history, genetic testing results, reproductive history, AH, LCIS, Gail and Tyrer-Cuzick scores, risk reduction strategies, and outcomes. All clinical data are obtained from detailed questionnaires filled out by patients who consent to the database studies and from a review of electronic medical records. Descriptive statistics were performed. Results: A total of 604 women were enrolled between 1/2011-2/2016. The median age was 51 years (range 20-87). The majority of women were Caucasian (83%). 52% had a strong FH, 13% were BRCA1 and 2 positive, 48% had AH, and 22% had LCIS. 47% of patients in our high risk program were not eligible for Gail model analysis (age 84 years. For patients who were eligible for Gail model analysis, 26 (8%) women did not meet criteria (5-year risk ≥1.7%) for being designated as high risk for breast cancer. 34 (6%) of our patients did not have Tyrer-Cuzick scores over 20% (criterion for high risk). Notably, majority of the patients (69%) who were not defined as high-risk based on Gail scores ≥1.7% or Tyrer-Cuzick scores ≥20%, had a strong family history of breast cancer. Only 14 (2%) patients developed breast cancer during our study period, and the majority (93%) of the cancers were early stage (stage 0,I). Conclusions: Our institutional high-risk database includes women who are at high risk based on well-established risk factors for developing breast cancer (FH, BRCA mutations, AH, LCIS). Current mathematical models including the Gail and Tyrer-Cuzick models did not capture the increased risk of breast cancer in 8% of our population. While the models are helpful, in clinical practice they are not necessarily the be-all and end-all. Using heuristic risk factors is more time efficient and comprehensive risk assessment allows the clinicians and patients to better understand risk. Identifying patients as high risk and enrolling them in a high-risk database and progra","PeriodicalId":9487,"journal":{"name":"Cancer Epidemiology and Prevention Biomarkers","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90548521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-IA18
H. Katki, S. Kovalchik, C. Berg, L. Cheung, A. Chaturvedi
The US Preventive Services Task Force (USPSTF) recommends computed-tomography (CT) lung-cancer screening for ever-smokers ages 55-80 years who smoked at least 30 pack-years with no more than 15 years since quitting. However, selecting ever-smokers for screening using individualized lung-cancer risk calculations may be more effective and efficient than current USPSTF recommendations. We compare of modeled outcomes from risk-based CT lung-screening strategies versus USPSTF recommendations. We developed empirical risk models for lung-cancer incidence and death in the absence of CT screening using data on ever-smokers from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO; 1993-2009) control group. Covariates included age, education, sex, race, smoking intensity/duration/quit-years, Body Mass Index, family history of lung-cancer, and self-reported emphysema. Models were validated in the chest radiography groups of the PLCO and the National Lung Screening Trial (NLST; 2002-2009), with additional validation of the death model in the National Health Interview Survey (NHIS; 1997-2001), a representative sample of the US. Models applied to US ever-smokers ages 50-80 (NHIS 2010-2012) to estimate outcomes of risk-based selection for annual CT lung-screening for 3 years, assuming screening for all ever-smokers yields the percent changes in lung-cancer detection and death observed in the NLST. Lung-cancer incidence and death risk models were well-calibrated in PLCO and NLST. The lung-cancer death model calibrated and discriminated well for US ever-smokers ages 50-80 (NHIS 1997-2001: Estimated/Observed=0.94, 95%CI=0.84-1.05; AUC=0.78, 95%CI=0.76-0.80). Under USPSTF recommendations, the models estimated 9.0 million US ever-smokers would qualify for lung-cancer screening and 46,488 (95%CI=43,924-49,053) lung-cancer deaths were estimated as screen-avertable over 5 years (estimated NNS=194, 95%CI=187-201). In contrast, risk-based selection screened the same number of ever-smokers (9.0 million) at highest 5-year lung-cancer risk (≥1.9%), was estimated to avert 20% more deaths (55,717; 95%CI=53,033-58,400) and was estimated to reduce the estimated NNS by 17% (NNS=162, 95%CI=157-166). Among a cohort of US ever-smokers age 50-80 years, application of a risk-based model for CT screening for lung cancer compared with a model based on USPSTF recommendations was estimated to be associated with a greater number of lung-cancer deaths prevented over 5 years along with a lower NNS to prevent 1 lung-cancer death. Citation Format: Hormuzd A. Katki, Stephanie A. Kovalchik, Christine D. Berg, Li C. Cheung, Anil K. Chaturvedi. Development and validation of risk models to select ever-smokers for CT lung-cancer screening. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract n
美国预防服务工作组(USPSTF)建议对年龄在55-80岁、吸烟至少30包年、戒烟不超过15年的吸烟者进行计算机断层扫描(CT)肺癌筛查。然而,选择曾经吸烟的人进行筛查,使用个性化的肺癌风险计算可能比目前USPSTF的建议更有效和高效。我们比较了基于风险的CT肺部筛查策略和USPSTF推荐的模型结果。我们利用来自前列腺癌、肺癌、结直肠癌和卵巢癌筛查试验(PLCO;1993-2009)对照组。协变量包括年龄、教育程度、性别、种族、吸烟强度/持续时间/戒烟年限、身体质量指数、肺癌家族史和自报肺气肿。模型在PLCO的胸片组和国家肺筛查试验(NLST;2002-2009年),并在全国健康访谈调查(NHIS;1997-2001),是美国的代表性样本。应用于美国50-80岁的吸烟者(NHIS 2010-2012)的模型来估计基于风险选择3年年度CT肺部筛查的结果,假设所有吸烟者的筛查产生NLST中观察到的肺癌检出率和死亡率的百分比变化。肺癌发病率和死亡风险模型在PLCO和NLST中得到了很好的校准。肺癌死亡模型对50-80岁的美国吸烟者进行了很好的校准和区分(NHIS 1997-2001:估计/观察=0.94,95%CI=0.84-1.05;AUC = 0.78, 95% ci -0.80 = 0.76)。根据USPSTF的建议,这些模型估计有900万美国吸烟者有资格进行肺癌筛查,估计有46,488例(95%CI=43,924-49,053)肺癌死亡在5年内是筛查可避免的(估计NNS=194, 95%CI=187-201)。相比之下,基于风险的选择筛查了相同数量的吸烟者(900万),5年肺癌风险最高(≥1.9%),估计可避免20%以上的死亡(55,717;95%CI=53,033-58,400),估计可使估计NNS降低17% (NNS=162, 95%CI=157-166)。在美国50-80岁的吸烟者队列中,与基于USPSTF建议的模型相比,应用基于风险的模型进行肺癌CT筛查估计与5年内预防的肺癌死亡人数更多以及预防1例肺癌死亡的较低NNS相关。引文格式:Hormuzd A. Katki, Stephanie A. Kovalchik, Christine D. Berg, Li C. Cheung, Anil K. Chaturvedi。发展和验证的风险模型,以选择曾经吸烟的CT肺癌筛查。[摘要]。摘自:AACR特别会议论文集:改进癌症风险预测以预防和早期发现;2016年11月16日至19日;费城(PA): AACR;Cancer epidemiology Biomarkers pre2017;26(5增刊):摘要nr IA18。
{"title":"Abstract IA18: Development and validation of risk models to select ever-smokers for CT lung-cancer screening","authors":"H. Katki, S. Kovalchik, C. Berg, L. Cheung, A. Chaturvedi","doi":"10.1158/1538-7755.CARISK16-IA18","DOIUrl":"https://doi.org/10.1158/1538-7755.CARISK16-IA18","url":null,"abstract":"The US Preventive Services Task Force (USPSTF) recommends computed-tomography (CT) lung-cancer screening for ever-smokers ages 55-80 years who smoked at least 30 pack-years with no more than 15 years since quitting. However, selecting ever-smokers for screening using individualized lung-cancer risk calculations may be more effective and efficient than current USPSTF recommendations. We compare of modeled outcomes from risk-based CT lung-screening strategies versus USPSTF recommendations. We developed empirical risk models for lung-cancer incidence and death in the absence of CT screening using data on ever-smokers from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO; 1993-2009) control group. Covariates included age, education, sex, race, smoking intensity/duration/quit-years, Body Mass Index, family history of lung-cancer, and self-reported emphysema. Models were validated in the chest radiography groups of the PLCO and the National Lung Screening Trial (NLST; 2002-2009), with additional validation of the death model in the National Health Interview Survey (NHIS; 1997-2001), a representative sample of the US. Models applied to US ever-smokers ages 50-80 (NHIS 2010-2012) to estimate outcomes of risk-based selection for annual CT lung-screening for 3 years, assuming screening for all ever-smokers yields the percent changes in lung-cancer detection and death observed in the NLST. Lung-cancer incidence and death risk models were well-calibrated in PLCO and NLST. The lung-cancer death model calibrated and discriminated well for US ever-smokers ages 50-80 (NHIS 1997-2001: Estimated/Observed=0.94, 95%CI=0.84-1.05; AUC=0.78, 95%CI=0.76-0.80). Under USPSTF recommendations, the models estimated 9.0 million US ever-smokers would qualify for lung-cancer screening and 46,488 (95%CI=43,924-49,053) lung-cancer deaths were estimated as screen-avertable over 5 years (estimated NNS=194, 95%CI=187-201). In contrast, risk-based selection screened the same number of ever-smokers (9.0 million) at highest 5-year lung-cancer risk (≥1.9%), was estimated to avert 20% more deaths (55,717; 95%CI=53,033-58,400) and was estimated to reduce the estimated NNS by 17% (NNS=162, 95%CI=157-166). Among a cohort of US ever-smokers age 50-80 years, application of a risk-based model for CT screening for lung cancer compared with a model based on USPSTF recommendations was estimated to be associated with a greater number of lung-cancer deaths prevented over 5 years along with a lower NNS to prevent 1 lung-cancer death. Citation Format: Hormuzd A. Katki, Stephanie A. Kovalchik, Christine D. Berg, Li C. Cheung, Anil K. Chaturvedi. Development and validation of risk models to select ever-smokers for CT lung-cancer screening. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract n","PeriodicalId":9487,"journal":{"name":"Cancer Epidemiology and Prevention Biomarkers","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85017991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-B02
D. Brenner, Demetra Yannitsos, M. Warkentin, E. Shaw, N. Brockton, S. Mcgregor, Susanna Town, R. Hilsden
Background: Despite the consistent association between regular recreational moderate to vigorous physical activity (rMVPA) and reduced risk of colorectal cancer (CRC), few studies have examined the effect of physical activity on carcinogenic development by examining colorectal adenomas (polyps). Furthermore, even fewer studies have examined the impact of sedentary behavior/time (ST) on the development of polyps. In this study we examined the associations between rMVPA and ST and the presence, number and type of colorectal polyps in a population undergoing screening for colorectal cancer in Calgary, Alberta, Canada. Methods: A cross-sectional study of 2,499 individuals undergoing colonoscopy at the Forzani & MacPhail Colon Cancer Screening Centre in Calgary, Canada was conducted. Physical activity levels and ST were characterized using hours of rMVPA, meeting cancer prevention recommendations (≥150 mins/wk of rMVPA) and hours of ST using self-reported data from the Long Form International Physical Activity Questionnaire. Unconditional logistic regression models were used to estimate the crude and adjusted odds ratios (OR) for presence of polyps associated with rMVP and ST. Results: Crude estimates for meeting cancer prevention guidelines (ORunadj=0.83, 95% CI: 0.70-0.98) and increasing rMVPA (ORunadj=0.75, 95% CI: 0.60-0.93 for 1-3 hrs/wk vs. 0) were associated with lower odds of having ≥1 polyp at screening. Effect estimates were attenuated in adjusted models. Threshold effects were observed for ST with significant associations observed for up to 20 hours/week of sitting time (ORadj per hour sitting=1.05, 95% CI: 1.01-1.09). Associations were strongest for rMVPA among females (ORadj=0.68, 95% CI: 0.48-0.97 for 1-3 hrs/wk vs. 0) and for ST among males (ORadj=1.74, 95% CI: 1.06-2.86 for 14-35hrs/wk of ST vs. 0-14 hrs/wk) Conclusions: In this large population undergoing colonoscopy screening for colorectal cancer, rMVPA was associated with reduced prevalence of polyps at screening, particularly among females. Even low amounts of regular ST (2-5hrs/day) were associated with the presence of polyps, particularly among males. Strategies aimed at reducing the amount of pre-carcinogenic colon lesions should combine increasing rMVPA and reducing ST. Citation Format: Darren R. Brenner, Demetra H. Yannitsos, Matthew Warkentin, Eileen Shaw, Nigel T. Brockton, S. Elizabeth McGregor, Susanna Town, Robert J. Hilsden. Recreational physical activity, sedentary time and the incidence of colorectal polyps in a screening population for colon cancer. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr B02.
背景:尽管有规律的娱乐性、中度至剧烈的体育活动(rMVPA)与降低结直肠癌(CRC)风险之间存在一致的关联,但很少有研究通过检查结直肠腺瘤(息肉)来检验体育活动对致癌发展的影响。此外,很少有研究调查久坐行为/时间(ST)对息肉发展的影响。在这项研究中,我们研究了rMVPA和ST与在加拿大阿尔伯塔省卡尔加里接受结直肠癌筛查的人群中结肠息肉的存在、数量和类型之间的关系。方法:在加拿大卡尔加里的Forzani & MacPhail结肠癌筛查中心对2499名接受结肠镜检查的患者进行了横断面研究。身体活动水平和ST采用rMVPA小时(≥150分钟/周rMVPA)和ST小时(来自Long Form International Physical activity Questionnaire的自我报告数据)进行表征。使用无条件逻辑回归模型来估计与rMVP和st相关的息肉存在的粗比值比和调整比值比(OR)。结果:符合癌症预防指南的粗比值比(ORunadj=0.83, 95% CI: 0.70-0.98)和增加rMVPA (ORunadj=0.75, 95% CI: 0.60-0.93, 1-3小时/周vs. 0)与筛查时出现≥1个息肉的几率较低相关。在调整后的模型中,效应估计被减弱。在ST中观察到阈值效应,并且在长达20小时/周的坐着时间中观察到显著关联(每小时坐着的ORadj =1.05, 95% CI: 1.01-1.09)。rMVPA与女性的相关性最强(1-3小时/周vs. 0)和男性ST的相关性最强(14-35小时/周vs. 0-14小时/周,ORadj=0.68, 95% CI: 0.48-0.97)。结论:在接受结直肠癌结肠镜筛查的大量人群中,rMVPA与息肉患病率降低有关,尤其是在女性中。即使少量的常规睡眠(每天2-5小时)也与息肉的存在有关,尤其是在男性中。旨在减少结肠癌前病变数量的策略应结合增加rMVPA和减少ST.引文形式:Darren R. Brenner, Demetra H. Yannitsos, Matthew Warkentin, Eileen Shaw, Nigel T. Brockton, S. Elizabeth McGregor, Susanna Town, Robert J. Hilsden。娱乐性体育活动,久坐时间和结肠癌筛查人群中结肠息肉的发病率[摘要]。摘自:AACR特别会议论文集:改进癌症风险预测以预防和早期发现;2016年11月16日至19日;费城(PA): AACR;Cancer epidemiology Biomarkers pre2017;26(5增刊):摘要nr B02。
{"title":"Abstract B02: Recreational physical activity, sedentary time and the incidence of colorectal polyps in a screening population for colon cancer","authors":"D. Brenner, Demetra Yannitsos, M. Warkentin, E. Shaw, N. Brockton, S. Mcgregor, Susanna Town, R. Hilsden","doi":"10.1158/1538-7755.CARISK16-B02","DOIUrl":"https://doi.org/10.1158/1538-7755.CARISK16-B02","url":null,"abstract":"Background: Despite the consistent association between regular recreational moderate to vigorous physical activity (rMVPA) and reduced risk of colorectal cancer (CRC), few studies have examined the effect of physical activity on carcinogenic development by examining colorectal adenomas (polyps). Furthermore, even fewer studies have examined the impact of sedentary behavior/time (ST) on the development of polyps. In this study we examined the associations between rMVPA and ST and the presence, number and type of colorectal polyps in a population undergoing screening for colorectal cancer in Calgary, Alberta, Canada. Methods: A cross-sectional study of 2,499 individuals undergoing colonoscopy at the Forzani & MacPhail Colon Cancer Screening Centre in Calgary, Canada was conducted. Physical activity levels and ST were characterized using hours of rMVPA, meeting cancer prevention recommendations (≥150 mins/wk of rMVPA) and hours of ST using self-reported data from the Long Form International Physical Activity Questionnaire. Unconditional logistic regression models were used to estimate the crude and adjusted odds ratios (OR) for presence of polyps associated with rMVP and ST. Results: Crude estimates for meeting cancer prevention guidelines (ORunadj=0.83, 95% CI: 0.70-0.98) and increasing rMVPA (ORunadj=0.75, 95% CI: 0.60-0.93 for 1-3 hrs/wk vs. 0) were associated with lower odds of having ≥1 polyp at screening. Effect estimates were attenuated in adjusted models. Threshold effects were observed for ST with significant associations observed for up to 20 hours/week of sitting time (ORadj per hour sitting=1.05, 95% CI: 1.01-1.09). Associations were strongest for rMVPA among females (ORadj=0.68, 95% CI: 0.48-0.97 for 1-3 hrs/wk vs. 0) and for ST among males (ORadj=1.74, 95% CI: 1.06-2.86 for 14-35hrs/wk of ST vs. 0-14 hrs/wk) Conclusions: In this large population undergoing colonoscopy screening for colorectal cancer, rMVPA was associated with reduced prevalence of polyps at screening, particularly among females. Even low amounts of regular ST (2-5hrs/day) were associated with the presence of polyps, particularly among males. Strategies aimed at reducing the amount of pre-carcinogenic colon lesions should combine increasing rMVPA and reducing ST. Citation Format: Darren R. Brenner, Demetra H. Yannitsos, Matthew Warkentin, Eileen Shaw, Nigel T. Brockton, S. Elizabeth McGregor, Susanna Town, Robert J. Hilsden. Recreational physical activity, sedentary time and the incidence of colorectal polyps in a screening population for colon cancer. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr B02.","PeriodicalId":9487,"journal":{"name":"Cancer Epidemiology and Prevention Biomarkers","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85364004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-B09
V. Mehrotra, Ashutosh Sharma
Introduction: In the field of cancer, vitamin D has emerged as the most creative research connecting it with risk reduction in various epithelial cancers. Aside from calcium homeostasis, vitamin D exerts a wide range of immunogenic and antiproliferative activities in the human body. Vitamin D exerts its antiproliferative outcome by binding to vitamin D receptor (VDR) found in various tissues and cells of the body. Several human genes contain vitamin D response elements (specific DNA sequences) that encode for proteins important in regulation of cell proliferation, differentiation, apoptosis, and angiogenesis. When the serum vitamin D levels are suboptimal these activities are impaired and as a result enhanced cellular growth, neo-angiogenesis, and cancer development takes place. The breast cells have VDRs in their nuclei and it is postulated that polymorphism of genes for these VDRs results in increased risk for breast cancer. Serum concentration of 25(OH) 2 D are more sensitive to exogenous sources like: dietary and supplemental intake and endogenous production through synthesis in the skin of vitamin D which is the best indicator of vitamin D status of the body. There are data showing that locally advanced breast cancer patients had more severe vitamin D deficiency than those with early stage disease. The aim of the study was to determine serum vitamin D levels in breast cancer patients related with grade and stage of the tumor and to assess its risk prediction to improve health. Materials and Methods: Study samples: The study was conducted on indoor and outdoor patients for a period of one year (January to December), and an equal number of age and sex matched controls were taken which included total of 500 adults. Clinical Aassessment: Body mass index (BMI) was categorized as normal weight ( 28 kg/m2), fasting blood glucose (60 to 100 mg/dl) and Glycosylated Hemoglobin (controlled 7% uncontrolled). Vitamin D nutritional status was based on 25(OH) D levels, which were assessed as mild/sufficient (30-50 nmol/L), moderate/insufficient (12.5-29.9 nmol/L), and severe/deficient ( Results: The mean age was 42±1.5 years. Age, marital status, menopausal, residential area and BMI were similar in distribution among cases and controls. The mean serum vitamin D level in the breast cancer patients was Conclusion: Invariably almost all patients with breast cancer were vitamin D deficient. Tumor characteristics and BMI did not show any significant associations with serum levels of vitamin D. Note: This abstract was not presented at the conference. Citation Format: Vinit Mehrotra, Ashutosh Sharma. Serum vitamin D levels in breast cancer patients to assess its risk prediction to improve health. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr B09.
{"title":"Abstract B09: Serum vitamin D levels in breast cancer patients to assess its risk prediction to improve health","authors":"V. Mehrotra, Ashutosh Sharma","doi":"10.1158/1538-7755.CARISK16-B09","DOIUrl":"https://doi.org/10.1158/1538-7755.CARISK16-B09","url":null,"abstract":"Introduction: In the field of cancer, vitamin D has emerged as the most creative research connecting it with risk reduction in various epithelial cancers. Aside from calcium homeostasis, vitamin D exerts a wide range of immunogenic and antiproliferative activities in the human body. Vitamin D exerts its antiproliferative outcome by binding to vitamin D receptor (VDR) found in various tissues and cells of the body. Several human genes contain vitamin D response elements (specific DNA sequences) that encode for proteins important in regulation of cell proliferation, differentiation, apoptosis, and angiogenesis. When the serum vitamin D levels are suboptimal these activities are impaired and as a result enhanced cellular growth, neo-angiogenesis, and cancer development takes place. The breast cells have VDRs in their nuclei and it is postulated that polymorphism of genes for these VDRs results in increased risk for breast cancer. Serum concentration of 25(OH) 2 D are more sensitive to exogenous sources like: dietary and supplemental intake and endogenous production through synthesis in the skin of vitamin D which is the best indicator of vitamin D status of the body. There are data showing that locally advanced breast cancer patients had more severe vitamin D deficiency than those with early stage disease. The aim of the study was to determine serum vitamin D levels in breast cancer patients related with grade and stage of the tumor and to assess its risk prediction to improve health. Materials and Methods: Study samples: The study was conducted on indoor and outdoor patients for a period of one year (January to December), and an equal number of age and sex matched controls were taken which included total of 500 adults. Clinical Aassessment: Body mass index (BMI) was categorized as normal weight ( 28 kg/m2), fasting blood glucose (60 to 100 mg/dl) and Glycosylated Hemoglobin (controlled 7% uncontrolled). Vitamin D nutritional status was based on 25(OH) D levels, which were assessed as mild/sufficient (30-50 nmol/L), moderate/insufficient (12.5-29.9 nmol/L), and severe/deficient ( Results: The mean age was 42±1.5 years. Age, marital status, menopausal, residential area and BMI were similar in distribution among cases and controls. The mean serum vitamin D level in the breast cancer patients was Conclusion: Invariably almost all patients with breast cancer were vitamin D deficient. Tumor characteristics and BMI did not show any significant associations with serum levels of vitamin D. Note: This abstract was not presented at the conference. Citation Format: Vinit Mehrotra, Ashutosh Sharma. Serum vitamin D levels in breast cancer patients to assess its risk prediction to improve health. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr B09.","PeriodicalId":9487,"journal":{"name":"Cancer Epidemiology and Prevention Biomarkers","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86255863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-05-01DOI: 10.1158/1538-7755.CARISK16-IA20
W. Klein
The most promising new medications are doomed to be ineffective if not adequately prescribed and taken as directed by patients, highlighting the grave importance of understanding the vicissitudes of human behavior. The same might be said of risk prediction tools. Irrespective of their quality and validity, the successful use and impact of such tools hinges firmly on a thorough understanding of human motivation, emotion, and cognition – the building blocks of human behavior and decision-making. In general, people desire to minimize loss, uncertainty, and ambiguity, and they hold defensive self-serving beliefs about their risk and risk factors, particularly when they compare themselves to other people. People also construe risk in terms of dimensions such as dread, absolute frequency, controllability, and intuition rather than objective likelihood, and fail to consider base rates when assessing risk (rendering their risk judgments non-Bayesian). They also endeavor to appear to themselves and others as rational actors, often leading to the paradoxical choice of non-dominant options, and are influenced – often beyond awareness – by incidental emotions and secondary motives such as managing existential anxiety when evaluating personal risk and making consequential decisions. People also vary greatly in how they use and comprehend numerical information and in the comfort with which they do so. Risk communication strategies have been developed to reduce the undesired consequences of these phenomena on risk perception and decision making, and in some cases can be implemented quite easily into the outward design of a risk prediction tool as well as the manner in which it is used in clinical practice. Citation Format: William MP Klein. Maximizing the impact of risk prediction models: Leveraging lessons learned from risk communication research. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr IA20.
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