BACKGROUNDAccurate information on childhood cancer survival is essential for improving health systems. Survival is believed to be low in low-resource countries, but population-based survival estimates are scant. We aim to provide reliable and comparable survival estimates in these settings.METHODSWe included 16 821 patients from 47 population-based cancer registries in 23 countries in Africa, Latin America and the Caribbean, and Asia. We used the Cancer Survival in Countries in Transition project data (children aged younger than 15 years, diagnosed 2008-2012, followed until 2014) and data from Rwanda (2013-2017, followed until 2022). We estimated 1-year, 3-year, and 5-year observed survival using the Kaplan-Meier method, by diagnostic group, country, region, Human Development Index, income, and sex.RESULTSSurvival was higher in registries included from the Caribbean (namely, Puerto Rico [United States], Martinique [France]) and Central America (Costa Rica), Asia, and the Middle East and North Africa compared with those included from South America and sub-Saharan Africa. Survival correlated with the Human Development Index. For leukemia, 3-year survival varied from 30.4% (95% confidence interval [CI] = 12.4% to 50.6%) in Kenya to 89.5% (95% CI = 83.8% to 93.2%) in Puerto Rico; for central nervous system tumors from 32.0% (95% CI = 13.9% to 51.8%) in Algeria to 79.3% (95% CI = 69.1% to 86.5%) in Puerto Rico. The findings should be interpreted with care, as registry coverage varies and may not reflect national and regional survival.CONCLUSIONThe variability of the population-based survival estimates across predominantly low- and middle-income countries highlights gaps in cancer registration, access to care, and quality of care. This study provides benchmark data for the World Health Organization Global Initiative for Childhood Cancer generated by population-based cancer registries, which should be supported in all countries.
关于儿童癌症生存的准确信息对于改善卫生系统至关重要。据信，在资源匮乏的国家，存活率很低，但基于人口的存活率估计不足。我们的目标是在这些情况下提供可靠和可比的生存估计。方法：我们纳入了来自非洲、拉丁美洲和加勒比地区以及亚洲23个国家的47个基于人群的癌症登记处的16821名患者。我们使用了转型国家癌症生存项目的数据（15岁以下儿童，2008-2012年确诊，随访至2014年）和卢旺达的数据（2013-2017年随访至2022年）。我们根据诊断组、国家、地区、人类发展指数、收入和性别，使用Kaplan-Meier法估计1年、3年和5年观察生存率。结果加勒比地区（即波多黎各[美国]、马提尼克岛[法国]）、中美洲（哥斯达黎加）、亚洲、中东和北非的生存率高于南美洲和撒哈拉以南非洲的生存率。生存与人类发展指数相关。白血病的3年生存率从肯尼亚的30.4%（95%可信区间[CI] = 12.4%至50.6%）到波多黎各的89.5% （95% CI = 83.8%至93.2%）不等；从阿尔及利亚的32.0% （95% CI = 13.9%至51.8%）到波多黎各的79.3% （95% CI = 69.1%至86.5%）。研究结果应谨慎解释，因为登记范围各不相同，可能不能反映国家和地区的生存情况。结论：主要在低收入和中等收入国家中，基于人群的生存估计的可变性突出了癌症登记、获得护理和护理质量方面的差距。这项研究为世界卫生组织儿童癌症全球倡议提供了基准数据，该倡议由基于人群的癌症登记处产生，应在所有国家得到支持。
{"title":"Childhood cancer survival in Africa, Asia, Latin America and the Caribbean, during 2008-2017 (SURVCAN-3): a population-based benchmarking study of 16 821 children.","authors":"Dagrun Slettebø Daltveit,Eileen Morgan,Aude Bardot,Eva Steliarova-Foucher,Amanuel Damie,Marc Hagenimana,Nisrine Khoubila,Florencia Moreno,Isabelle Soerjomataram","doi":"10.1093/jnci/djaf321","DOIUrl":"https://doi.org/10.1093/jnci/djaf321","url":null,"abstract":"BACKGROUNDAccurate information on childhood cancer survival is essential for improving health systems. Survival is believed to be low in low-resource countries, but population-based survival estimates are scant. We aim to provide reliable and comparable survival estimates in these settings.METHODSWe included 16 821 patients from 47 population-based cancer registries in 23 countries in Africa, Latin America and the Caribbean, and Asia. We used the Cancer Survival in Countries in Transition project data (children aged younger than 15 years, diagnosed 2008-2012, followed until 2014) and data from Rwanda (2013-2017, followed until 2022). We estimated 1-year, 3-year, and 5-year observed survival using the Kaplan-Meier method, by diagnostic group, country, region, Human Development Index, income, and sex.RESULTSSurvival was higher in registries included from the Caribbean (namely, Puerto Rico [United States], Martinique [France]) and Central America (Costa Rica), Asia, and the Middle East and North Africa compared with those included from South America and sub-Saharan Africa. Survival correlated with the Human Development Index. For leukemia, 3-year survival varied from 30.4% (95% confidence interval [CI] = 12.4% to 50.6%) in Kenya to 89.5% (95% CI = 83.8% to 93.2%) in Puerto Rico; for central nervous system tumors from 32.0% (95% CI = 13.9% to 51.8%) in Algeria to 79.3% (95% CI = 69.1% to 86.5%) in Puerto Rico. The findings should be interpreted with care, as registry coverage varies and may not reflect national and regional survival.CONCLUSIONThe variability of the population-based survival estimates across predominantly low- and middle-income countries highlights gaps in cancer registration, access to care, and quality of care. This study provides benchmark data for the World Health Organization Global Initiative for Childhood Cancer generated by population-based cancer registries, which should be supported in all countries.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145752528","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}
Lindsey J Mattick,Chin-Shang Li,Po-Ju Lin,Luke J Peppone,Allison Magnuson,Marianne Melnik,Howard Gross,Adedayo A Onitilo,Amber S Kleckner,Karen M Mustian,Michelle C Janelsins
BACKGROUNDCancer-related fatigue (CRF) is a debilitating side effect among patients with cancer. While exercise is recommended to manage CRF, clinical guidelines lack specificity on modality, intensity, and duration. This study aimed to determine the optimal doses of walking to mitigate CRF.METHODSIn a nationwide, prospective cohort study of patients with stage I-IIIC breast cancer, we assessed walking volume (MET-hours/week) via Aerobics Center Longitudinal Study Physical Activity measure and CRF via Multidimensional Fatigue Symptom Inventory (MFSI) at pre-chemotherapy (T1), one month post-chemotherapy (T2), and six months post-chemotherapy (T3). A receiver operating characteristic curve analysis identified a cut-point for walking volume needed for a clinically meaningful CRF reduction from T1 to T2 (-4.5 points MFSI score). Linear mixed models controlling for age, BMI, and other modes of moderate-vigorous intensity exercise characterized CRF at each time point.RESULTSAmong 577 participants (mean age 53.4 years; 76% stage I/II) higher walking volume was associated with lower general, emotional, physical, overall CRF and higher vigor post-chemotherapy (T2; all p < .05). Those who walked ≥4.3 MET-hours/week, equivalent to walking 88-172 minutes at a low-intensity pace (<2.5 mph) or 43-83 minutes at a moderate-intensity pace (2.6-4.5 mph) at pre-, during, and post-chemotherapy demonstrated significantly lower CRF at post-chemotherapy (T2) compared to those who walked <4.3 MET-hours/week (p < .05).CONCLUSIONSOur data indicate that higher walking volume was associated with lower CRF and a minimum walking volume of 88-172 minutes at a low-intensity pace or 43-83 minutes of moderate-intensity pace, may attenuate CRF following chemotherapy.
癌症相关疲劳（CRF）是癌症患者中一种使人衰弱的副作用。虽然运动被推荐用于治疗慢性肾功能衰竭，但临床指南在运动方式、强度和持续时间方面缺乏特异性。本研究旨在确定步行减轻CRF的最佳剂量。方法在一项全国范围的I-IIIC期乳腺癌患者的前瞻性队列研究中，我们通过有氧运动中心纵向研究身体活动测量评估了化疗前（T1）、化疗后1个月（T2）和化疗后6个月（T3）的步行量（MET-hours/week）和多维疲劳症状量表（MFSI）评估了CRF。接受者工作特征曲线分析确定了从T1到T2有临床意义的CRF降低所需的步行量的切割点（-4.5分MFSI评分）。控制年龄、BMI和其他中等强度运动模式的线性混合模型表征了每个时间点的CRF。结果在577名参与者中（平均年龄53.4岁，76%为I/II期），较高的步行量与化疗后较低的总体、情绪、身体、总体CRF和较高的活力相关（T2；均p < 0.05）。那些在化疗前、化疗期间和化疗后步行≥4.3 met -小时/周的患者，相当于以低强度速度（<2.5英里/小时）步行88-172分钟或以中等强度速度（2.6-4.5英里/小时）步行43-83分钟，与步行<4.3 met -小时/周的患者相比，化疗后（T2）的CRF显着降低（p < 0.05）。结论较高的步行量与较低的CRF相关，最低步行量88 ~ 172分钟的低强度配速或43 ~ 83分钟的中强度配速可减轻化疗后的CRF。
{"title":"Walking dose associated with lower cancer-related fatigue among patients with breast cancer.","authors":"Lindsey J Mattick,Chin-Shang Li,Po-Ju Lin,Luke J Peppone,Allison Magnuson,Marianne Melnik,Howard Gross,Adedayo A Onitilo,Amber S Kleckner,Karen M Mustian,Michelle C Janelsins","doi":"10.1093/jnci/djaf360","DOIUrl":"https://doi.org/10.1093/jnci/djaf360","url":null,"abstract":"BACKGROUNDCancer-related fatigue (CRF) is a debilitating side effect among patients with cancer. While exercise is recommended to manage CRF, clinical guidelines lack specificity on modality, intensity, and duration. This study aimed to determine the optimal doses of walking to mitigate CRF.METHODSIn a nationwide, prospective cohort study of patients with stage I-IIIC breast cancer, we assessed walking volume (MET-hours/week) via Aerobics Center Longitudinal Study Physical Activity measure and CRF via Multidimensional Fatigue Symptom Inventory (MFSI) at pre-chemotherapy (T1), one month post-chemotherapy (T2), and six months post-chemotherapy (T3). A receiver operating characteristic curve analysis identified a cut-point for walking volume needed for a clinically meaningful CRF reduction from T1 to T2 (-4.5 points MFSI score). Linear mixed models controlling for age, BMI, and other modes of moderate-vigorous intensity exercise characterized CRF at each time point.RESULTSAmong 577 participants (mean age 53.4 years; 76% stage I/II) higher walking volume was associated with lower general, emotional, physical, overall CRF and higher vigor post-chemotherapy (T2; all p < .05). Those who walked ≥4.3 MET-hours/week, equivalent to walking 88-172 minutes at a low-intensity pace (<2.5 mph) or 43-83 minutes at a moderate-intensity pace (2.6-4.5 mph) at pre-, during, and post-chemotherapy demonstrated significantly lower CRF at post-chemotherapy (T2) compared to those who walked <4.3 MET-hours/week (p < .05).CONCLUSIONSOur data indicate that higher walking volume was associated with lower CRF and a minimum walking volume of 88-172 minutes at a low-intensity pace or 43-83 minutes of moderate-intensity pace, may attenuate CRF following chemotherapy.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"44 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145777327","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}
Jerome Jourquin,James C Dickerson,Emily G Marks,Jessica Epps,Kimberly Sabelko,Allison W Kurian,Melissa L Bondy
ShareForCures® is a newly launched and growing dataset, crowd-sourced from participants, that comprises self-reported, clinical, and genomics data. ShareForCures seeks to advance breast cancer research by expanding patient participation in research therefore accelerating discoveries. It is designed to 1) provide opportunities for individuals who have or had breast cancer to participate in research; 2) create a longitudinal cohort that represents the diversity of individuals diagnosed with breast cancer; and 3) facilitate collaboration among researchers from various backgrounds and institutions to improve breast cancer care and outcomes for all. ShareForCures is a user-friendly, direct-to-consumer, online platform that collects demographic, genetic, and clinical information from or on behalf of breast cancer research participants. All adults in the United States diagnosed with breast cancer are eligible. As of September 30, 2025, 1,327 participants have enrolled. The platform aims to enroll 2,500 diverse participants by 2027, with a long-term goal of reaching 10,000 participants in the next decade. With ShareForCures, Komen is engaging a diverse population of individuals with breast cancer, including those from groups typically underrepresented in research, to drive discoveries that benefit everyone. With the first research projects already leveraging the dataset, ShareForCures has the potential to become a unique national platform for generating insights and real-world data that will drive patient-centered research.
{"title":"Susan G. Komen's ShareForCures®: a patient-engaged, nationwide breast cancer research registry.","authors":"Jerome Jourquin,James C Dickerson,Emily G Marks,Jessica Epps,Kimberly Sabelko,Allison W Kurian,Melissa L Bondy","doi":"10.1093/jnci/djaf353","DOIUrl":"https://doi.org/10.1093/jnci/djaf353","url":null,"abstract":"ShareForCures® is a newly launched and growing dataset, crowd-sourced from participants, that comprises self-reported, clinical, and genomics data. ShareForCures seeks to advance breast cancer research by expanding patient participation in research therefore accelerating discoveries. It is designed to 1) provide opportunities for individuals who have or had breast cancer to participate in research; 2) create a longitudinal cohort that represents the diversity of individuals diagnosed with breast cancer; and 3) facilitate collaboration among researchers from various backgrounds and institutions to improve breast cancer care and outcomes for all. ShareForCures is a user-friendly, direct-to-consumer, online platform that collects demographic, genetic, and clinical information from or on behalf of breast cancer research participants. All adults in the United States diagnosed with breast cancer are eligible. As of September 30, 2025, 1,327 participants have enrolled. The platform aims to enroll 2,500 diverse participants by 2027, with a long-term goal of reaching 10,000 participants in the next decade. With ShareForCures, Komen is engaging a diverse population of individuals with breast cancer, including those from groups typically underrepresented in research, to drive discoveries that benefit everyone. With the first research projects already leveraging the dataset, ShareForCures has the potential to become a unique national platform for generating insights and real-world data that will drive patient-centered research.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"231 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746690","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}
Carmen L Wilson, Rikeenkumar Dhaduk, Xin Zhou, Gavriel Matt, Yutaka Yasui, Cindy Im, Gregory T Armstrong, Stephanie B Dixon, Yadav Sapkota, Zhaoming Wang, Melissa M Hudson, Kirsten K Ness
BACKGROUND As traditional cardiovascular risk factors (CVRFs) increase cardiovascular risk with a near-multiplicative effect among childhood cancer survivors (CCS), our purpose was to evaluate the combined contributions of population-based polygenic risk scores (PRSs) and lifestyle behaviors to CVRF risk to identify targets for surveillance and risk prevention. METHODS Participants included 2,610 European ancestry CCS, (mean age = 34.6-years [±9.5]). Using phenotype-specific, population-based PRSs for LDL- and HDL-cholesterol, triglycerides, fasting glucose (FG), hemoglobin A1c, systolic (SBP), and diastolic blood pressure (DBP), CCS were classified with low- (lowest quintile), intermediate- (middle three quintiles), or high genetic-risk (highest quintile). Lifestyle (good, intermediate, poor) was based on four factors (smoking, physical activity, diet quality, obesity). Multiple linear regression was used to assess associations between lifestyle and genetic risk with each CVRFs, adjusting for cancer therapies and medications. RESULTS Worsening CVRF profiles were associated with poorer lifestyle (ie, decreasing number of positive health habits) and increasing genetic-risk. For example, poor lifestyle and high genetic-risk were associated with 5.4 (±1.0) and 5.0 (±1.1) mmHg increase in SBP compared to good lifestyle and low genetic-risk, respectively, and 3.4 (±0.7) and 4.4 (±0.7) mmHg increase in DBP. Among CCS with high genetic-risk and poor lifestyle, mean DBP (-4.6 [±2.2] mmHg, p = .034) and FG (-5.0 [±2.1] mg/dL, p < .001) were lower among CCS with good versus poor lifestyle, while mean HDL was higher (12.9 [±1.9] mg/dL, p < .001). CONCLUSION Among CCS, lifestyle is associated with increased risk of CVRFs independent of genetic-risk and treatment, highlighting the importance of developing interventions targeting lifestyle in this population.
背景：由于传统心血管危险因素（CVRF）在儿童癌症幸存者（CCS）中以近乎倍增的效应增加心血管风险，我们的目的是评估基于人群的多基因风险评分（prs）和生活方式行为对CVRF风险的综合贡献，以确定监测和风险预防的目标。方法纳入2610例欧洲血统CCS患者（平均年龄34.6岁[±9.5]）。使用表型特异性、基于人群的LDL-胆固醇和hdl -胆固醇、甘油三酯、空腹血糖（FG）、血红蛋白A1c、收缩压（SBP）和舒张压（DBP）的prs，将CCS分为低（最低五分位数）、中（中间三个五分位数）或高遗传风险（最高五分位数）。生活方式（良好，中等，差）基于四个因素（吸烟，体育活动，饮食质量，肥胖）。多元线性回归用于评估生活方式和遗传风险与每个cvrf之间的关联，并根据癌症治疗和药物进行调整。结果CVRF谱恶化与生活方式不良（即积极健康习惯数量减少）和遗传风险增加有关。例如，与良好生活方式和低遗传风险相比，不良生活方式和高遗传风险分别与收缩压升高5.4（±1.0）和5.0（±1.1）mmHg相关，与舒张压升高3.4（±0.7）和4.4（±0.7）mmHg相关。在高遗传风险和不良生活方式的CCS患者中，平均DBP（-4.6[±2.2]mmHg, p = 0.034）和FG(-5.0[±2.1]mg/dL, p <；生活方式良好与生活方式不良的CCS患者的HDL较低，而平均HDL较高（12.9[±1.9]mg/dL, p < .001）。结论：在CCS人群中，生活方式与cvrf风险增加相关，独立于遗传风险和治疗，强调了针对这一人群制定针对生活方式的干预措施的重要性。
{"title":"Influence of treatment, genetic predisposition, and lifestyle on cardiovascular risk factors among cancer survivors","authors":"Carmen L Wilson, Rikeenkumar Dhaduk, Xin Zhou, Gavriel Matt, Yutaka Yasui, Cindy Im, Gregory T Armstrong, Stephanie B Dixon, Yadav Sapkota, Zhaoming Wang, Melissa M Hudson, Kirsten K Ness","doi":"10.1093/jnci/djaf356","DOIUrl":"https://doi.org/10.1093/jnci/djaf356","url":null,"abstract":"BACKGROUND As traditional cardiovascular risk factors (CVRFs) increase cardiovascular risk with a near-multiplicative effect among childhood cancer survivors (CCS), our purpose was to evaluate the combined contributions of population-based polygenic risk scores (PRSs) and lifestyle behaviors to CVRF risk to identify targets for surveillance and risk prevention. METHODS Participants included 2,610 European ancestry CCS, (mean age = 34.6-years [±9.5]). Using phenotype-specific, population-based PRSs for LDL- and HDL-cholesterol, triglycerides, fasting glucose (FG), hemoglobin A1c, systolic (SBP), and diastolic blood pressure (DBP), CCS were classified with low- (lowest quintile), intermediate- (middle three quintiles), or high genetic-risk (highest quintile). Lifestyle (good, intermediate, poor) was based on four factors (smoking, physical activity, diet quality, obesity). Multiple linear regression was used to assess associations between lifestyle and genetic risk with each CVRFs, adjusting for cancer therapies and medications. RESULTS Worsening CVRF profiles were associated with poorer lifestyle (ie, decreasing number of positive health habits) and increasing genetic-risk. For example, poor lifestyle and high genetic-risk were associated with 5.4 (±1.0) and 5.0 (±1.1) mmHg increase in SBP compared to good lifestyle and low genetic-risk, respectively, and 3.4 (±0.7) and 4.4 (±0.7) mmHg increase in DBP. Among CCS with high genetic-risk and poor lifestyle, mean DBP (-4.6 [±2.2] mmHg, p = .034) and FG (-5.0 [±2.1] mg/dL, p &lt; .001) were lower among CCS with good versus poor lifestyle, while mean HDL was higher (12.9 [±1.9] mg/dL, p &lt; .001). CONCLUSION Among CCS, lifestyle is associated with increased risk of CVRFs independent of genetic-risk and treatment, highlighting the importance of developing interventions targeting lifestyle in this population.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145759711","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}
Pathology and oncology education are at an inflection point. Beyond abbreviated preclinical blocks, the central problem is pedagogical misalignment with learners who expect relevance, interactivity, and clinical application. We advocate a shift from content delivery to concept integration anchored in clinical reasoning and data literacy. In oncology, trainees must learn to interpret next‑generation sequencing and biomarker profiles, participate in molecular tumor boards, sequence precision therapies, manage toxicities, and incorporate patient‑reported outcomes-competencies rarely taught in a structured way. The digitization of histopathology and the integration of artificial intelligence demand exposure to digital pathology and critical appraisal of algorithmic outputs, including AI‑supported IHC quantification, variant classification, and methylation‑based classifiers. Large language models may enhance self‑directed learning but require faculty oversight, instruction in appraisal and ethics, and safeguards against inaccuracy and overconfidence. Operationalizing these reforms requires institutional commitment, curriculum redesign that integrates pathology, oncology, genomics, and decision‑making, and expanded residency time to acquire competencies in informatics and AI (machine learning, deep learning, supervised and unsupervised methods, and validation). Faculty development, adoption of digital platforms and virtual microscopy, competency‑based assessment, and collaboration with computer scientists, bioinformaticians, and ethicists are essential. Implementation barriers-including limited faculty time, resource constraints, and accreditation requirements-can be mitigated by pilot programs, strategic partnerships, phased integration, and attention to transparency, equity, and accountability. Absent deliberate reform within LCME and ACGME frameworks that currently do not mandate genomics or AI literacy, future physicians will enter practice unprepared for precision medicine. Modernizing curricula to meet the genomics and AI era is therefore urgent.
{"title":"Modernizing pathology and oncology education: integrating genomics, artificial intelligence, and clinical relevance into medical training.","authors":"Ana Carolina de Jesus Paniza,Fabio Ynoe Moraes","doi":"10.1093/jnci/djaf358","DOIUrl":"https://doi.org/10.1093/jnci/djaf358","url":null,"abstract":"Pathology and oncology education are at an inflection point. Beyond abbreviated preclinical blocks, the central problem is pedagogical misalignment with learners who expect relevance, interactivity, and clinical application. We advocate a shift from content delivery to concept integration anchored in clinical reasoning and data literacy. In oncology, trainees must learn to interpret next‑generation sequencing and biomarker profiles, participate in molecular tumor boards, sequence precision therapies, manage toxicities, and incorporate patient‑reported outcomes-competencies rarely taught in a structured way. The digitization of histopathology and the integration of artificial intelligence demand exposure to digital pathology and critical appraisal of algorithmic outputs, including AI‑supported IHC quantification, variant classification, and methylation‑based classifiers. Large language models may enhance self‑directed learning but require faculty oversight, instruction in appraisal and ethics, and safeguards against inaccuracy and overconfidence. Operationalizing these reforms requires institutional commitment, curriculum redesign that integrates pathology, oncology, genomics, and decision‑making, and expanded residency time to acquire competencies in informatics and AI (machine learning, deep learning, supervised and unsupervised methods, and validation). Faculty development, adoption of digital platforms and virtual microscopy, competency‑based assessment, and collaboration with computer scientists, bioinformaticians, and ethicists are essential. Implementation barriers-including limited faculty time, resource constraints, and accreditation requirements-can be mitigated by pilot programs, strategic partnerships, phased integration, and attention to transparency, equity, and accountability. Absent deliberate reform within LCME and ACGME frameworks that currently do not mandate genomics or AI literacy, future physicians will enter practice unprepared for precision medicine. Modernizing curricula to meet the genomics and AI era is therefore urgent.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746715","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}
Joanne Kotsopoulos, Marta Seca, Jacek Gronwald, Tomasz Huzarski, Pål Møller, Raymond H Kim, Christian F Singer, Beth Karlan, Amber Aeilts, Teresa Ramón y Cajal, Tuya Pal, Andrea Eisen, Louise Bordeleau, William D Foulkes, Nadine Tung, Fergus Couch, Susan L Neuhausen, Dana Zakalik, Cezary Cybulski, Olufunmilayo Olopade, Kelly Metcalfe, Robert Fruscio, Ping Sun, Jan Lubinski, Steven A Narod
Background Women with a pathogenic variant in BRCA1 or BRCA2 are at high risk of developing ovarian cancer and often recommended to undergo bilateral salpingo-oophorectomy at an early age resulting in surgical menopause. Menopausal hormone therapy (MHT) is an effective way to mitigate the adverse outcomes of early menopause; however, the safety of MHT on breast cancer risk in this population has not been established. Methods We conducted a prospective matched analysis of MHT use following menopause and breast cancer risk in BRCA carriers. Women who initiated MHT were matched one-to-one with women who had not initiated MHT by gene, year of birth, and age at menopause, resulting in 676 matched pairs. MHT use collected by questionnaire included formulation and mode of administration. Results After a mean of 5.6 years there were 87 incident breast cancer cases in the 676 exposed women (12·9%) and 128 cases in the 676 unexposed women (18·9%) (P = 0·002). Compared to their unexposed matched controls, women who used estrogen alone (E) experienced a significantly decreased risk of breast cancer (HR = 0·37; 95%: CI 0·24-0·57). There was no protective or adverse effect associated with the use of E plus progestogen (E + P) (HR = 0·94; 95%CI 0·54-1·63). Conclusions Our findings suggest there is no significant increase in the risk of breast cancer in BRCA carriers with the use of MHT and that E alone might be protective.
{"title":"Menopausal hormone therapy and the risk of breast cancer in women with a pathogenic variant in BRCA1 or BRCA2","authors":"Joanne Kotsopoulos, Marta Seca, Jacek Gronwald, Tomasz Huzarski, Pål Møller, Raymond H Kim, Christian F Singer, Beth Karlan, Amber Aeilts, Teresa Ramón y Cajal, Tuya Pal, Andrea Eisen, Louise Bordeleau, William D Foulkes, Nadine Tung, Fergus Couch, Susan L Neuhausen, Dana Zakalik, Cezary Cybulski, Olufunmilayo Olopade, Kelly Metcalfe, Robert Fruscio, Ping Sun, Jan Lubinski, Steven A Narod","doi":"10.1093/jnci/djaf363","DOIUrl":"https://doi.org/10.1093/jnci/djaf363","url":null,"abstract":"Background Women with a pathogenic variant in BRCA1 or BRCA2 are at high risk of developing ovarian cancer and often recommended to undergo bilateral salpingo-oophorectomy at an early age resulting in surgical menopause. Menopausal hormone therapy (MHT) is an effective way to mitigate the adverse outcomes of early menopause; however, the safety of MHT on breast cancer risk in this population has not been established. Methods We conducted a prospective matched analysis of MHT use following menopause and breast cancer risk in BRCA carriers. Women who initiated MHT were matched one-to-one with women who had not initiated MHT by gene, year of birth, and age at menopause, resulting in 676 matched pairs. MHT use collected by questionnaire included formulation and mode of administration. Results After a mean of 5.6 years there were 87 incident breast cancer cases in the 676 exposed women (12·9%) and 128 cases in the 676 unexposed women (18·9%) (P = 0·002). Compared to their unexposed matched controls, women who used estrogen alone (E) experienced a significantly decreased risk of breast cancer (HR = 0·37; 95%: CI 0·24-0·57). There was no protective or adverse effect associated with the use of E plus progestogen (E + P) (HR = 0·94; 95%CI 0·54-1·63). Conclusions Our findings suggest there is no significant increase in the risk of breast cancer in BRCA carriers with the use of MHT and that E alone might be protective.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765248","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}
BACKGROUNDLynch Syndrome (LS), caused by pathogenic variants (PVs) in mismatch repair (MMR) genes, increases the risk of several cancers. Surveillance guidelines vary internationally due to inconsistent risk estimates. This study refines cancer risk estimates by gene, sex, and age to support personalized recommendations.METHODSThis meta-analysis included studies reporting cumulative cancer risks in genetically confirmed LS PV carriers. PubMed was searched until December 31, 2024. Following the MOOSE guideline, data were extracted independently by two reviewers and analyzed using fixed (n = 2 estimates) or random-effects models (n > 2 estimates), stratified by gene, sex, cancer site, and study design LS retrospective family studies (LSRF), LS prospective cohort (LSPC), and population-based case-control (PBCC).RESULTSThirty-three studies were included, mostly LSRF. Meta-analysis of LSRF showed that colorectal cancer risk by age 40 was markedly lower in MSH6 and PMS2 carriers (<2%) than in MLH1 and MSH2 (>4%). For endometrial cancer, risks at 50 y were 8.3%[5.1-13.4], 8.7%[3.8-18.7], 5.2%[2.3-11.2] and 3.0%[1.0-8.0] for MLH1, MSH2, MSH6 and PMS2 respectively. For ovarian cancer, risks at 40 y were 1.2%[0.6-2.7] and 0.9%[0.5-1.8] for MLH1 and MSH2, respectively. Few studies addressed other cancer types, highlighting the need for additional data.CONCLUSIONSThis is the first meta-analysis providing stratified cancer risk estimates by cancer site, gene, and study design. These findings support gene-specific surveillance strategies, such as initiating colonoscopy at age 30-35 for MSH6 and PMS2 carriers, postponing hysterectomy after 50 y for PMS2 carriers, and delaying oophorectomy after 45 y for MLH1 and MSH2 PV carriers.
{"title":"Cancer risks in lynch syndrome carriers: a systematic review and meta-analysis.","authors":"Séphora Campoy,Youenn Drouet,Pauline Rochefort,Valérie Bonadona,Christine Lasset","doi":"10.1093/jnci/djaf349","DOIUrl":"https://doi.org/10.1093/jnci/djaf349","url":null,"abstract":"BACKGROUNDLynch Syndrome (LS), caused by pathogenic variants (PVs) in mismatch repair (MMR) genes, increases the risk of several cancers. Surveillance guidelines vary internationally due to inconsistent risk estimates. This study refines cancer risk estimates by gene, sex, and age to support personalized recommendations.METHODSThis meta-analysis included studies reporting cumulative cancer risks in genetically confirmed LS PV carriers. PubMed was searched until December 31, 2024. Following the MOOSE guideline, data were extracted independently by two reviewers and analyzed using fixed (n = 2 estimates) or random-effects models (n > 2 estimates), stratified by gene, sex, cancer site, and study design LS retrospective family studies (LSRF), LS prospective cohort (LSPC), and population-based case-control (PBCC).RESULTSThirty-three studies were included, mostly LSRF. Meta-analysis of LSRF showed that colorectal cancer risk by age 40 was markedly lower in MSH6 and PMS2 carriers (<2%) than in MLH1 and MSH2 (>4%). For endometrial cancer, risks at 50 y were 8.3%[5.1-13.4], 8.7%[3.8-18.7], 5.2%[2.3-11.2] and 3.0%[1.0-8.0] for MLH1, MSH2, MSH6 and PMS2 respectively. For ovarian cancer, risks at 40 y were 1.2%[0.6-2.7] and 0.9%[0.5-1.8] for MLH1 and MSH2, respectively. Few studies addressed other cancer types, highlighting the need for additional data.CONCLUSIONSThis is the first meta-analysis providing stratified cancer risk estimates by cancer site, gene, and study design. These findings support gene-specific surveillance strategies, such as initiating colonoscopy at age 30-35 for MSH6 and PMS2 carriers, postponing hysterectomy after 50 y for PMS2 carriers, and delaying oophorectomy after 45 y for MLH1 and MSH2 PV carriers.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746689","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}
Alison M Schram,Soo-Ryum Yang,Genessa Kahn,Rogelio Velasco,Matteo Repetto,Richard Kinh Gian Do,Sara DiNapoli,Purvil Sukhadia,Megan Troxel,Kerem Ozcan,Zeynep Tarcan,Marc Ladanyi,James J Harding,Alexander Drilon,Olca Basturk,Eileen M O'Reilly
BACKGROUNDNRG1 fusions are unique oncogenic drivers that activate the HER3/HER2/PI3K pathway. The FDA granted Accelerated Approval to a HER2/HER3 antibody, zenocutuzumab, for treatment of NRG1 fusion-positive (NRG1+) non-small-cell lung and pancreatic cancer (PDAC). The optimal detection methods and clinicopathologic features of patients with NRG1+ cancer have not been systematically studied. We review NRG1+ cancer and focus on outcomes in PDAC.METHODSNRG1+ patients at Memorial Sloan Kettering were identified using institutional databases. Clinicopathologic data were extracted from the medical record. NRG1+ PDAC cases underwent review of radiology, pathology, treatment data, and assessment of progression-free and overall survival.RESULTSOut of 76,531 patients, 48 NRG1+ cases were identified. The most common tumor types were lung (60%), PDAC (21%), and breast (10%). Approximately half (46%) received HER2 and/or HER3-directed therapy. Patients were identified by RNA (n = 34), DNA (n = 11), or both (n = 3). RNA was superior to DNA for fusion identification. Twenty-one fusion partners were detected, most commonly CD74 (40%) and ATP1B1 (10%). Lung cancers were otherwise driver-negative and PDAC were KRAS wild-type. NRG1+ PDAC exhibited distinct histopathologic and clinical features. Median age was 48.5 years, median PFS on 1st-line chemotherapy was 12.6 months (n = 7; 95% CI 2.9-NR), and median OS from diagnosis was 39.6 months (n = 9; 95% CI 23.2-NR).CONCLUSIONSNRG1 fusions are a newly described clinically actionable target in solid tumors. We report the landscape of NRG1+ cancers and highlight the importance of RNA testing. NRG1+ PDAC is enriched in younger patients with KRAS wild-type disease and has a unique biology.
{"title":"NRG1 fusion-positive solid tumors: clinical detection, genomic landscape, and real-world data in pancreatic cancer.","authors":"Alison M Schram,Soo-Ryum Yang,Genessa Kahn,Rogelio Velasco,Matteo Repetto,Richard Kinh Gian Do,Sara DiNapoli,Purvil Sukhadia,Megan Troxel,Kerem Ozcan,Zeynep Tarcan,Marc Ladanyi,James J Harding,Alexander Drilon,Olca Basturk,Eileen M O'Reilly","doi":"10.1093/jnci/djaf361","DOIUrl":"https://doi.org/10.1093/jnci/djaf361","url":null,"abstract":"BACKGROUNDNRG1 fusions are unique oncogenic drivers that activate the HER3/HER2/PI3K pathway. The FDA granted Accelerated Approval to a HER2/HER3 antibody, zenocutuzumab, for treatment of NRG1 fusion-positive (NRG1+) non-small-cell lung and pancreatic cancer (PDAC). The optimal detection methods and clinicopathologic features of patients with NRG1+ cancer have not been systematically studied. We review NRG1+ cancer and focus on outcomes in PDAC.METHODSNRG1+ patients at Memorial Sloan Kettering were identified using institutional databases. Clinicopathologic data were extracted from the medical record. NRG1+ PDAC cases underwent review of radiology, pathology, treatment data, and assessment of progression-free and overall survival.RESULTSOut of 76,531 patients, 48 NRG1+ cases were identified. The most common tumor types were lung (60%), PDAC (21%), and breast (10%). Approximately half (46%) received HER2 and/or HER3-directed therapy. Patients were identified by RNA (n = 34), DNA (n = 11), or both (n = 3). RNA was superior to DNA for fusion identification. Twenty-one fusion partners were detected, most commonly CD74 (40%) and ATP1B1 (10%). Lung cancers were otherwise driver-negative and PDAC were KRAS wild-type. NRG1+ PDAC exhibited distinct histopathologic and clinical features. Median age was 48.5 years, median PFS on 1st-line chemotherapy was 12.6 months (n = 7; 95% CI 2.9-NR), and median OS from diagnosis was 39.6 months (n = 9; 95% CI 23.2-NR).CONCLUSIONSNRG1 fusions are a newly described clinically actionable target in solid tumors. We report the landscape of NRG1+ cancers and highlight the importance of RNA testing. NRG1+ PDAC is enriched in younger patients with KRAS wild-type disease and has a unique biology.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746688","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}
BACKGROUND: Deleterious DPYD variants are the primary identified cause of severe fluoropyrimidine-related toxicity. The objective was to improve the sensitivity of current DPYD genotyping recommendations and develop a predictive model for severe toxicity.METHODS: This pooled analysis included colorectal cancer (CRC) patients from seven prospective studies. Full DPYD sequencing was performed. Depending on their minor allele frequency (MAF), relevant DPYD variants were identified using Bolasso, or SKAT coupled with in silico functionality predictions. The primary end-point was 12-week grade 4-5 fluoropyrimidine-related hematological and digestive toxicities. Multivariate logistic regression models were developed.RESULTSOf 4,496 eligible patients, 3,437 were analyzed (267 events). The final model included patient/treatment characteristics, variants *2A/*13/p.D949V, common variants rs1801160 (p.V732I (*6), OR 1.93 [95%CI 1.37-2.70] if heterozygous) and rs2297595 (p.M166V, OR 1.49 [95%CI 1.13-1.96] if heterozygous), and aggregation of all very rare (MAF < 0.01) in silico-predicted deleterious variants (OR 3.20 [95%CI 1.43-7.14] if one allele). Model performance was supported by discrimination (AUC = 0.76, 95%CI 0.73-0.78), calibration, and internal validation. Crude sensitivity of DPYD testing increased from 11.2% for *2A/*13/p.D949V to 47.5% when including the 44 variants. An exploratory analysis of 1,138 stage III CRC patients revealed, for the first time, that carriers of deleterious DPYD variants exhibited significantly longer overall survival: HR = 0.65 [95%CI 0.43-0.98] for p. V732I and 0.62 [95%CI 0.43-0.90] for p. M166V.CONCLUSIONDPYD sequencing identified additional relevant variants and improved the sensitivity of DPYD testing. An online calculator (https://fluoropyrimidine-toxicity-predictor.gustaveroussy.fr/) is provided to estimate the individual probability of developing life-threatening toxicity, based on clinical covariates and extended DPYD genotype.
{"title":"A predictive model for life-threatening fluoropyrimidine toxicity based on DPYD sequencing in colorectal cancer.","authors":"Valérie Boige,Estelle Menoret,Gwénaël Le Teuff,Jean-Christophe Boyer,Nathalie Cozic,Jean-Pierre Desvignes,Julien Taieb,Pierre Laurent-Puig,Yvonne Wettergren,Matthias Schwab,Stephen Ackland,Barbara Jennings,Anne Sudaka,Eva Seutin,Christophe Beroud,Yves Koudou,Marie-Christine Etienne-Grimaldi, ","doi":"10.1093/jnci/djaf357","DOIUrl":"https://doi.org/10.1093/jnci/djaf357","url":null,"abstract":"BACKGROUND: Deleterious DPYD variants are the primary identified cause of severe fluoropyrimidine-related toxicity. The objective was to improve the sensitivity of current DPYD genotyping recommendations and develop a predictive model for severe toxicity.METHODS: This pooled analysis included colorectal cancer (CRC) patients from seven prospective studies. Full DPYD sequencing was performed. Depending on their minor allele frequency (MAF), relevant DPYD variants were identified using Bolasso, or SKAT coupled with in silico functionality predictions. The primary end-point was 12-week grade 4-5 fluoropyrimidine-related hematological and digestive toxicities. Multivariate logistic regression models were developed.RESULTSOf 4,496 eligible patients, 3,437 were analyzed (267 events). The final model included patient/treatment characteristics, variants *2A/*13/p.D949V, common variants rs1801160 (p.V732I (*6), OR 1.93 [95%CI 1.37-2.70] if heterozygous) and rs2297595 (p.M166V, OR 1.49 [95%CI 1.13-1.96] if heterozygous), and aggregation of all very rare (MAF < 0.01) in silico-predicted deleterious variants (OR 3.20 [95%CI 1.43-7.14] if one allele). Model performance was supported by discrimination (AUC = 0.76, 95%CI 0.73-0.78), calibration, and internal validation. Crude sensitivity of DPYD testing increased from 11.2% for *2A/*13/p.D949V to 47.5% when including the 44 variants. An exploratory analysis of 1,138 stage III CRC patients revealed, for the first time, that carriers of deleterious DPYD variants exhibited significantly longer overall survival: HR = 0.65 [95%CI 0.43-0.98] for p. V732I and 0.62 [95%CI 0.43-0.90] for p. M166V.CONCLUSIONDPYD sequencing identified additional relevant variants and improved the sensitivity of DPYD testing. An online calculator (https://fluoropyrimidine-toxicity-predictor.gustaveroussy.fr/) is provided to estimate the individual probability of developing life-threatening toxicity, based on clinical covariates and extended DPYD genotype.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145732817","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}
Xin Hu,Clara Cai,Sara Arshad,Janeane N Anderson,Mylin A Torres,Gregory A Vidal,Lee Schwartzberg,Ilana Graetz
BACKGROUNDAdjuvant endocrine therapy reduces breast cancer recurrence, but symptom burden contributes to nonadherence, particularly among Black women. We examined how patient sociodemographic factors and perceived discrimination are associated with symptoms and Black-White differences in symptoms during early treatment course of adjuvant endocrine therapy.METHODSWe conducted a post hoc analysis using survey data collected at study enrollment in the THRIVE trial from November 15, 2018, to June 11, 2021, among women with early-stage breast cancer. Symptom burden was assessed by the Functional Assessment of Cancer Therapy-Endocrine Subscale within 8 weeks of adjuvant endocrine therapy initiation. Covariates included sociodemographic and clinical information and perceived discrimination. Multivariable regressions and Kitagawa-Oaxaca-Blinder decomposition evaluated how these patient characteristics are associated with Black-White differences in symptoms.RESULTSAmong 272 participants, 35.7% self-identified as Black and 64.3% as White. Black women reported more symptoms (lower Functional Assessment of Cancer Therapy-Endocrine Subscale scores) than White women (60.7 vs 64.3, P = .004) and similar discrimination scores (5.44 vs 5.54, P = .17). Experiencing less discrimination (ie, each unit increase in discrimination score, 1.93, 95% confidence interval [CI] = 0.08 to 3.78), older age groups (65-83 vs 30-49 years: 4.84, 95% CI = 1.15 to 8.54), and higher income (≥400% vs <200% federal poverty level = 5.72, 95% CI = 2.12 to 9.33) was associated with lower symptom burden. Decomposition analyses attributed 84.6% of Black-White symptom differences to patient characteristics, with income explaining the largest proportion, while perceived discrimination did not explain symptom burden differences.CONCLUSIONSBlack women experienced higher early symptoms during adjuvant endocrine therapy. Although perceived discrimination was associated with greater symptom burden, it did not clinically or statistically significantly explain Black-White differences in symptoms. Income explained the largest portion of Black-White symptom differences. Addressing income inequality is essential for equitable symptom management.
背景：辅助内分泌治疗减少乳腺癌复发，但症状负担导致不依从，尤其是黑人妇女。我们研究了患者的社会人口因素和感知歧视如何与早期辅助内分泌治疗过程中的症状和黑白症状差异相关。方法：我们使用THRIVE试验在2018年11月15日至2021年6月11日期间收集的调查数据，对早期乳腺癌女性进行了事后分析。在辅助内分泌治疗开始后8周内，采用肿瘤治疗功能评估-内分泌亚量表评估症状负担。协变量包括社会人口学和临床信息以及感知歧视。多变量回归和Kitagawa-Oaxaca-Blinder分解评估了这些患者特征与黑白症状差异的关系。结果272名被调查者中，黑人占35.7%，白人占64.3%。黑人妇女报告的症状比白人妇女更多（癌症治疗功能评估-内分泌亚量表得分较低）(60.7比64.3,P =。004)和相似判别分数（5.44 vs 5.54, P = 0.17）。较少的歧视（即歧视评分每单位增加1.93,95%可信区间[CI] = 0.08至3.78）、年龄较大的年龄组（65-83岁vs 30-49岁：4.84,95% CI = 1.15至8.54）和收入较高的年龄组（≥400% vs <200%联邦贫困水平= 5.72,95% CI = 2.12至9.33）与较低的症状负担相关。分解分析将84.6%的黑白症状差异归因于患者特征，其中收入解释的比例最大，而感知歧视并不能解释症状负担差异。结论黑人妇女在辅助内分泌治疗中有较高的早期症状。尽管感知歧视与更大的症状负担相关，但它并不能在临床上或统计学上显著解释黑人和白人在症状上的差异。收入解释了黑人和白人症状差异的最大部分。解决收入不平等问题对于公平的症状管理至关重要。
{"title":"Potential role of perceived discrimination and sociodemographics on racial disparities in breast cancer symptom burden.","authors":"Xin Hu,Clara Cai,Sara Arshad,Janeane N Anderson,Mylin A Torres,Gregory A Vidal,Lee Schwartzberg,Ilana Graetz","doi":"10.1093/jnci/djaf301","DOIUrl":"https://doi.org/10.1093/jnci/djaf301","url":null,"abstract":"BACKGROUNDAdjuvant endocrine therapy reduces breast cancer recurrence, but symptom burden contributes to nonadherence, particularly among Black women. We examined how patient sociodemographic factors and perceived discrimination are associated with symptoms and Black-White differences in symptoms during early treatment course of adjuvant endocrine therapy.METHODSWe conducted a post hoc analysis using survey data collected at study enrollment in the THRIVE trial from November 15, 2018, to June 11, 2021, among women with early-stage breast cancer. Symptom burden was assessed by the Functional Assessment of Cancer Therapy-Endocrine Subscale within 8 weeks of adjuvant endocrine therapy initiation. Covariates included sociodemographic and clinical information and perceived discrimination. Multivariable regressions and Kitagawa-Oaxaca-Blinder decomposition evaluated how these patient characteristics are associated with Black-White differences in symptoms.RESULTSAmong 272 participants, 35.7% self-identified as Black and 64.3% as White. Black women reported more symptoms (lower Functional Assessment of Cancer Therapy-Endocrine Subscale scores) than White women (60.7 vs 64.3, P = .004) and similar discrimination scores (5.44 vs 5.54, P = .17). Experiencing less discrimination (ie, each unit increase in discrimination score, 1.93, 95% confidence interval [CI] = 0.08 to 3.78), older age groups (65-83 vs 30-49 years: 4.84, 95% CI = 1.15 to 8.54), and higher income (≥400% vs <200% federal poverty level = 5.72, 95% CI = 2.12 to 9.33) was associated with lower symptom burden. Decomposition analyses attributed 84.6% of Black-White symptom differences to patient characteristics, with income explaining the largest proportion, while perceived discrimination did not explain symptom burden differences.CONCLUSIONSBlack women experienced higher early symptoms during adjuvant endocrine therapy. Although perceived discrimination was associated with greater symptom burden, it did not clinically or statistically significantly explain Black-White differences in symptoms. Income explained the largest portion of Black-White symptom differences. Addressing income inequality is essential for equitable symptom management.","PeriodicalId":501635,"journal":{"name":"Journal of the National Cancer Institute","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145704702","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}
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