Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology最新文献

{"title":"Achieving the National Cancer Plan's Goals: The Role of Nationwide and State-Level Health Data Infrastructure.","authors":"Gabriel Seidman, Ahmad Alkasir, Anna D Barker","doi":"10.1158/1055-9965.EPI-24-1731","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-1731","url":null,"abstract":"<p><p>Nationwide enterprise architecture for health data would enable the effective reuse of existing data assets for applications across cancer care, prevention, and research and is arguably a prerequisite for meeting the NCI goal of halving cancer mortality in 25 years. This study builds on and extends existing calls for a federal initiative that incentivizes the creation of state-designated entities with mandates and authorities to implement and oversee a state's enterprise architecture to collect, integrate, analyze, and share multisource health data for reuse. Granting the proposed state-designated entities relevant authorities would allow them to serve as de facto population-level registries with critical multisource datasets to support cancer research. We describe how these capabilities could contribute to improvements in precision oncology clinical research and care, primary prevention and research on risk factors, secondary prevention, screening and diagnosis, and more effectively measuring progress against cancer. We also propose a framework for moving forward on this initiative, beginning with the development of a Master Plan by a consortium of research, professional, and patient advocacy organizations; a single nonprofit cancer organization; and/or a group of states. This Master Plan would be presented to the federal government for adoption and implementation.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":"34 7","pages":"1059-1065"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532656","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}

{"title":"Achieving Maximum Benefit from Colorectal Cancer Screening: Start Younger, Offer Choice, Find Advanced Precancerous Lesions.","authors":"Richard C Wender","doi":"10.1158/1055-9965.EPI-25-0678","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-25-0678","url":null,"abstract":"<p><p>Colorectal cancer screening is one of the most effective interventions in all of preventive care. Screening programs in many high-resource nations have resulted in marked declines in colorectal cancer mortality rates in the screening age population. For several decades, the incidence of colorectal cancer in individuals below 50 years of age (early-onset colorectal cancer) has been steadily increasing in each successive birth cohort. This increase in incidence has driven rising colorectal cancer mortality in people below 55 years of age. Two studies in this issue of the journal provide useful guidance for addressing this shifting incidence and information about choice of screening test to cost-effectively reach a higher percentage of the total population. Moving screening to 45 years of age should occur in all high-resource countries experiencing rising incidence. Although a menu of screening options is needed to reach the highest possible number of eligible individuals, detecting advanced precancerous lesions is a critical aspect of any screening program. Affordable, acceptable noninvasive screening options with high sensitivity for cancer and advanced precancerous lesions combined with primary and follow-up colonoscopy should be deployed to reach the most people and prevent the most deaths from colorectal cancer. See related article by Chia and colleagues, Cancer Epidemiol Biomarkers Prev 2025;34:990-7 See related article by Rui et al., p. 1111.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":"34 7","pages":"1053-1054"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532655","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}

{"title":"Misclassification Matters: A Case for Utilization of Histologic Coding in UK Biobank Analyses.","authors":"Michael A O'Rorke, Isaac R Werner, Bradley D McDowell, Elizabeth A Chrischilles","doi":"10.1158/1055-9965.EPI-25-0286","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-25-0286","url":null,"abstract":"<p><p>Misclassification and measurement error is a significant issue in epidemiologic research. When utilizing large datasets like the UK Biobank in particular, we found that pancreatic neuroendocrine neoplasms are often erroneously included in studies focused on exocrine pancreatic cancer. This happens when studies use only International Classification of Diseases codes to define their cases. The use of International Classification of Diseases for Oncology, Third Edition histologic coding can prevent this problem. This commentary examines the prevalence of this issue in published literature and highlights its potential impact on existing studies. Implementing rigorous coding practices and promoting their consistent use among researchers are crucial for ensuring valid and reliable findings in future pancreatic cancer studies using the UK Biobank.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":"34 7","pages":"1055-1058"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532657","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}

{"title":"Family history of early onset or lethal prostate cancer and the risk of prostate cancer death in Sweden.","authors":"E Lin, Hans Garmo, Kerri Beckmann, Ola Bratt, Par Stattin, Rolf Gedeborg","doi":"10.1158/1055-9965.EPI-25-0198","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-25-0198","url":null,"abstract":"<p><strong>Background: </strong>A family history (FH) of prostate cancer (PCa) increases the risk of PCa, but its association with PCa mortality remains unclear.</p><p><strong>Methods: </strong>FH was defined as having a first-degree relative who was diagnosed before age 60 or died from PCa. We used Cox regression to estimate associations between FH and PCa characteristics at diagnosis, radical treatment, and PCa death in men born after 1932 and diagnosed with PCa between 1998-2020 in Sweden.</p><p><strong>Results: </strong>Among 125 272 men with PCa, 13 193 had a FH of early onset or lethal PCa. At diagnosis, men with FH had 1.4 years lower median age, 0.87 ng/ml lower serum PSA, lower proportion of Gleason score 8-10 cancer (14.8% vs. 17.6%), lower odds for metastatic disease (odds ratio [OR], 0.79; 95% confidence interval [CI], 0.73-0.86), and higher odds for radical treatment (OR, 1.25; 95% CI, 1.18-1.32). With a median follow-up of 6.9 years and 12 773 PCa deaths, mortality was lower (crude hazard ratio (HR), 0.77; 95% CI, 0.73-0.82) in men with FH. Adjustment for PCa characteristics attenuated this association (adjusted HR, 0.94; 95% CI, 0.88-1.00).</p><p><strong>Conclusions: </strong>Men with PCa and a FH of early onset or lethal PCa had more favorable cancer characteristics, higher likelihood of radical treatment, and similar PCa mortality compared with men without FH.</p><p><strong>Impact: </strong>In men with PCa, the risk of PCa death appears unaffected by a FH of early onset or lethal PCa after controlling for clinical characteristics. More research is needed about the potential role of screening.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546785","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}

{"title":"Projected Trends in the Incidence and Mortality of Uterine Cancer in the United States.","authors":"Jason D Wright, Matthew T Prest, Jennifer S Ferris, Ling Chen, Xiao Xu, Kevin J Rouse, Alexander Melamed, Chin Hur, Brandy M Heckman-Stoddard, Goli Samimi, Nina A Bickell, Tracy M Layne, Evan R Myers, Laura J Havrilesky, Stephanie V Blank, Natasha K Stout, William D Hazelton, Chung Yin Kong, Elena B Elkin","doi":"10.1158/1055-9965.EPI-24-1422","DOIUrl":"10.1158/1055-9965.EPI-24-1422","url":null,"abstract":"<p><strong>Background: </strong>To develop a natural history model for uterine cancer calibrated to population-based incidence and mortality data to project future trends in the disease through 2050.</p><p><strong>Methods: </strong>We developed a state-transition microsimulation model of uterine cancer. The model begins at 18 years of age and simulates Black and White patients, includes transition states for precursor lesions, and separately models endometrioid and nonendometrioid tumors. The model was calibrated to population-based incidence and mortality data using parameter extrapolation.</p><p><strong>Results: </strong>The model closely fit population-based incidence and mortality data of uterine cancer. From 2020 to 2050, the incidence of uterine cancer is projected to increase in White women to 74.2 cases per 100,000 (compared with 57.7 cases per 100,000 in 2018) and increase to 86.9 per 100,000 (compared with 56.8 cases per 100,000 in 2018) in Black women. Among White women, incidence-based mortality will increase from 6.1 per 100,000 in 2018 to 11.2 per 100,000 in 2050, whereas incidence-based mortality in Black women will increase from 14.1 per 100,000 to 27.9 per 100,000. Endometrioid tumors are expected to increase considerably in both White and Black women; White women will experience only a slight increase in nonendometrioid tumors, whereas the incidence of these tumors will increase substantially in Black women.</p><p><strong>Conclusions: </strong>The incidence and mortality of uterine cancer are projected to increase substantially over the next three decades. Black women will experience a disproportionate increase in the disease.</p><p><strong>Impact: </strong>Projecting the incidence and mortality of uterine cancer can facilitate future cancer control efforts.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":"34 7","pages":"1156-1166"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12221196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144532674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Translational Research Program in Cancer Differences across Populations.","authors":"Jane C Figueiredo, Diana Redwood, Li Li, Elizabeth Donato, Daniel Fort, Eric E Fox, William M Grady, Heather Green, Tabitha A Harrison, Carl Haupt, Li Hsu, Meredith A J Hullar, Jeroen R Huyghe, Wenora Johnson, Amanda L Koehne, Scott D LaBrie, Meredith A Lakey, MingGang Lin, Nicole C Loroña, Grace A Maresh, Marc Matrana, Jonathan D Mizrahi, Sarah H Nash, Nathalie T Nguyen, Jennifer L Paruch, Amanda I Phipps, Conghui Qu, Timothy W Randolph, Stephanie Romo, Claire E Thomas, Sushma Thomas, James Tiesinga, Charles Whitlow, Cecilia C S Yeung, Hang Yin, Craig M Zibilich, Christopher I Li, Timothy K Thomas, Ulrike Peters","doi":"10.1158/1055-9965.EPI-24-1711","DOIUrl":"10.1158/1055-9965.EPI-24-1711","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) incidence and mortality vary substantially across populations. The Translational Research Program in Cancer Differences across Populations (TRPCDP) was established in 2020 to address differences in CRC incidence and mortality rates within the United States.</p><p><strong>Methods: </strong>TRPCDP centralized data acquisition and harmonization across three sites in the U.S. to create a well-annotated resource of CRC tumors across four populations: African American/Black, Alaska Native, Hispanic/Latino/a, and non-Hispanic White. Using a case-control framework, patients with lethal CRC were matched to two controls with non-lethal CRC. Formalin-fixed paraffin-embedded tumor and normal tissue were retrieved and sent for centralized pathology review, followed by DNA and RNA extraction and tissue microarray development. Multi-omics and spatial profiling are underway to evaluate the transcriptome, proteome, and microbiome. Patient demographic and clinical data were obtained by medical record review, patient self-report, or linkage to cancer registries. Additional health-related factors were assessed using geospatial linkage.</p><p><strong>Results: </strong>The virtual biorepository includes 7,181 patients [African American (n=1,345), Alaska Native (n=1,640), Hispanic (n=1,659), and non-Hispanic White (n=2,537)]. Tissue blocks (1,594 tumor, 728 normal colon) were selected for 938 patients. To date, DNA and RNA have been extracted (n=831) and tissue microarrays have been constructed (n=414). Transcriptomic, spatial tumor profiling (multiplex immunofluorescence, PhenoCycler, GeoMx) and microbiome data (16S rRNAseq, ddPCR) are available.</p><p><strong>Conclusion: </strong>The TRPCDP has developed a clinically annotated biorepository for future molecular epidemiology studies.</p><p><strong>Impact: </strong>TRPCDP is a unique program that supports collaborative research, community engagement, and pipeline development for the next generation of scientists.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144510294","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}

{"title":"Associations of Type 2 Diabetes with risk of overall and site-specific cancers in a cohort of predominantly low-income racially diverse populations.","authors":"Pranoti Pradhan, Wanqing Wen, Alvin C Powers, Shaneda Warren Andersen, Maureen Sanderson, Loren Lipworth, Wei Zheng","doi":"10.1158/1055-9965.EPI-23-1079","DOIUrl":"10.1158/1055-9965.EPI-23-1079","url":null,"abstract":"<p><strong>Background: </strong>The prevalence of type 2 diabetes (T2D) is higher in Black than white Americans, and individuals with T2D have an increased cancer risk. We investigated the association of T2D with the risk of all cancer combined and 21 site-specific cancers, among predominantly low-income participants who experienced a disproportionately high risk of both T2D and cancer.</p><p><strong>Methods: </strong>The study included 76,121 participants (mean age: 52.0 years; 67.2% Black) from the Southern Community Cohort Study (SCCS). T2D was ascertained at the baseline survey. Incident cancer was ascertained via linkage to state cancer registries. Cox proportional hazard models were used to estimate the associations between T2D and cancer after adjusting for confounders.</p><p><strong>Results: </strong>Among participants, 21.2% (N=16,137) had baseline T2D, and 9.7% (N=7,376) were diagnosed with incident cancer. Compared to individuals without T2D, individuals with T2D had a significantly elevated risk of all cancer combined (HR: 1.07; 95% CI: 1.01-1.13) and several site-specific cancers, including cancers of the stomach, colorectum, pancreas, liver/intrahepatic bile duct, kidney, and renal pelvis as well as leukemia. The significant association for most cancers was largely observed within 15 years after T2D diagnosis, except for cancer of the pancreas and liver/intrahepatic bile duct, for which elevated risks remain statistically significant 15 to 30 years after T2D diagnosis Conclusion: T2D was associated with the risk of overall and certain site-specific cancers in this predominant low-income population.</p><p><strong>Impact: </strong>Preventive measures to reduce the burden from T2D could help reduce the risk of overall cancer and several site-specific cancers.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12284803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144500251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SECONDARY LUNG CANCER AMONG SURVIVORS OF ADOLESCENT AND YOUNG ADULT CANCER: A POPULATION-BASED STUDY.","authors":"Amy M Berkman, Michelle Tran, Laura K Thompson, Caryn Lerman, Jorge Nieva, Yueh-Yun Chi, Michael E Roth, Myles Cockburn, David R Freyer","doi":"10.1158/1055-9965.EPI-25-0360","DOIUrl":"10.1158/1055-9965.EPI-25-0360","url":null,"abstract":"<p><strong>Background: </strong>Survivors of adolescent and young adult cancer (AYA, age 15 to 39 years at diagnosis) are at increased risk for second malignant neoplasms (SMNs) of which lung cancer is the most lethal. Factors contributing to lung SMN development and outcomes are not well-characterized.</p><p><strong>Methods: </strong>Survivors of AYA cancer diagnosed between 1998 and 2020 were identified in the California Cancer Registry (n=251,632). Pearson's chi-square and Fisher's exact tests were used to determine associations between sociodemographic and cancer characteristics with SMN status. Multivariable Cox proportional hazard regression, adjusting for age, time from primary diagnosis, race/ethnicity, insurance, primary cancer site, stage, and treatment, evaluated associations between these characteristics and lung SMN incidence and mortality.</p><p><strong>Results: </strong>A total of 675 (0.7%) survivors were diagnosed with lung SMN, of whom 487 (72.1%) died. Median time from primary diagnosis to lung SMN was 13.0 years (IQR 4.0-20.0 years). Nearly half (46.5%) of survivors with lung SMN had metastatic disease. Non-Hispanic Black survivors were more likely than non-Hispanic White survivors to develop lung SMN (adjusted hazard ratio [aHR] 1.47, 95% confidence interval [95%CI] 1.13-1.91) but not more likely to die from lung SMN (aHR 0.84, 95%CI 0.56, 1.27). Primary cancer treatment with both chemotherapy and radiation was associated with greater likelihood of lung SMN (aHR 1.41, 95%CI 1.11-1.80) compared to receiving neither.</p><p><strong>Conclusions: </strong>Lung SMN has a long latency and high mortality among survivors of AYA cancer.</p><p><strong>Impact: </strong>More research is needed regarding lung cancer prevention, education, and early detection, particularly among survivors at higher risk.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12286616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144478531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of circulating proteins and their role in mediating adiposity's effect on endometrial cancer risk: Mendelian randomisation and colocalization analyses.","authors":"Sabrina E Wang, Vanessa Y Tan, James Yarmolinsky, Yadi Zheng, Tracy A O'Mara, Nicholas J Timpson, Marc J Gunter, Laure Dossus, Matthew A Lee","doi":"10.1158/1055-9965.EPI-25-0165","DOIUrl":"10.1158/1055-9965.EPI-25-0165","url":null,"abstract":"<p><strong>Background: </strong>Proteomics could enhance our understanding of endometrial carcinogenesis. However, addressing confounding in traditional observational studies remains challenging, especially given the strong impact of adiposity on the plasma proteome and endometrial cancer risk.</p><p><strong>Methods: </strong>Using Mendelian randomization (MR) and colocalization analyses, we examined the causal association between 2,751 unique proteins from the UK Biobank (N proteins=2,031; N=52,363) and deCODE (N proteins=1,667; N=35,559) with endometrial cancer risk [overall (N cases=12,270; N controls=46,126), endometrioid (N cases=8,758), and non-endometrioid (N cases=1,230)]. We performed enrichment analyses to explore pathways overrepresented among plasma proteins in endometrioid and non-endometrioid cancer subtypes. We assessed whether circulating proteins mediated the effect of body mass index (BMI) on endometrial cancer risk using univariable and multivariable MR.</p><p><strong>Results: </strong>20 proteins were associated with endometrial cancer risk in MR and colocalization analyses. GSTO1-1 and SKAP1 were positively and MMP10 was negatively associated with overall and endometrioid endometrial cancer; DTYMK and ABO were positively and TSSC4 was negatively associated with overall endometrial cancer; IGF2R was positively associated with endometrioid cancer; MAPK9 was positively and DNAJB14, IFI16, LCN2, and SCT were negatively associated with non-endometrioid endometrial cancer. Distinct pathways were overrepresented in endometrioid (e.g., PDGF signalling and PTEN gene regulation) and non-endometrioid (e.g., non-canonical NF-kB signalling) cancer subtypes. There was weak evidence of associated proteins mediating the relationship between BMI and endometrial cancer risk.</p><p><strong>Conclusions: </strong>We identified distinct plasma proteins and pathways associated with endometrioid and non-endometrioid endometrial cancer risk.</p><p><strong>Impact: </strong>Prioritised proteins may support non-invasive methods to differentiate endometrial cancer subtypes.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144478532","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}

{"title":"Pubertal timing and incident ovarian cancer in the Sister Study cohort.","authors":"Sydney A Lash, Katie M O'Brien, Dale P Sandler, Mandy Goldberg","doi":"10.1158/1055-9965.EPI-25-0541","DOIUrl":"10.1158/1055-9965.EPI-25-0541","url":null,"abstract":"<p><strong>Background: </strong>Pubertal milestones such as menarche (first period) and thelarche (onset of breast development) are markers of hormonal changes that may be relevant to the hormonal etiology of ovarian cancer. Prior studies of the association of age at menarche with ovarian cancer risk have been inconsistent, while age at thelarche has not been examined in relation to ovarian cancer incidence.</p><p><strong>Methods: </strong>With data from 40,809 women in the Sister Study, we used multivariable-adjusted Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations of self-reported ages at thelarche and menarche with incident ovarian cancer, both overall and by histotype.</p><p><strong>Results: </strong>During a median follow-up of 13.3 years, 291 women reported a diagnosis of ovarian cancer. Ages at thelarche (HR 0.94, 95% CI 0.87-1.02 per one-year older) and menarche (HR 0.99, 95% CI 0.91-1.07 per one-year older) were not associated with ovarian cancer overall. Although imprecise, HRs suggested a possible inverse association of ages at thelarche (HR 0.71, 95% CI 0.48-1.04) and menarche (HR 0.79, 95% CI 0.59-1.04) with incidence of clear cell tumors.</p><p><strong>Conclusions: </strong>Ages at thelarche and menarche were not associated with ovarian cancer incidence overall.</p><p><strong>Impact: </strong>Though our results do not provide clear evidence of associations of pubertal timing with ovarian cancer incidence, possible associations of earlier thelarche and menarche with increased incidence of ovarian clear cell carcinoma may warrant further investigation, especially considering secular trends towards earlier thelarche.</p>","PeriodicalId":520580,"journal":{"name":"Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144478530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}