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Enhancing Clinical Cancer Research Through Sharing of Data and Biospecimens. 通过数据和生物标本共享加强临床癌症研究。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-18 DOI: 10.1001/jamaoncol.2025.5376
Hans Wildiers,Virginie Adam,Seamus O'Reilly,Josephine Van Cauwenberge,Amal Arahmani,Carlos L Arteaga,Philippe L Bedard,Judith Bliss,Panayota Boussis,Etienne Brain,Marc Buyse,Carmela Caballero,David Cameron,Fatima Cardoso,Eva Carrasco,Ana Casas,Boon Chua,Giuseppe Curigliano,Angela DeMichele,Laura Esserman,Giuseppe Floris,Matthew P Goetz,Theodora Goulioti,Benjamin Haibe-Kains,Christine Hodgdon,Michail Ignatiadis,Marleen Kok,Denis Lacombe,Barbro Linderholm,Sherene Loi,Christopher J Lord,Mairead MacKenzie,Julia Maues,Lydie Meheus,Judy Needham,Patrick Neven,Heather Parsons,Martine Piccart,Lajos Pusztai,Evangelia Razis,Shigehira Saji,Eva Schumacher-Wulf,Gabe S Sonke,Tania Spanic,Ian F Tannock,Andrew Tutt,Ander Urruticoechea,Laura van 't Veer,Ines Vaz-Luis,Gustavo Werutsky,Douglas Yee,Khalil Zaman,Christine Desmedt
ImportanceMolecular analyses of biospecimens collected from study participants are essential for identifying biomarkers that can tailor treatments to specific subsets of patients who are most likely to benefit. Sharing of data and biospecimens from clinical trials enables personalized, patient-centric use of cancer therapies and accelerates the development of new treatments.ObjectiveTo describe obstacles to sharing data and biospecimens and to propose strategies to enhance access and collaboration.Evidence ReviewThis is a Special Communication authored by 53 academic investigators and patient representatives from the breast cancer community with extensive experience in conducting clinical and translational research. The article also evaluates the impact of biomarker research on specifying responsive subpopulations in the 29 registrational clinical trials that have led to approval of a new drug for treatment of breast cancer between 2017 and 2024.FindingsClinical trial participants are increasingly asked to provide tissue and/or body fluid biospecimens for biomarker research that is typically controlled by the sponsoring pharmaceutical company, but published biomarker studies are rare. Among 29 breast cancer registrational studies reported in the past 8 years, none resulted in biomarker research that restricted a drug's approved indication. Herein, strategies to maximize the value of clinical data and biospecimens contributed by participants are proposed, thereby supporting the shared goals of the pharmaceutical industry and academia to improve patient care. These strategies include (1) establishing coleadership structures involving academia and patients in clinical trial design and conduct, (2) ensuring that informed consent forms state that data and biospecimens will be shared with academia for future research, (3) requiring the sharing of clinical data as a condition for regulatory approval, and (4) enabling access to biospecimens and translational research data for independent studies on biomarkers that may indicate drug efficacy and toxicity.Conclusions and RelevanceData and biospecimen sharing from registrational trials has been suboptimal. Improving clinical data, biospecimens, and biospecimens' related data sharing requires concrete actions and a multidimensional stakeholder approach to accelerate the impact of clinical cancer research on the quality of patient care.
重要性从研究参与者收集的生物标本的分子分析对于确定生物标记物至关重要,这些生物标记物可以针对最有可能受益的特定亚群患者定制治疗。临床试验数据和生物标本的共享使癌症治疗的个性化、以患者为中心的使用成为可能,并加速了新治疗方法的开发。目的描述数据和生物标本共享的障碍,并提出加强获取和合作的策略。这是一份特别通讯,由53名来自乳腺癌社区的学术研究者和患者代表撰写,他们在进行临床和转化研究方面具有丰富的经验。本文还评估了生物标志物研究对2017年至2024年间29项注册临床试验中指定反应性亚群的影响,这些临床试验已导致一种治疗乳腺癌的新药获得批准。越来越多的临床试验参与者被要求提供组织和/或体液生物标本,用于通常由赞助制药公司控制的生物标志物研究,但已发表的生物标志物研究很少。在过去8年的29项乳腺癌注册研究中,没有一项生物标志物研究限制了药物的批准适应症。在此,提出了最大化参与者贡献的临床数据和生物标本价值的策略,从而支持制药行业和学术界改善患者护理的共同目标。这些策略包括:(1)在临床试验设计和实施中建立涉及学术界和患者的领导结构;(2)确保知情同意书声明数据和生物标本将与学术界共享,用于未来的研究;(3)要求共享临床数据作为监管部门批准的条件;(4)允许获取生物标本和转化研究数据,用于可能指示药物疗效和毒性的生物标志物的独立研究。结论和相关性注册试验的数据和生物标本共享并不理想。改善临床数据、生物标本和生物标本相关数据共享需要具体行动和多维利益相关者方法,以加速临床癌症研究对患者护理质量的影响。
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引用次数: 0
Glucagon-Like Peptide-1 Receptor Agonists and Cancer. 胰高血糖素样肽-1受体激动剂与癌症。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-18 DOI: 10.1001/jamaoncol.2025.5364
Mahyar Etminan,Connor Frey,Mohammad A Mansournia
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引用次数: 0
Glucagon-Like Peptide-1 Receptor Agonists and Cancer-Reply. 胰高血糖素样肽-1受体激动剂与癌症应答。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-18 DOI: 10.1001/jamaoncol.2025.5370
Hao Dai,Jingchuan Guo,Jiang Bian
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引用次数: 0
Managing Nonfinancial Conflicts of Interest in Oncology Research-A Guide for Practice. 管理肿瘤学研究中的非财务利益冲突——实践指南。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-18 DOI: 10.1001/jamaoncol.2025.5247
Annabelle D Robinson,Anthony M Joshua,Wendy Lipworth
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引用次数: 0
Glucagon-Like Peptide-1 Receptor Agonists and Cancer. 胰高血糖素样肽-1受体激动剂与癌症。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-18 DOI: 10.1001/jamaoncol.2025.5367
Matthew Harris,Duncan Wilson,Andrew G Renehan
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引用次数: 0
Quadrivalent Human Papillomavirus Vaccine and High-Grade Vulvovaginal Lesions. 四价人乳头瘤病毒疫苗与高级别外阴阴道病变。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-18 DOI: 10.1001/jamaoncol.2025.5511
Yunyang Deng,Shiqiang Wu,Lina Schollin Ask,Tiia Lepp,Mark Clements,Hanna Milerad,Christina Carlander,Jiayao Lei
ImportanceHuman papillomavirus (HPV) vaccination has been associated with reduced risk of high-grade cervical lesions. However, evidence on its association with high-grade vulvovaginal lesions remains scarce.ObjectiveTo evaluate the association between quadrivalent HPV vaccination and high-grade vulvovaginal lesions and assess the population-level incidence reduction among birth cohorts eligible for various vaccination programs.Design, Setting, and ParticipantsThis population-based cohort study included women who were born between 1985 and 1998 and resided in Sweden between 2006 and 2022. Eligible participants had not previously received an HPV vaccination and did not have high-grade vulvovaginal lesions. Data were analyzed from February to October 2025.ExposureHPV vaccination status was treated as a time-varying exposure, and birth cohorts corresponded to different vaccination programs: 1985 to 1988 (opportunistic vaccination program), 1989 to 1992 (subsidized vaccination), and 1993 to 1998 (catch-up vaccination).Main Outcome and MeasuresThe main outcome was incidence of high-grade vulvovaginal lesions, including cancers. Poisson regression models were used to estimate incidence rate ratios with 95% CIs.ResultsAmong 778 943 women, a total of 256 353 (32.9%) received at least 1 dose of the quadrivalent HPV vaccine. The median (IQR) follow-up duration was 17.0 (17.0-17.0) years for unvaccinated women, 12.2 (10.6-13.4) years for those vaccinated between ages 10 and 16 years, and 10.8 (9.3-13.5) years for those vaccinated at 17 years or older. During follow-up, 98 cases of high-grade vulvovaginal lesions were found in vaccinated women, and 547 cases were found in unvaccinated women. Compared with unvaccinated women, the fully adjusted incidence rate ratio of high-grade vulvovaginal lesions was 0.63 (95% CI, 0.50-0.81) in vaccinated women. Stratified by age at vaccination, the incidence rate ratios for those vaccinated at 10 to 16 years and 17 years or older were 0.45 (95% CI, 0.32-0.65) and 0.80 (95% CI, 0.61-1.06), respectively. Compared with women born between 1985 and 1988, the incidence rate ratios for those born in 1989 to 1992 and 1993 to 1998 were 0.81 (95% CI, 0.67-0.97) and 0.62 (95% CI, 0.49-0.80), respectively.Conclusions and RelevanceIn this cohort study, vaccinated women had a lower incidence of high-grade vulvovaginal lesions compared with unvaccinated women, with a greater incidence reduction for those vaccinated at younger ages (before 17 years of age). Population-level incidence reduction was observed in cohorts vaccinated through subsidized or catch-up programs. These findings support that scaling up coverage of HPV vaccination at younger ages may help prevent high-grade vulvovaginal lesions.
人乳头瘤病毒(HPV)疫苗接种与降低高级别宫颈病变的风险相关。然而,其与高级别外阴阴道病变相关的证据仍然很少。目的评估四价HPV疫苗接种与高级别外阴阴道病变之间的关系,并评估不同疫苗接种计划的出生队列中人群水平发病率的降低。设计、环境和参与者这项以人群为基础的队列研究包括1985年至1998年出生、2006年至2022年居住在瑞典的女性。符合条件的参与者以前没有接受过HPV疫苗接种,也没有高度外阴阴道病变。数据分析时间为2025年2月至10月。hpv疫苗接种状况被视为时变暴露,出生队列对应于不同的疫苗接种计划:1985年至1988年(机会性疫苗接种计划),1989年至1992年(补贴疫苗接种)和1993年至1998年(补种疫苗接种)。主要结局和测量主要结局是外阴阴道高级病变(包括癌症)的发生率。泊松回归模型用于估计95% ci的发病率比。结果在778 943名女性中,共有256 353名(32.9%)接受了至少一剂四价HPV疫苗。未接种疫苗的妇女随访时间中位数(IQR)为17.0(17.0-17.0)年,10 - 16岁接种疫苗的妇女随访时间为12.2(10.6-13.4)年,17岁或以上接种疫苗的妇女随访时间为10.8(9.3-13.5)年。在随访期间,接种疫苗的妇女中发现了98例高度外阴阴道病变,未接种疫苗的妇女中发现了547例。与未接种疫苗的妇女相比,接种疫苗的妇女高度外阴阴道病变的完全调整发生率比为0.63 (95% CI, 0.50-0.81)。按接种年龄分层,10 - 16岁和17岁及以上接种者的发病率比分别为0.45 (95% CI, 0.32-0.65)和0.80 (95% CI, 0.61-1.06)。与1985年至1988年出生的妇女相比,1989年至1992年和1993年至1998年出生的妇女的发病率分别为0.81 (95% CI, 0.67-0.97)和0.62 (95% CI, 0.49-0.80)。结论和相关性在这项队列研究中,与未接种疫苗的女性相比,接种疫苗的女性外阴阴道高度病变的发生率较低,年龄较小(17岁之前)接种疫苗的女性发病率降低幅度更大。在通过补贴或追赶计划接种疫苗的队列中,观察到人群水平的发病率降低。这些发现支持在年轻年龄扩大HPV疫苗接种覆盖率可能有助于预防高度外阴阴道病变。
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引用次数: 0
Cognitive Impairment and Chemoendocrine vs Endocrine Therapy in Pre- and Postmenopausal Women 绝经前和绝经后妇女的认知障碍和化学内分泌与内分泌治疗
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-11 DOI: 10.1001/jamaoncol.2025.5220
Irene M. Kang, Jamie K. Forschmiedt, Michelle M. Loch, Danika L. Lew, William E. Barlow, Julie R. Gralow, Funda Meric-Bernstam, Kathy S. Albain, Daniel F. Hayes, Nancy U. Lin, Edith A. Perez, Lori J. Goldstein, Priya Rastogi, Anne F. Schott, Rick Baehner, Priyanka Sharma, Debasish Tripathy, Lajos Pusztai, Gabriel N. Hortobagyi, Kevin Kalinsky, N. Lynn Henry
Importance Breast cancer treatment is associated with cancer-related cognitive impairment (CRCI). However, the association of endocrine therapy (ET) vs chemotherapy plus endocrine therapy (CET) with CRCI is poorly understood. Objective To compare patient-reported CRCI between women with breast cancer treated with ET vs CET and to consider whether menopausal status may be associated. Design, Settings, and Participants This was a prespecified secondary analysis of RxPONDER (SWOG S1007), a multinational phase 3 randomized clinical trial of more than 5000 women with hormone receptor−positive <jats:italic>ERBB2</jats:italic> -negative (formerly <jats:italic>HER2</jats:italic> -negative) breast cancer with 1 to 3 involved lymph nodes and Oncotype DX (21-gene recurrence score) of 25 or less. Participants were enrolled from February 2011 to September 2017, with results first reported in December 2020. Participants were randomly assigned to CET or ET, with ongoing follow-up. This secondary analysis assessed cognitive function using the Patient-Reported Outcomes Measurement Information System Perceived Cognitive Function Concerns (PCF) questionnaire at baseline, 6, 12, and 36 months. Data were analyzed from July 2022 to August 2025. Intervention Random assignment to CET or ET. Main Outcomes and Measures Mean PCF standardized (T) scores by menopausal status over time using generalized estimating equations analysis for continuous outcomes. Results Of the 568 patients who completed the baseline questionnaire and were included in the analysis, 139 (24%) were premenopausal (median [range] age, 47.8 [28.0-56.3] years) and 429 (76%) were postmenopausal (median [range] age, 62.3 [37.3-87.6] years). Among the 274 (48%) who received CET and the 294 (52%) who received ET alone, CET was determined to have a greater negative association with patient-reported CRCI in both the pre- and postmenopausal participants during the 36-month follow-up. In the ET alone group, PCF scores for premenopausal participants decreased from baseline to 6 and 12 months (53.53, 51.51, and 51.72, respectively) but recovered to baseline (54.36) at 36 months. For postmenopausal participants, mean PCF scores were essentially stable (51.72, 51.13, 51.11, and 51.70, respectively); however, in the CET group, PCF scores for both pre- and postmenopausal participants decreased from baseline to 6 and 12 months (premenopausal, 52.84, 49.27, 48.04; postmenopausal, 50.65, 48.39, 47.13, respectively) and did not return to baseline at 36 months (premenopausal, 49.25; postmenopausal, 48.44). The difference in longitudinal mean PCF scores over time between CET and ET groups was −3.02 (95% CI, −5.33 to −0.72; <jats:italic>P</jats:italic> = .01) for premenopausal and −2.37 (95% CI, −3.92 to −0.82; <jats:italic>P</jats:italic> = .003) for postmenopausal participants. Conclusions and Relevance This secondary analysis of the RxPONDER found that CET had a greater negative association with patient-reported CRCI comp
乳腺癌治疗与癌症相关认知障碍(CRCI)相关。然而,内分泌治疗(ET)与化疗+内分泌治疗(CET)与CRCI的关系尚不清楚。目的比较ET与CET治疗的乳腺癌患者报告的CRCI,并探讨绝经状态是否与之相关。这是一项预先指定的RxPONDER (SWOG S1007)的二次分析,这是一项多国3期随机临床试验,有5000多名妇女患有激素受体阳性ERBB2阴性(以前为HER2阴性)乳腺癌,伴有1至3个淋巴结,Oncotype DX(21基因复发评分)为25或更低。参与者于2011年2月至2017年9月入组,结果于2020年12月首次报告。参与者被随机分配到CET或ET,并持续随访。在基线、6、12和36个月时,使用患者报告结果测量信息系统感知认知功能关注(PCF)问卷评估认知功能。数据分析时间为2022年7月至2025年8月。干预措施随机分配至CET或ET。主要结果和测量方法使用连续结果的广义估计方程分析,通过绝经状态随时间的平均PCF标准化(T)评分。结果在完成基线问卷并纳入分析的568例患者中,139例(24%)为绝经前(年龄中位数为47.8[28.0-56.3]岁),429例(76%)为绝经后(年龄中位数为62.3[37.3-87.6]岁)。在接受CET治疗的274名患者(48%)和单独接受ET治疗的294名患者(52%)中,在36个月的随访中,我们确定CET与绝经前和绝经后患者报告的CRCI有更大的负相关。在单独使用ET的组中,绝经前参与者的PCF评分从基线下降到6个月和12个月(分别为53.53、51.51和51.72),但在36个月时恢复到基线(54.36)。绝经后参与者的平均PCF评分基本稳定(分别为51.72、51.13、51.11和51.70);然而,在CET组中,绝经前和绝经后参与者的PCF评分从基线下降到6个月和12个月(绝经前,52.84,49.27,48.04;绝经后,50.65,48.39,47.13),并且在36个月时没有恢复到基线(绝经前,49.25;绝经后,48.44)。CET组和ET组纵向平均PCF评分随时间的差异,绝经前为- 3.02 (95% CI, - 5.33至- 0.72;P = 0.01),绝经后为- 2.37 (95% CI, - 3.92至- 0.82;P = 0.003)。结论和相关性RxPONDER的二次分析发现,在36个月的随访期间,绝经前和绝经后参与者中,与单独ET相比,CET与患者报告的CRCI有更大的负相关。为了改善这些接受化疗的患者的长期生活质量,需要采取预防或治疗CRCI的干预措施。临床试验注册:ClinicalTrials.gov标识符:NCT01272037
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引用次数: 0
Error in Denominator in Results Text. 结果文本中的分母错误。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-11 DOI: 10.1001/jamaoncol.2025.5629
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引用次数: 0
Stroke in Patients With Cancer-Time Is Brain. 癌症患者的中风——时间就是大脑。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-11 DOI: 10.1001/jamaoncol.2025.5234
Ronda Lun,Jeffrey Q Cao,Andrew Demchuk,Umberto Pensato
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引用次数: 0
Unraveling the Complexity of Cancer-Related Cognitive Impairment in Breast Cancer-Effect of Differing Treatments and Menopausal Status. 揭示乳腺癌中癌症相关认知障碍的复杂性——不同治疗和绝经状态的影响。
IF 28.4 1区 医学 Q1 ONCOLOGY Pub Date : 2025-12-11 DOI: 10.1001/jamaoncol.2025.5088
Michelle C Janelsins,Allison Magnuson
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引用次数: 0
期刊
JAMA Oncology
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