Pub Date : 2024-08-06DOI: 10.1158/1055-9965.EPI-24-0490
Mengmeng Ji, Yi-Hsuan Shih, John H Huber, Mei Wang, Eric J Feuer, Ruth Etzioni, Shi-Yi Wang, Su-Hsin Chang
Background Monoclonal gammopathy of undetermined significance (MGUS) is the premalignant condition of multiple myeloma (MM). Given a lack of population-based screening for MGUS and its asymptomatic nature, the epidemiology of MGUS remains unknown. This study estimated age- and race/ethnicity-specific MGUS incidence and preclinical duration from MGUS to MM in the United States. Methods A previously published modeling approach was used to calculate national MGUS incidence using estimates of MGUS prevalence, MM incidence, MM-specific and all-cause mortality, and population age distribution from the National Health and Nutrition Examination Survey, 1999-2004, and Surveillance, Epidemiology, and End Results, 2000-2021. The estimated MGUS prevalence was divided by MGUS incidence to obtain preclinical duration of MM. Results MGUS incidence for non-Hispanic white (NHW) populations was 52, 86, 142, and 181 and for non-Hispanic black (NHB) population was 110, 212, 392, and 570 per 100,000 person-years at ages 50, 60, 70, and 80, respectively. The average preclinical duration was 20.5 (95% confidence interval, CI: 16.5, 26.1) years for the NHW population and 14.2 (95% CI: 11.5, 17.6) years for the NHB population. The cumulative risk of developing MGUS in age 50-85 was 2.8% (95% CI: 1.7%, 4.2%) for the NHW population and 6.1% (95% CI: 3.8%, 10.0%) for the NHB population. Conclusion NHB populations had a higher MGUS incidence rate at all ages and a shorter preclinical duration of MM compared to their NHW counterparts. Impact This study provides insights into the epidemiology of MGUS and enhances our understanding of the natural history of MM.
{"title":"Asymptomatic Incidence of Monoclonal Gammopathy of Undetermined Significance and Preclinical Duration to Myeloma Diagnosis: A Modeling Study.","authors":"Mengmeng Ji, Yi-Hsuan Shih, John H Huber, Mei Wang, Eric J Feuer, Ruth Etzioni, Shi-Yi Wang, Su-Hsin Chang","doi":"10.1158/1055-9965.EPI-24-0490","DOIUrl":"10.1158/1055-9965.EPI-24-0490","url":null,"abstract":"<p><p>Background Monoclonal gammopathy of undetermined significance (MGUS) is the premalignant condition of multiple myeloma (MM). Given a lack of population-based screening for MGUS and its asymptomatic nature, the epidemiology of MGUS remains unknown. This study estimated age- and race/ethnicity-specific MGUS incidence and preclinical duration from MGUS to MM in the United States. Methods A previously published modeling approach was used to calculate national MGUS incidence using estimates of MGUS prevalence, MM incidence, MM-specific and all-cause mortality, and population age distribution from the National Health and Nutrition Examination Survey, 1999-2004, and Surveillance, Epidemiology, and End Results, 2000-2021. The estimated MGUS prevalence was divided by MGUS incidence to obtain preclinical duration of MM. Results MGUS incidence for non-Hispanic white (NHW) populations was 52, 86, 142, and 181 and for non-Hispanic black (NHB) population was 110, 212, 392, and 570 per 100,000 person-years at ages 50, 60, 70, and 80, respectively. The average preclinical duration was 20.5 (95% confidence interval, CI: 16.5, 26.1) years for the NHW population and 14.2 (95% CI: 11.5, 17.6) years for the NHB population. The cumulative risk of developing MGUS in age 50-85 was 2.8% (95% CI: 1.7%, 4.2%) for the NHW population and 6.1% (95% CI: 3.8%, 10.0%) for the NHB population. Conclusion NHB populations had a higher MGUS incidence rate at all ages and a shorter preclinical duration of MM compared to their NHW counterparts. Impact This study provides insights into the epidemiology of MGUS and enhances our understanding of the natural history of MM.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141896780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-02DOI: 10.1158/1055-9965.EPI-24-0494
Zahna Bigham, Etienne X Holder, Angie Mae Rodday, Janis Breeze, Kerrie P Nelson, Julie R Palmer, Karen M Freund, Kimberly A Bertrand
Background: High mammographic density is one of the strongest breast cancer risk factors; however, determinants of high mammographic density are understudied in Black women. We assessed growth and development factors across the lifecourse in relation to mammographic density.
Methods: Within the Black Women's Health Study (BWHS), we used Cumulus software to assess percent mammographic density from digital screening mammograms for 5,905 women ages 40-74. We fit linear regression models to quantify the association of lifecourse characteristics including birth weight, childhood somatotype, age at menarche, body mass index (BMI) at age 18, height, BMI at mammography, and adulthood waist-to-hip ratio with density overall and by age. We also performed a path analysis to assess the total and mediating effects of the growth and development factors on density.
Results: BMI at age 18, height, BMI at mammography, and waist-to-hip ratio were significantly and inversely associated with density. On path analysis, total effects of childhood somatotype (standardized = -0.05, p <0.001), BMI at age 18 (standardized = -0.13, p <0.001), BMI at mammography (standardized = -0.22, p <0.001), and waist-to-hip ratio (standardized = -0.04, p <0.001) were associated with density.
Conclusions: Several factors across the lifecourse - greater childhood somatotype, BMI at age 18, height, BMI at mammography, and waist-to-hip ratio - were associated with lower mammographic density in this cohort of Black women.
Impact: Body size closer to the time of mammography may be more meaningful in determining mammographic density, though early life adiposity also influences mammographic density.
背景:高乳房X线照相密度是乳腺癌风险最高的因素之一;然而,对黑人女性高乳房X线照相密度的决定因素研究不足。我们评估了与乳房X线摄影密度相关的整个生命过程中的生长和发育因素:在 "黑人妇女健康研究"(BWHS)中,我们使用Cumulus软件评估了5905名40-74岁女性的数字筛查乳房X光照片中的乳房X光密度百分比。我们拟合了线性回归模型,以量化生命过程特征(包括出生体重、童年体型、初潮年龄、18 岁时的体重指数 (BMI)、身高、乳房 X 光检查时的体重指数以及成年后的腰臀比等)与总体和各年龄段密度的关联。我们还进行了路径分析,以评估生长发育因素对密度的总体影响和中介影响:结果:18 岁时的体重指数、身高、乳房 X 射线照相时的体重指数和腰臀比与密度呈显著的反向关系。在路径分析中,童年体型的总效应(标准化 = -0.05,p 结论:童年体型的总效应与密度之间存在着明显的反向关系:在这个黑人妇女队列中,几个贯穿生命过程的因素--较大的童年体型、18 岁时的体重指数、身高、乳房 X 光检查时的体重指数和腰臀比--与较低的乳房 X 光密度有关:影响:虽然早年的肥胖也会影响乳房X光密度,但乳房X光造影时的体型可能对确定乳房X光密度更有意义。
{"title":"Lifecourse growth and development determinants of mammographic density in Black women.","authors":"Zahna Bigham, Etienne X Holder, Angie Mae Rodday, Janis Breeze, Kerrie P Nelson, Julie R Palmer, Karen M Freund, Kimberly A Bertrand","doi":"10.1158/1055-9965.EPI-24-0494","DOIUrl":"10.1158/1055-9965.EPI-24-0494","url":null,"abstract":"<p><strong>Background: </strong>High mammographic density is one of the strongest breast cancer risk factors; however, determinants of high mammographic density are understudied in Black women. We assessed growth and development factors across the lifecourse in relation to mammographic density.</p><p><strong>Methods: </strong>Within the Black Women's Health Study (BWHS), we used Cumulus software to assess percent mammographic density from digital screening mammograms for 5,905 women ages 40-74. We fit linear regression models to quantify the association of lifecourse characteristics including birth weight, childhood somatotype, age at menarche, body mass index (BMI) at age 18, height, BMI at mammography, and adulthood waist-to-hip ratio with density overall and by age. We also performed a path analysis to assess the total and mediating effects of the growth and development factors on density.</p><p><strong>Results: </strong>BMI at age 18, height, BMI at mammography, and waist-to-hip ratio were significantly and inversely associated with density. On path analysis, total effects of childhood somatotype (standardized = -0.05, p <0.001), BMI at age 18 (standardized = -0.13, p <0.001), BMI at mammography (standardized = -0.22, p <0.001), and waist-to-hip ratio (standardized = -0.04, p <0.001) were associated with density.</p><p><strong>Conclusions: </strong>Several factors across the lifecourse - greater childhood somatotype, BMI at age 18, height, BMI at mammography, and waist-to-hip ratio - were associated with lower mammographic density in this cohort of Black women.</p><p><strong>Impact: </strong>Body size closer to the time of mammography may be more meaningful in determining mammographic density, though early life adiposity also influences mammographic density.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1158/1055-9965.EPI-24-0046
Kelsi R Kroon, Johannes A Bogaards, Daniëlle A M Heideman, Chris J L M Meijer, Johannes Berkhof
Background: High-risk human papillomavirus (hrHPV)-based cervical cancer screening in the Netherlands led to a substantial increase in number of colposcopy referrals and low-grade lesions detected. Genotyping strategies may be employed to lower the screening-related burden.
Methods: We evaluated 14 triage strategies with genotyping (HPV16/18 or HPV16/18/31/33/45/52/58) for hrHPV-positive borderlineormilddyskaryosis (BMD)ornormal cytology,usingdata from a population-based hrHPV-based screening trial with 5-year interval (POBASCAM). We considered colposcopy referral at baseline, after 6-month repeat cytology and after 5-year hrHPV testing. Performance was evaluated by one-round positive and negative predictive value (PPVandNPV) for CIN3+ and by two-roundcolposcopy referral rate. To identify efficient strategies, they were ordered by the one-round colposcopy referral rate. Adjacent strategies were compared by the marginal PPV for detecting one additional CIN3+ (mPPV).
Results: The most conservative strategy (repeat cytology after BMD and HPV16/18/31/33/45/52/58-positive normal cytology, next round otherwise) yielded an mPPV of 28%, NPV of 98.2%, and two-round colposcopy referral rate of 47.2%. Adding direct referral after BMD or genotype-positive BMD yielded an mPPV ≤ 8.2%, NPV ≥ 98.5% and an increase in colposcopy referral rate of 1.9% to 6.5%. Adding direct referral after HPV16/18-positive normal cytology yielded an mPPV ≤ 3.5%, NPV ≥ 99.5% and an increase in colposcopy referral rate of 13.9%.
Conclusions: Direct colposcopy referral of women with BMD or normal cytology is unlikely to be efficient, but genotype-guided direct referral after BMD may be considered because the increase in colposcopies is limited.
Impact: hrHPV screening programs can become very efficient when immediate colposcopy referral is limited to women at highest CIN3+ risk. See related In the Spotlight, p. 979.
{"title":"Colposcopy Referral and CIN3+ Risk of Human Papillomavirus Genotyping Strategies in Cervical Cancer Screening.","authors":"Kelsi R Kroon, Johannes A Bogaards, Daniëlle A M Heideman, Chris J L M Meijer, Johannes Berkhof","doi":"10.1158/1055-9965.EPI-24-0046","DOIUrl":"10.1158/1055-9965.EPI-24-0046","url":null,"abstract":"<p><strong>Background: </strong>High-risk human papillomavirus (hrHPV)-based cervical cancer screening in the Netherlands led to a substantial increase in number of colposcopy referrals and low-grade lesions detected. Genotyping strategies may be employed to lower the screening-related burden.</p><p><strong>Methods: </strong>We evaluated 14 triage strategies with genotyping (HPV16/18 or HPV16/18/31/33/45/52/58) for hrHPV-positive borderlineormilddyskaryosis (BMD)ornormal cytology,usingdata from a population-based hrHPV-based screening trial with 5-year interval (POBASCAM). We considered colposcopy referral at baseline, after 6-month repeat cytology and after 5-year hrHPV testing. Performance was evaluated by one-round positive and negative predictive value (PPVandNPV) for CIN3+ and by two-roundcolposcopy referral rate. To identify efficient strategies, they were ordered by the one-round colposcopy referral rate. Adjacent strategies were compared by the marginal PPV for detecting one additional CIN3+ (mPPV).</p><p><strong>Results: </strong>The most conservative strategy (repeat cytology after BMD and HPV16/18/31/33/45/52/58-positive normal cytology, next round otherwise) yielded an mPPV of 28%, NPV of 98.2%, and two-round colposcopy referral rate of 47.2%. Adding direct referral after BMD or genotype-positive BMD yielded an mPPV ≤ 8.2%, NPV ≥ 98.5% and an increase in colposcopy referral rate of 1.9% to 6.5%. Adding direct referral after HPV16/18-positive normal cytology yielded an mPPV ≤ 3.5%, NPV ≥ 99.5% and an increase in colposcopy referral rate of 13.9%.</p><p><strong>Conclusions: </strong>Direct colposcopy referral of women with BMD or normal cytology is unlikely to be efficient, but genotype-guided direct referral after BMD may be considered because the increase in colposcopies is limited.</p><p><strong>Impact: </strong>hrHPV screening programs can become very efficient when immediate colposcopy referral is limited to women at highest CIN3+ risk. See related In the Spotlight, p. 979.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"1037-1045"},"PeriodicalIF":3.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140304964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1158/1055-9965.EPI-24-0313
Leslie V Farland, Kimberly E Lind, Denise J Roe, Nazmus Saquib, Howard D Strickler, Lihong Qi, Cynthia A Thomson, Holly R Harris
Background: There has been limited prior research on the association between infertility and risk of colorectal cancer.
Methods: Data from postmenopausal women in the Women's Health Initiative were used to estimate the association between self-reported infertility (12 months of trying to get pregnant without achieving a pregnancy) and the risk of colorectal cancer using Cox proportional hazard models.
Results: No association was observed between infertility and risk of postmenopausal colorectal cancer [RR, 0.97; 95% confidence interval (CI), 0.87-1.08], invasive colorectal cancer (RR, 0.99; 95% CI, 0.88-1.10), or colorectal cancer mortality (RR, 0.89; 95% CI, 0.71-1.12).
Conclusions: Infertility was not found to be associated with colorectal cancer risk among postmenopausal women. Risk did not vary by specific infertility diagnoses.
Impact: Infertility may not be associated with colorectal cancer risk.
{"title":"History of Infertility and Risk of Colorectal Cancer.","authors":"Leslie V Farland, Kimberly E Lind, Denise J Roe, Nazmus Saquib, Howard D Strickler, Lihong Qi, Cynthia A Thomson, Holly R Harris","doi":"10.1158/1055-9965.EPI-24-0313","DOIUrl":"10.1158/1055-9965.EPI-24-0313","url":null,"abstract":"<p><strong>Background: </strong>There has been limited prior research on the association between infertility and risk of colorectal cancer.</p><p><strong>Methods: </strong>Data from postmenopausal women in the Women's Health Initiative were used to estimate the association between self-reported infertility (12 months of trying to get pregnant without achieving a pregnancy) and the risk of colorectal cancer using Cox proportional hazard models.</p><p><strong>Results: </strong>No association was observed between infertility and risk of postmenopausal colorectal cancer [RR, 0.97; 95% confidence interval (CI), 0.87-1.08], invasive colorectal cancer (RR, 0.99; 95% CI, 0.88-1.10), or colorectal cancer mortality (RR, 0.89; 95% CI, 0.71-1.12).</p><p><strong>Conclusions: </strong>Infertility was not found to be associated with colorectal cancer risk among postmenopausal women. Risk did not vary by specific infertility diagnoses.</p><p><strong>Impact: </strong>Infertility may not be associated with colorectal cancer risk.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"1129-1131"},"PeriodicalIF":3.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11293956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141086881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1158/1055-9965.EPI-24-0204
Kush R Lohani, Andrea M Nibbe, Robert A Vierkant, Laura M Pacheco-Spann, Lisa R Seymour, Celine M Vachon, Mark E Sherman, Stacey J Winham, Amy C Degnim, Deirdre A Hill
Introduction: Although Hispanic White (HW) females have a lower incidence of breast cancer than non-Hispanic White (NHW) females, breast cancer risk is unclear for HW females after benign breast disease (BBD).
Methods: We compared BBD characteristics and subsequent breast cancer risk among HW and NHW females in New Mexico using a population-based collection of benign breast biopsies (1996-2007). BBD was categorized as nonproliferative disease (NPD), proliferative disease without atypia (PDWA), or atypical hyperplasia (AH). Breast cancer risk was assessed as absolute risk (AR) using cumulative incidence and RR by comparing the number of breast cancer events in BBDs to non-BBD.
Results: This study included 3,684 HW and 6,587 NHW females with BBD. HW females had similar proportions of NPD (58.6% vs. 54.3%), PDWA (21.4% vs. 23.5%), and AH (3.6% vs. 3.3%) as NHW females. Breast cancer risk among all females with BBD was higher than population-based expected rates (RR, 1.87) and was similar for HW and NHW subgroups (RR = 1.99 vs. 1.84). As expected, breast cancer risk increased with increasing BBD severity, both overall [RR, 1.81 (NPD), 1.85 (PDWA), and 3.10 (AH)] and in the HW and NHW subgroups. Adjusted AR of breast cancer at 5 years also increased with the severity of BBD (HW vs. NHW; NPD: 1.4% vs. 2.1%; PDWA: 1.5% vs. 2.7%; AH: 6% vs. 4.8%).
Conclusions: We found similar breast cancer RRs and ARs in HW and NHW. Risk counseling should ensure that HW females receive breast cancer clinical management warranted by their similar absolute risks.
Impact: The present population-based provides evidence for the clinical management of HW females with BBD for the prevention of breast cancer.
背景 西班牙裔白人女性(HW)的乳腺癌(BC)发病率低于非西班牙裔白人女性(NHW),但HW女性患良性乳腺疾病(BBD)后的BC风险尚不清楚。方法 我们通过基于人群的良性乳腺活检收集(1996-2007 年),比较了新墨西哥州华裔女性和非西语裔白人女性的良性乳腺疾病特征及其后的乳腺癌风险。BBD分为非增生性疾病(NPD)、无不典型性的增生性疾病(PDWA)或非典型性增生(AH)。BC风险的评估方式包括:使用累积发病率评估绝对风险(AR);通过比较BBD与非BBD的BC事件数量评估相对风险(RR)。结果 这项研究包括 3,684 名患有 BBD 的 HW 女性和 6,587 名患有 BBD 的 NHW 女性。HW女性中NPD(58.6%vs.54.3%)、PDWA(21.4%vs.23.5%)和AH(3.6%vs.3.3%)的比例与NHW相似。在所有患有 BBD 的女性中,BC 风险高于基于人群的预期比率(RR=1.87),而在 HW 和 NHW 亚群中,BC 风险相似(RR=1.99vs.1.84)。正如预期的那样,随着BBD严重程度的增加,BC风险也会增加,无论是在总体上[RR=1.81(NPD)、1.85(PDWA)和3.10(AH)],还是在HW和NHW亚组中。5年后BC的调整AR也随着BBD严重程度的增加而增加(HW vs. NHW;NPD:1.4 vs. 2.1%;PDWA:1.5 vs. 2.7%;AH:6 vs. 4.8%)。结论 我们发现 HW 和 NHW 的 BC RRs 和 ARs 相似。风险咨询应确保女性高危人群接受与其绝对风险相似的乳腺癌临床治疗。影响 本研究以人群为基础,提供了对患有 BBD 的华裔女性进行临床管理以预防乳腺癌的证据。
{"title":"Understanding Benign Breast Disease and Subsequent Breast Cancer in Hispanic White Females: A Step Closer to Evidence-Based Management.","authors":"Kush R Lohani, Andrea M Nibbe, Robert A Vierkant, Laura M Pacheco-Spann, Lisa R Seymour, Celine M Vachon, Mark E Sherman, Stacey J Winham, Amy C Degnim, Deirdre A Hill","doi":"10.1158/1055-9965.EPI-24-0204","DOIUrl":"10.1158/1055-9965.EPI-24-0204","url":null,"abstract":"<p><strong>Introduction: </strong>Although Hispanic White (HW) females have a lower incidence of breast cancer than non-Hispanic White (NHW) females, breast cancer risk is unclear for HW females after benign breast disease (BBD).</p><p><strong>Methods: </strong>We compared BBD characteristics and subsequent breast cancer risk among HW and NHW females in New Mexico using a population-based collection of benign breast biopsies (1996-2007). BBD was categorized as nonproliferative disease (NPD), proliferative disease without atypia (PDWA), or atypical hyperplasia (AH). Breast cancer risk was assessed as absolute risk (AR) using cumulative incidence and RR by comparing the number of breast cancer events in BBDs to non-BBD.</p><p><strong>Results: </strong>This study included 3,684 HW and 6,587 NHW females with BBD. HW females had similar proportions of NPD (58.6% vs. 54.3%), PDWA (21.4% vs. 23.5%), and AH (3.6% vs. 3.3%) as NHW females. Breast cancer risk among all females with BBD was higher than population-based expected rates (RR, 1.87) and was similar for HW and NHW subgroups (RR = 1.99 vs. 1.84). As expected, breast cancer risk increased with increasing BBD severity, both overall [RR, 1.81 (NPD), 1.85 (PDWA), and 3.10 (AH)] and in the HW and NHW subgroups. Adjusted AR of breast cancer at 5 years also increased with the severity of BBD (HW vs. NHW; NPD: 1.4% vs. 2.1%; PDWA: 1.5% vs. 2.7%; AH: 6% vs. 4.8%).</p><p><strong>Conclusions: </strong>We found similar breast cancer RRs and ARs in HW and NHW. Risk counseling should ensure that HW females receive breast cancer clinical management warranted by their similar absolute risks.</p><p><strong>Impact: </strong>The present population-based provides evidence for the clinical management of HW females with BBD for the prevention of breast cancer.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"1107-1113"},"PeriodicalIF":3.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11490305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141261099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1158/1055-9965.EPI-24-0010
Claire Ducos, Naïla Aba, Filippo Rosselli, Brice Fresneau, Baraah Al Ahmad Nachar, Monia Zidane, Florent de Vathaire, Simone Benhamou, Nadia Haddy
Second malignant neoplasm (SMN) is one of the most severe long-term risks for childhood cancer survivors (CCS), significantly impacting long-term patient survival. While radiotherapy and chemotherapy are known risk factors, the observed inter-individual variability suggests a genetic component contributing to the risk of SMN. This article aims to conduct a systematic review of genetic factors implicated in the SMN risk among CCS. Searches were performed in PubMed, Scopus, and Web of Sciences. Eighteen studies were included (eleven candidate gene studies, three genome-wide association studies, and four whole exome/genome sequencing studies). The included studies were based on different types of first cancers, investigated any or specific types of SMN, and focused mainly on genes involved in drug metabolism and DNA repair pathways. These differences in study design and methods used to characterize genetic variants limit the scope of the results and highlight the need for further extensive and standardized investigations. However, this review provides a valuable compilation of SMN risk-associated variants and genes, facilitating efficient replication and advancing our understanding of the genetic basis for this major risk for CCS.
二次恶性肿瘤(SMN)是儿童癌症幸存者(CCS)最严重的长期风险之一,严重影响患者的长期生存。虽然放疗和化疗是已知的风险因素,但观察到的个体间差异表明,遗传因素也是导致第二次恶性肿瘤风险的原因之一。本文旨在对与癌症幸存者 SMN 风险有关的遗传因素进行系统综述。我们在 PubMed、Scopus 和 Web of Sciences 上进行了搜索。共纳入 18 项研究(11 项候选基因研究、3 项全基因组关联研究和 4 项全外显子组/基因组测序研究)。所纳入的研究基于不同类型的首发癌症,调查了任何或特定类型的 SMN,并主要侧重于涉及药物代谢和 DNA 修复途径的基因。研究设计和表征基因变异所用方法的这些差异限制了研究结果的范围,并凸显了进一步开展广泛和标准化研究的必要性。不过,本综述对 SMN 风险相关变异和基因进行了有价值的汇编,有助于有效复制,并推进我们对这一 CCS 主要风险遗传基础的了解。
{"title":"Genetic Risk of Second Malignant Neoplasm after Childhood Cancer Treatment: A Systematic Review.","authors":"Claire Ducos, Naïla Aba, Filippo Rosselli, Brice Fresneau, Baraah Al Ahmad Nachar, Monia Zidane, Florent de Vathaire, Simone Benhamou, Nadia Haddy","doi":"10.1158/1055-9965.EPI-24-0010","DOIUrl":"10.1158/1055-9965.EPI-24-0010","url":null,"abstract":"<p><p>Second malignant neoplasm (SMN) is one of the most severe long-term risks for childhood cancer survivors (CCS), significantly impacting long-term patient survival. While radiotherapy and chemotherapy are known risk factors, the observed inter-individual variability suggests a genetic component contributing to the risk of SMN. This article aims to conduct a systematic review of genetic factors implicated in the SMN risk among CCS. Searches were performed in PubMed, Scopus, and Web of Sciences. Eighteen studies were included (eleven candidate gene studies, three genome-wide association studies, and four whole exome/genome sequencing studies). The included studies were based on different types of first cancers, investigated any or specific types of SMN, and focused mainly on genes involved in drug metabolism and DNA repair pathways. These differences in study design and methods used to characterize genetic variants limit the scope of the results and highlight the need for further extensive and standardized investigations. However, this review provides a valuable compilation of SMN risk-associated variants and genes, facilitating efficient replication and advancing our understanding of the genetic basis for this major risk for CCS.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"999-1011"},"PeriodicalIF":3.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141154587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1158/1055-9965.EPI-24-0121
Meredith S Shiels, Anika T Haque, Neal D Freedman, Hae-Rin Kim, Amy Berrington de González, Paul S Albert
Background: It is important to understand the impact of the COVID-19 pandemic on cancer death rates in 2020 in the US. We estimated whether there were larger-than-expected changes in cancer mortality rates from March to December 2020 after accounting for temporal and seasonal patterns using data from January 2011 to February 2020 by cancer type and age.
Methods: We obtained death counts and underlying causes of death by cancer type, month/year (2011-2020), and age group from the National Center for Health Statistics and population estimates from the US Census Bureau. Poisson regression was used to test for significant changes in cancer death rates from March to December 2020 compared with prior years.
Results: After accounting for temporal trends and seasonal patterns, total cancer death rates were significantly lower than expected during March to December 2020 among 55- to 64-year-olds and ≥75-year-olds, but not in other age groups. Cancer death rates were 2% lower than expected from March to June among 55- to 64-year-olds and 2% to 3% lower from March to July and December among ≥75-year-olds. Among ≥75-year-olds, colorectal cancer death rates were lower from March to June [rate ratios (RR) = 0.94-0.96; P < 0.05]; however, lung cancer death rates were 5% lower across each month (all RRs = 0.95; P < 0.05).
Conclusions: In the US, cancer death rates based on the underlying cause of death were broadly similar to expected rates from March to December 2020. However, cancer death rates were lower than expected among 55- to 64-year-olds and ≥75-year-olds, likely due to COVID-19 as a competing cause of death.
Impact: Cancer mortality rates from 2020 should be interpreted with caution.
{"title":"Age-Specific Cancer Mortality in the US During the COVID-19 Pandemic, March to December 2020.","authors":"Meredith S Shiels, Anika T Haque, Neal D Freedman, Hae-Rin Kim, Amy Berrington de González, Paul S Albert","doi":"10.1158/1055-9965.EPI-24-0121","DOIUrl":"10.1158/1055-9965.EPI-24-0121","url":null,"abstract":"<p><strong>Background: </strong>It is important to understand the impact of the COVID-19 pandemic on cancer death rates in 2020 in the US. We estimated whether there were larger-than-expected changes in cancer mortality rates from March to December 2020 after accounting for temporal and seasonal patterns using data from January 2011 to February 2020 by cancer type and age.</p><p><strong>Methods: </strong>We obtained death counts and underlying causes of death by cancer type, month/year (2011-2020), and age group from the National Center for Health Statistics and population estimates from the US Census Bureau. Poisson regression was used to test for significant changes in cancer death rates from March to December 2020 compared with prior years.</p><p><strong>Results: </strong>After accounting for temporal trends and seasonal patterns, total cancer death rates were significantly lower than expected during March to December 2020 among 55- to 64-year-olds and ≥75-year-olds, but not in other age groups. Cancer death rates were 2% lower than expected from March to June among 55- to 64-year-olds and 2% to 3% lower from March to July and December among ≥75-year-olds. Among ≥75-year-olds, colorectal cancer death rates were lower from March to June [rate ratios (RR) = 0.94-0.96; P < 0.05]; however, lung cancer death rates were 5% lower across each month (all RRs = 0.95; P < 0.05).</p><p><strong>Conclusions: </strong>In the US, cancer death rates based on the underlying cause of death were broadly similar to expected rates from March to December 2020. However, cancer death rates were lower than expected among 55- to 64-year-olds and ≥75-year-olds, likely due to COVID-19 as a competing cause of death.</p><p><strong>Impact: </strong>Cancer mortality rates from 2020 should be interpreted with caution.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"1023-1027"},"PeriodicalIF":3.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11293979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141282996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1158/1055-9965.EPI-23-1491
Jennifer L Lund, M Patricia Rivera, I-Hsuan Su, Jason M Long, Xiaomeng Chen, Joyce Pak, Michael G Hudgens, Til Stürmer, Daniel S Reuland, Louise M Henderson
Randomized controlled trials (RCT) are the gold standard in determining efficacy of cancer screening tests. Yet, systematic differences between RCT and the general populations eligible for screening raise concerns about the generalizability and relevance of RCT findings to guide the development and dissemination of cancer screening programs. Observational studies from clinical practice settings have documented selective uptake in screening-i.e., variation across subgroups regarding who is screened and not screened-as well as suboptimal adherence to screening recommendations, including follow-up of positive findings with subsequent imaging studies and diagnostic invasive procedures. When the effectiveness of a screening intervention varies across subgroups, and there is selective uptake and suboptimal adherence to screening in clinical practice relative to that in the RCT, the effects of screening reported in RCTs are not expected to generalize to clinical practice settings. Understanding the impacts of selective uptake and suboptimal adherence on estimates of the effectiveness of cancer screening in clinical practice will generate evidence that can be used to inform future screening recommendations and enhance shared decision-making tools.
{"title":"Estimating the Effects of Cancer Screening in Clinical Practice Settings: The Role of Selective Uptake and Suboptimal Adherence along the Cancer Screening Continuum.","authors":"Jennifer L Lund, M Patricia Rivera, I-Hsuan Su, Jason M Long, Xiaomeng Chen, Joyce Pak, Michael G Hudgens, Til Stürmer, Daniel S Reuland, Louise M Henderson","doi":"10.1158/1055-9965.EPI-23-1491","DOIUrl":"10.1158/1055-9965.EPI-23-1491","url":null,"abstract":"<p><p>Randomized controlled trials (RCT) are the gold standard in determining efficacy of cancer screening tests. Yet, systematic differences between RCT and the general populations eligible for screening raise concerns about the generalizability and relevance of RCT findings to guide the development and dissemination of cancer screening programs. Observational studies from clinical practice settings have documented selective uptake in screening-i.e., variation across subgroups regarding who is screened and not screened-as well as suboptimal adherence to screening recommendations, including follow-up of positive findings with subsequent imaging studies and diagnostic invasive procedures. When the effectiveness of a screening intervention varies across subgroups, and there is selective uptake and suboptimal adherence to screening in clinical practice relative to that in the RCT, the effects of screening reported in RCTs are not expected to generalize to clinical practice settings. Understanding the impacts of selective uptake and suboptimal adherence on estimates of the effectiveness of cancer screening in clinical practice will generate evidence that can be used to inform future screening recommendations and enhance shared decision-making tools.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"984-988"},"PeriodicalIF":3.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11351907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1158/1055-9965.EPI-24-0716
Jennifer C Spencer, Cosette M Wheeler
Cervical cancer screening has reduced morbidity and mortality in many countries, but efforts to optimize screening modalities and schedules are ongoing. Using data from a randomized trial conducted in British Columbia, Canada, in conjunction with a provincial screening registry, Gottschlich and colleagues demonstrated that the estimated risk for precancerous disease (cervical intraepithelial neoplasia grades 2 or worse) at 8 years following a negative human papillomavirus (HPV) test was similar to the current standard of care (Pap testing after 3 years). The study supports extending screening intervals for those with a negative HPV test beyond currently recommended 5-year intervals. In an ideal world, the resources saved through less frequent routine cervical screening could be redirected to increasing screening uptake and follow-up of abnormalities to improve equity in cervical cancer prevention. However, implementation of extending screening intervals remains less than straightforward in settings with fragmented healthcare systems that lack information systems to support patient call/recall, such as the United States. To achieve the full promise of primary HPV testing, stakeholders at every level must commit to identifying and addressing the diverse spectrum of barriers that undergird existing inequities in care access, appropriately resource implementation strategies, and improve health information systems. See related article by Gottschlich et al., p. 904.
{"title":"Promise and Perils of Primary HPV Testing.","authors":"Jennifer C Spencer, Cosette M Wheeler","doi":"10.1158/1055-9965.EPI-24-0716","DOIUrl":"10.1158/1055-9965.EPI-24-0716","url":null,"abstract":"<p><p>Cervical cancer screening has reduced morbidity and mortality in many countries, but efforts to optimize screening modalities and schedules are ongoing. Using data from a randomized trial conducted in British Columbia, Canada, in conjunction with a provincial screening registry, Gottschlich and colleagues demonstrated that the estimated risk for precancerous disease (cervical intraepithelial neoplasia grades 2 or worse) at 8 years following a negative human papillomavirus (HPV) test was similar to the current standard of care (Pap testing after 3 years). The study supports extending screening intervals for those with a negative HPV test beyond currently recommended 5-year intervals. In an ideal world, the resources saved through less frequent routine cervical screening could be redirected to increasing screening uptake and follow-up of abnormalities to improve equity in cervical cancer prevention. However, implementation of extending screening intervals remains less than straightforward in settings with fragmented healthcare systems that lack information systems to support patient call/recall, such as the United States. To achieve the full promise of primary HPV testing, stakeholders at every level must commit to identifying and addressing the diverse spectrum of barriers that undergird existing inequities in care access, appropriately resource implementation strategies, and improve health information systems. See related article by Gottschlich et al., p. 904.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"33 8","pages":"982-983"},"PeriodicalIF":3.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11292190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141859126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.1158/1055-9965.EPI-23-1185
Elif Inan-Eroglu, Matthew Ahmadi, Raaj Kishore Biswas, Ding Ding, Leandro F M Rezende, I-Min Lee, Edward L Giovannucci, Emmanuel Stamatakis
Background: We examined the joint associations of diet and device-measured intensity-specific physical activity (PA) with all-cause mortality (ACM), cardiovascular disease (CVD), and cancer incidence.
Methods: We used data from 79,988 participants from the UK Biobank, a population-based prospective cohort study. Light PA (LPA), moderate-to-vigorous PA (MVPA), vigorous PA (VPA), and total PA (TPA) were measured using a wrist-worn accelerometer. Diet quality score (DQS) was based on 10 foods and ranged from 0 (unhealthiest) to 100 (healthiest) points. We derived joint PA and diet variables. Outcomes were ACM, CVD, and cancer incidence including PA, diet and adiposity-related (PDAR) cancer.
Results: During a median follow-up of 8 years, 2,863 deaths occurred, 11,053 participants developed CVD, 7,005 developed cancer, and 3,400 developed PDAR cancer. Compared with the least favorable referent group (bottom PA tertile/low DQS), participants with middle and high (total and intensity specific) PA, except for LPA, had lower ACM risk and incident CVD risk, regardless of DQS. For example, among middle and high VPA and high DQS groups, CVD HR were 0.79 (95% CI, 0.74-0.86) and 0.75 (95% CI, 0.69-0.82), respectively. The pattern of cancer results was less pronounced but in agreement with the ACM and CVD incidence findings (e.g., HR, 0.90, 95% CI, 0.81-0.99; 0.88, 0.79-0.98; and 0.82, 0.74-0.92 among high VPA for low, moderate, and high DQS groups, respectively).
Conclusions: Device-measured PA reveals novel joint associations with diet on health outcomes.
Impact: Our results emphasize the crucial role of PA in addition to a healthy diet for reducing chronic diseases and mortality risk.
{"title":"Joint Associations of Diet and Device-Measured Physical Activity with Mortality and Incident CVD and Cancer: A Prospective Analysis of the UK Biobank Study.","authors":"Elif Inan-Eroglu, Matthew Ahmadi, Raaj Kishore Biswas, Ding Ding, Leandro F M Rezende, I-Min Lee, Edward L Giovannucci, Emmanuel Stamatakis","doi":"10.1158/1055-9965.EPI-23-1185","DOIUrl":"10.1158/1055-9965.EPI-23-1185","url":null,"abstract":"<p><strong>Background: </strong>We examined the joint associations of diet and device-measured intensity-specific physical activity (PA) with all-cause mortality (ACM), cardiovascular disease (CVD), and cancer incidence.</p><p><strong>Methods: </strong>We used data from 79,988 participants from the UK Biobank, a population-based prospective cohort study. Light PA (LPA), moderate-to-vigorous PA (MVPA), vigorous PA (VPA), and total PA (TPA) were measured using a wrist-worn accelerometer. Diet quality score (DQS) was based on 10 foods and ranged from 0 (unhealthiest) to 100 (healthiest) points. We derived joint PA and diet variables. Outcomes were ACM, CVD, and cancer incidence including PA, diet and adiposity-related (PDAR) cancer.</p><p><strong>Results: </strong>During a median follow-up of 8 years, 2,863 deaths occurred, 11,053 participants developed CVD, 7,005 developed cancer, and 3,400 developed PDAR cancer. Compared with the least favorable referent group (bottom PA tertile/low DQS), participants with middle and high (total and intensity specific) PA, except for LPA, had lower ACM risk and incident CVD risk, regardless of DQS. For example, among middle and high VPA and high DQS groups, CVD HR were 0.79 (95% CI, 0.74-0.86) and 0.75 (95% CI, 0.69-0.82), respectively. The pattern of cancer results was less pronounced but in agreement with the ACM and CVD incidence findings (e.g., HR, 0.90, 95% CI, 0.81-0.99; 0.88, 0.79-0.98; and 0.82, 0.74-0.92 among high VPA for low, moderate, and high DQS groups, respectively).</p><p><strong>Conclusions: </strong>Device-measured PA reveals novel joint associations with diet on health outcomes.</p><p><strong>Impact: </strong>Our results emphasize the crucial role of PA in addition to a healthy diet for reducing chronic diseases and mortality risk.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"1028-1036"},"PeriodicalIF":3.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}