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Racial differences in multiple myeloma survival: Associations with stem cell transplantation, insurance, and Medicaid expansion 多发性骨髓瘤生存的种族差异:与干细胞移植、保险和医疗补助扩大的关系。
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-28 DOI: 10.1002/cncr.70596
F. Lennie Wong PhD, Scott R. Goldsmith MD, Kimlin Ashing PhD, Amrita Krishnan MD, Michael A. Rosenzweig MD, Saro H. Armenian DO, MPH

Background

At the population level, Black patients with multiple myeloma (MM) may experience worse survival than White patients. The authors examined how autologous stem cell transplantation (ASCT), insurance, and Medicaid expansion relate to racial differences in real-world overall survival (rwOS).

Methods

Data from 4932 patients with MM (24% Black) in the Flatiron Health Research Database were analyzed using Cox regression (rwOS), Fine and Gray competing-risk models (ASCT), and polytomous regression (insurance).

Results

Adjusted for demographic and clinical factors, Black patients had worse rwOS than White patients (adjusted hazard ratio [aHR], 1.11; 95% confidence interval [CI], 1.00–1.23), which became nonsignificant when adjusted for ASCT and/or health insurance. Lack of ASCT was associated with inferior rwOS (aHR, 0.59; 95% CI, 0.51–0.67). Black patients were less likely to receive ASCT (younger than 65 years: adjusted subdistribution HR [asHR], 0.64; 95% CI, 0.57–0.72; 65 years and older: asHR, 0.54; 95% CI, 0.42–0.69) and experienced a longer time to transplantation. Medicaid expansion was associated with a lower likelihood of ASCT in patients younger than 65 years (aHR, 0.50; 95% CI, 0.38–0.67) and was three times more common among Black than White patients. Among patients who received oncology care, Medicaid expansion was not associated with changes in Medicaid coverage, ASCT receipt, or rwOS.

Conclusions

Medicaid was associated with a lower likelihood of ASCT and was more prevalent among Black patients. Reduced receipt of ASCT was linked to inferior survival, contributing to survival disparities. Within this treated cohort, Medicaid expansion did not improve coverage, ASCT receipt, or survival, suggesting that structural barriers beyond insurance persist. Targeted efforts to improve ASCT access among Medicaid-insured patients are needed.

背景:在人群水平上,黑人多发性骨髓瘤(MM)患者的生存率可能比白人患者差。作者研究了自体干细胞移植(ASCT)、保险和医疗补助扩大与现实世界总生存(rwOS)的种族差异之间的关系。方法:采用Cox回归(rwOS)、Fine和Gray竞争风险模型(ASCT)和多元回归(保险)对Flatiron健康研究数据库中4932例MM患者(24%为黑人)的数据进行分析。结果:经人口统计学和临床因素校正后,黑人患者的rwOS比白人患者差(校正风险比[aHR], 1.11; 95%可信区间[CI], 1.00-1.23),经ASCT和/或健康保险校正后,这一差异变得不显著。缺乏ASCT与较差的rwOS相关(aHR, 0.59; 95% CI, 0.51-0.67)。黑人患者接受ASCT的可能性较小(65岁以下:调整亚分布HR [asHR], 0.64; 95% CI, 0.57-0.72; 65岁及以上:asHR, 0.54; 95% CI, 0.42-0.69),移植时间较长。医疗补助扩大与65岁以下患者发生ASCT的可能性较低相关(aHR, 0.50; 95% CI, 0.38-0.67),黑人患者发生ASCT的可能性是白人患者的三倍。在接受肿瘤治疗的患者中,医疗补助扩大与医疗补助覆盖范围、ASCT收据或rwOS的变化无关。结论:医疗补助与ASCT的可能性较低有关,并且在黑人患者中更为普遍。ASCT接受量减少与生存差有关,导致生存差异。在这个接受治疗的队列中,医疗补助的扩大并没有改善覆盖范围、ASCT接收或生存率,这表明保险之外的结构性障碍仍然存在。有针对性的努力,以提高ASCT在医疗保险患者的访问是必要的。
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引用次数: 0
Cancer statistics for Asian American, Native Hawaiian, and Pacific Islander people, 2026 2026年亚裔美国人、夏威夷原住民和太平洋岛民的癌症统计。
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-27 DOI: 10.1002/cncr.70584
Nikita Sandeep Wagle PhD, MBBS, MHA, Angela N. Giaquinto MSPH, Mandi Yu PhD, Hyuna Sung PhD, Tyler B. Kratzer MPH, Kekoa Taparra MD, PhD, MPH, Jessica Star MA, MPH, Ahmedin Jemal DVM, PhD, Rebecca L. Siegel MPH

Background

Cancer statistics for Asian American and Native Hawaiian and Pacific Islander (NHPI) people are usually aggregated, masking substantial variation within this heterogeneous population. Herein, the American Cancer Society reports cancer incidence and survival for 8 Asian American and 3 NHPI ethnic groups.

Methods

The authors used population-based cancer registry data from the National Cancer Institute’s Surveillance, Epidemiology, and End Results program, for Asian American and NHPI ethnic groups from 2000 through 2022.

Results

During 2018–2022, overall cancer incidence ranged from 218.3 per 100,000 Kampuchean people to 474.5 per 100,000 Native Hawaiian people, which was 1.5 times higher than the rate for the aggregated Asian American and NHPI population (307.3 per 100,000). High incidence among Native Hawaiian people is largely driven by the highest rates of female breast, colorectal, and prostate cancers, whereas infection-related cancers were highest among Asian American ethnic groups. For example, liver and stomach cancer incidence is highest among Vietnamese (22.2 per 100,000) and Korean people (17.8 per 100,000), respectively, both of which were nearly twice that in Native Hawaiian people (12.9 and 9.6 per 100,000, respectively). Native Hawaiian and Samoan women are twice and 3 times as likely, respectively, to be diagnosed with uterine corpus cancer as aggregated Asian American and NHPI women or White women. Five-year relative survival ranges from 42% in Laotians to 74% in Asian Indians/Pakistanis, with largest differences for colorectal (43% in Laotians to 72% in Asian Indians/Pakistanis) and prostate (63% in Kampucheans to 97% in Japanese) cancers.

Conclusions

Wide variation in cancer risk within the Asian American and NHPI population highlights the critical need for disaggregated data to effectively target cancer prevention and control interventions.

背景:亚裔美国人、夏威夷原住民和太平洋岛民(NHPI)的癌症统计数据通常是汇总的,掩盖了这一异质人群中的实质性差异。在此,美国癌症协会报告了8个亚裔美国人和3个NHPI族群的癌症发病率和生存率。方法:作者使用了来自美国国家癌症研究所监测、流行病学和最终结果项目的基于人群的癌症登记数据,这些数据来自2000年至2022年的亚裔美国人和NHPI族裔群体。结果:在2018-2022年期间,总体癌症发病率从每10万柬埔寨人中218.3人到每10万夏威夷原住民中474.5人不等,是亚裔美国人和NHPI人口总和(每10万人中307.3人)的1.5倍。夏威夷原住民的高发病率主要是由于女性乳腺癌、结肠直肠癌和前列腺癌的最高发病率,而与感染相关的癌症在亚裔美国人中最高。例如,肝癌发病率最高的是越南人(每10万人中有22.2人患肝癌),最高的是韩国人(每10万人中有17.8人患胃癌),几乎是夏威夷原住民(每10万人中有12.9人患肝癌)的两倍。夏威夷和萨摩亚土著妇女被诊断为子宫癌的可能性分别是亚裔和非裔美国人妇女或白人妇女的两倍和三倍。5年相对生存率从老挝人的42%到亚洲印度人/巴基斯坦人的74%不等,其中结肠直肠癌(老挝人43%,亚洲印度人/巴基斯坦人72%)和前列腺癌(柬埔寨人63%,日本人97%)的差异最大。结论:亚裔美国人和NHPI人群中癌症风险的广泛差异突出了对分类数据的迫切需要,以有效地针对癌症预防和控制干预措施。
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引用次数: 0
Vimseltinib for patients with tenosynovial giant cell tumor: A multicenter, open-label, phase 2 trial Vimseltinib用于腱鞘巨细胞瘤患者:一项多中心,开放标签,2期试验
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-25 DOI: 10.1002/cncr.70564
Silvia Stacchiotti MD, Jean-Yves Blay MD, PhD, Piotr Rutkowski MD, PhD, Hans Gelderblom MD, PhD, Alejandro Falcón MD, PhD, Axel Le Cesne MD, Jayesh Desai MBBS, FRACP, Emanuela Palmerini MD, PhD, César Serrano MD, PhD, Kristen N. Ganjoo MD, Gina Z. D’Amato MD, Christopher W. Ryan MD, Breelyn A. Wilky MD, Virginia Ferraresi MD, Ramy Saleh MD, MSc, FRCPC, Vinod Ravi MD, MS, MBA, Albiruni Abdul Razak MB BCh, BM BCh, Antonio Casado Herráez MD, PhD, Mahbubl Ahmed MBBS, PhD, Nicholas M. Bernthal MD, Michiel van de Sande MD, PhD, Mehdi Brahmi MD, PhD, Bartlomiej Szostakowski MD, PhD, Jasmine Sen MS, Nicholas A. Zeringo PhD, Brooke Harrow PhD, Supraja Narasimhan PhD, Amanda Saunders DO, Maitreyi G. Sharma MD, Matthew L. Sherman MD, Andrew J. Wagner MD, PhD, William D. Tap MD

Background

Tenosynovial giant cell tumor (TGCT) is a locally aggressive neoplasm caused by dysregulation of the colony-stimulating factor 1 (CSF1) gene. Patients report substantial pain, stiffness, and declining physical function; those whose disease is not amenable to surgery require systemic therapy. Vimseltinib is an oral, switch-control kinase inhibitor of the CSF1 receptor (CSF1R). Here, the authors report safety and efficacy of vimseltinib in patients with TGCT based on prior treatment. Cohort A included patients who did not receive prior specific anti-CSF1/CSF1R agents (n = 46; prior imatinib/nilotinib allowed), and cohort B included patients who received prior specific agents (n = 20).

Methods

The phase 2 (expansion) portion of this ongoing, multicenter, open-label, phase 1/2 study (NCT03069469) enrolled adults (≥18 years) with histologically-confirmed TGCT not amenable to surgery. Patients received vimseltinib 30 mg twice weekly (recommended phase 2 dose). The primary objectives were to assess safety and antitumor activity; secondary objectives included assessment of active range of motion (ROM) and patient-reported outcomes.

Results

Most treatment-emergent adverse events were grade 1/2, and there was no evidence of cholestatic hepatotoxicity or drug-induced liver injury. Best overall response rates were 64% (29 of 45) and 37% (7 of 19) for cohorts A and B after mean follow-up of 23 and 19 months, respectively. Most patients experienced meaningful improvements in active ROM and patient-reported physical function, stiffness, health status, and pain.

Conclusions

Vimseltinib had a manageable safety profile, demonstrated durable antitumor activity, and provided functional and symptomatic improvements in patients with TGCT, offering an effective treatment option regardless of previous treatment with anti-CSF1/CSF1R agents.

背景:腱鞘巨细胞瘤(TGCT)是一种由集落刺激因子1 (CSF1)基因失调引起的局部侵袭性肿瘤。患者报告严重疼痛、僵硬和身体功能下降;那些疾病不适合手术的人需要全身治疗。Vimseltinib是一种口服CSF1受体(CSF1R)的开关控制激酶抑制剂。在这里,作者报告了基于先前治疗的维姆西替尼在TGCT患者中的安全性和有效性。队列A包括先前未接受特异性抗csf1 /CSF1R药物治疗的患者(n = 46;允许接受伊马替尼/尼罗替尼治疗),队列B包括先前接受特异性药物治疗的患者(n = 20)。方法:这项正在进行的多中心、开放标签、1/2期研究(NCT03069469)的2期(扩展)部分招募了组织学证实的TGCT不适合手术的成人(≥18岁)。患者接受vimseltinib 30 mg,每周2次(推荐的2期剂量)。主要目的是评估安全性和抗肿瘤活性;次要目标包括评估活动度(ROM)和患者报告的结果。结果:大多数治疗后出现的不良事件为1/2级,没有证据表明存在胆汁淤积性肝毒性或药物性肝损伤。在平均随访23个月和19个月后,A组和B组的最佳总有效率分别为64%(45人中29人)和37%(19人中7人)。大多数患者在活动性ROM和患者报告的身体功能、僵硬度、健康状况和疼痛方面有了有意义的改善。结论:Vimseltinib具有可控的安全性,具有持久的抗肿瘤活性,并可改善TGCT患者的功能和症状,无论先前使用抗csf1 /CSF1R药物治疗,都是一种有效的治疗选择。
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引用次数: 0
Gynecologic cancers in low- and middle-income countries: Bridging the survival gap 低收入和中等收入国家的妇科癌症:弥合生存差距。
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-24 DOI: 10.1002/cncr.70518
Dewi Setiawati SpOG, Wachyudi Muchsin SKed, SH, MKes, CMed, Alfi Sophan SSi, MSi

Gynecologic malignancies—including cervical, endometrial, ovarian, vaginal, and vulvar cancers—represent a major and largely preventable source of mortality in low- and middle-income countries (LMICs). In 2022, an estimated 1.47 million new cases and over 680,000 deaths were reported globally, with mortality disproportionately concentrated in resource-constrained settings. The survival gap between LMICs and high-income countries (HICs) remains profound, reflecting systemic policy and health system failures in prevention, early detection, and access to treatment. This narrative review synthesizes evidence from PubMed/MEDLINE, Embase, Cochrane Library, and World Health Organization (WHO) databases, prioritizing literature published between January 2015 and December 2024, with a focus on epidemiology, health system constraints, and policy-relevant interventions. LMICs account for approximately 94% of global cervical cancer deaths, with the highest mortality observed in East Africa (age-standardized mortality rate 35.3 per 100,000). Persistent survival disparities are driven by late-stage diagnosis, limited screening coverage, inadequate radiotherapy infrastructure, workforce shortages, and restricted access to essential and novel therapies. However, evidence demonstrates that cost-effective and scalable interventions—including single-dose human papillomavirus (HPV) vaccination, screen-and-treat strategies, HPV self-sampling, task-shifting models, and international training partnerships—can substantially improve outcomes when embedded within national cancer control policies and supported by sustainable financing mechanisms. Reducing these inequities requires policy-driven, system-level reforms that prioritize prevention, strengthen service delivery, and expand equitable access to care, aligning national strategies with global frameworks such as the WHO 90–70–90 targets to achieve sustainable cancer control in LMICs.

妇科恶性肿瘤——包括子宫癌、子宫内膜癌、卵巢癌、阴道癌和外阴癌——是低收入和中等收入国家的一个主要且在很大程度上可预防的死亡来源。2022年,全球估计报告了147万新病例和68万多例死亡,死亡率不成比例地集中在资源有限的环境中。中低收入国家和高收入国家之间的生存差距仍然很大,反映出系统性政策和卫生系统在预防、早期发现和获得治疗方面的失败。本综述综合了PubMed/MEDLINE、Embase、Cochrane图书馆和世界卫生组织(WHO)数据库的证据,优先考虑了2015年1月至2024年12月期间发表的文献,重点关注流行病学、卫生系统限制和政策相关干预措施。中低收入国家约占全球宫颈癌死亡人数的94%,其中死亡率最高的是东非(年龄标准化死亡率为每10万人35.3人)。持续的生存差异是由晚期诊断、有限的筛查覆盖率、放射治疗基础设施不足、劳动力短缺以及限制获得基本和新疗法造成的。然而,有证据表明,具有成本效益和可扩展的干预措施,包括单剂量人乳头瘤病毒(HPV)疫苗接种、筛查和治疗策略、HPV自采样、任务转移模式和国际培训伙伴关系,如果纳入国家癌症控制政策并得到可持续融资机制的支持,可以大大改善结果。减少这些不公平现象需要政策驱动的系统级改革,以预防为重点,加强服务提供,扩大公平获得医疗服务的机会,使国家战略与世卫组织90-70-90目标等全球框架保持一致,以实现中低收入国家的可持续癌症控制。
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引用次数: 0
Beyond risk factors: A capacity framework for cancer survivorship research 超越风险因素:癌症生存研究的能力框架
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-20 DOI: 10.1002/cncr.70582
Keith M. Bellizzi PhD, MPH

Cancer survivorship research has identified numerous biological, behavioral, psychosocial, health care, and structural factors that influence recovery. However, these factors are typically studied as separate determinants rather than interacting influences. This commentary proposes available survivorship capacity as a unifying framework that explains how these diverse determinants collectively shape recovery and survivorship outcomes. Concepts from geroscience, health care delivery, rehabilitation, occupational therapy, and human factors science were synthesized to develop a conceptual framework of available survivorship capacity. The framework conceptualizes recovery as a function of the capacity remaining after competing health care and life demands draw upon survivors' finite physical, cognitive, emotional, social, financial, temporal, and health care resources. It generates testable propositions for measurement, intervention research, health care delivery, and implementation science while positioning available survivorship capacity as a common mechanism linking diverse determinants of recovery and identifying actionable targets for intervention. Available capacity offers a unifying conceptual framework for understanding heterogeneity in survivorship outcomes and intervention effectiveness while generating a research agenda for future survivorship science. Measuring and strengthening survivors' available capacity, while reducing unnecessary demands, may improve engagement in care, health behaviors, and long-term recovery.

癌症幸存者研究已经确定了许多影响康复的生物、行为、社会心理、卫生保健和结构因素。然而,这些因素通常是作为单独的决定因素而不是相互影响来研究的。这篇评论提出可用的生存能力作为一个统一的框架,解释了这些不同的决定因素如何共同影响恢复和生存结果。综合了来自老年科学、卫生保健、康复、职业治疗和人因科学的概念,形成了可用生存能力的概念框架。该框架将康复概念化为在医疗保健和生活需求相互竞争后剩余能力的函数,这些需求利用了幸存者有限的身体、认知、情感、社会、经济、时间和医疗保健资源。它为测量、干预研究、卫生保健提供和实施科学提供了可测试的命题,同时将可用的生存能力定位为连接恢复的各种决定因素和确定可操作的干预目标的共同机制。可用能力为理解生存结果和干预有效性的异质性提供了一个统一的概念框架,同时为未来的生存科学制定了研究议程。衡量和加强幸存者的现有能力,同时减少不必要的需求,可以改善对护理、卫生行为和长期康复的参与。
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引用次数: 0
Blinatumomab administration in the outpatient setting: Safety and health care utilization 布利纳单抗在门诊治疗中的应用:安全性和保健应用
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-18 DOI: 10.1002/cncr.70566
Yannis K. Valtis MD, Benjamin F. Frost MD, David Nemirovsky MA, Andriy Derkach PhD, Kuo-Kai Chin MD, Meira Yisraeli Salman MD, Leora Boussi MD, Natalia Tijaro Ovalle MD, Emilie Baxter BA, Ann Mercurio MD, Eytan M. Stein MD, Mark B. Geyer MD, Deborah Schrag MD, MPH, Amar H. Kelkar MD, Daniel J. DeAngelo MD, Marlise R. Luskin MD, Jae H. Park MD, Evan C. Chen MD

Background

Blinatumomab, a bispecific CD19 × CD3 antibody is effective for the treatment of B-cell acute lymphoblastic leukemia (ALL). Because of its immune toxicities, namely cytokine release syndrome (CRS) and immune effector cell–associated neurotoxicity syndrome (ICANS), the US Food and Drug Administration (FDA) recommends preemptive hospitalization for the initiation of cycle 1 (C1) and cycle 2 (C2). The necessity of this approach is unclear.

Methods

The authors conducted a retrospective cohort study among all patients treated with blinatumomab between 2012 and 2025 at two academic cancer centers: Memorial Sloan Kettering Cancer Center (MSK) and Dana-Farber Cancer Institute (DFCI).

Results

For C1, only nine of 308 (3%) patients initiated outpatient (OP) treatment. A total of 184 of 308 (60%) initiated C2: At DFCI, 10 of 83 (12%) initiated C2 OP and at MSK, and 74 of 101 (88%) initiated C2 OP. Demographic and clinical characteristics were similar between patients initiating C2 inpatient versus OP. No patients who initiated C2 (0 of 184) had Gr3+ CRS (across all cycles) and only two (1%) had Gr3+ ICANS; both were inpatient for C2. Of 84 patients treated without preemptive hospitalization for C2, 16 of 84 (19%) required hospitalization at some point during the cycle, largely for infections (50%).

Conclusions

OP administration of C2 of blinatumomab can be administered safely with no unexpected, severe, or life-threatening toxicities. The ability to safely manage treatment without preemptive hospitalization may support the patient experience and limit costs of care.

背景:双特异性CD19 × CD3抗体Blinatumomab可有效治疗b细胞急性淋巴细胞白血病(ALL)。由于其免疫毒性,即细胞因子释放综合征(CRS)和免疫效应细胞相关神经毒性综合征(ICANS),美国食品和药物管理局(FDA)建议在周期1 (C1)和周期2 (C2)开始时先住院治疗。这种做法的必要性尚不清楚。方法:作者对2012年至2025年间在两个学术癌症中心(Memorial Sloan Kettering cancer Center (MSK)和Dana-Farber cancer Institute (DFCI))接受blinatumomab治疗的所有患者进行了回顾性队列研究。结果对于C1, 308例患者中只有9例(3%)开始了门诊治疗。308例患者中有184例(60%)启动了C2:在DFCI, 83例患者中有10例(12%)启动了C2 OP和MSK, 101例患者中有74例(88%)启动了C2 OP。在住院患者和OP中启动C2的患者中,人口统计学和临床特征相似。启动C2的患者(184例中0例)没有Gr3+ CRS(所有周期),只有2例(1%)有Gr3+ ICANS;两人都因C2住院。在84例未因C2预先住院治疗的患者中,84例中有16例(19%)需要在周期内的某个时间点住院,主要是感染(50%)。结论:布利纳单抗C2的OP给药是安全的,没有意外的、严重的或危及生命的毒性。在没有预先住院的情况下安全管理治疗的能力可以支持患者体验并限制护理成本。
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引用次数: 0
Daraxonrasib doubles survival in patients with metastatic pancreatic cancer Daraxonrasib可使转移性胰腺癌患者的生存率提高一倍
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-18 DOI: 10.1002/cncr.70513
Leah Lawrence
<p>Compared with chemotherapy, treatment with daraxonrasib more than doubled overall survival (OS) and progression-free survival (PFS) for patients with previously treated metastatic pancreatic ductal adenocarcinoma (mPDAC) according to results from RASolute 302 presented at the 2026 annual meeting of the American Society of Clinical Oncology and published simultaneously in <i>The New England Journal of Medicine</i>.<span><sup>1</sup></span></p><p>“About 90% of pancreatic cancers harbor mutations in KRAS,” explains Vaia Florou, MD, an associate professor in the Division of Oncology at Huntsman Cancer Institute at the University of Utah in Salt Lake City. Previously approved <i>KRAS</i> inhibitors sotorasib and adagrasib both target <i>KRAS</i> G12C mutations, which are uncommon in pancreatic cancer. “Daraxonrasib is a pan-RAS inhibitor, covering multiple different RAS mutations.”</p><p>The RASolute 302 trial enrolled 500 patients with previously treated mPDAC and randomly assigned them to daraxonrasib or the investigator’s choice of chemotherapy. The trial had dual primary endpoints of OS and PFS in the subpopulation of patients with <i>RAS</i> G12 mutations, who composed 91.8% of the study patients.</p><p>Daraxonrasib yielded a 60% reduction in the risk for progression or death in patients with <i>RAS</i> G12 mutations and in the entire study population (hazard ratio [HR], 0.40; p < .001). The median OS was 13.2 months for patients with <i>RAS</i> G12 mutations who were assigned to daraxonrasib and 6.6 months for patients who were assigned to chemotherapy. For the entire study population, the median OS was 13.2 months with daraxonrasib and 3.6 months with chemotherapy.</p><p>Similarly, PFS was significantly improved in both populations. In patients with RAS G12 mutations, the median PFS was 7.3 months with daraxonrasib and 3.5 months with chemotherapy (HR, 0.45; <i>p</i> < .001), and in the entire population, the median PFS was 7.2 months with daraxonrasib and 3.6 months with chemotherapy (HR, 0.49; <i>p</i> < .001).</p><p>Treatment was discontinued because of adverse events in 1.2% of patients assigned to daraxonrasib and in 11.2% of patients assigned to chemotherapy.</p><p>“This is a landmark study in a way that is going to be a paradigm shift in how we treat this disease,” Dr Florou says.</p><p>Ongoing trials are evaluating daraxonrasib in newly diagnosed mPDAC (RASolute 303) and in the localized setting (RASolute 304). Additionally, other RAS inhibitors are being investigated in clinical trials targeting the G12D and G12V mutations, which are the most common <i>RAS</i> G12 variants in PDAC.</p><p>Before the publication of these results, the US Food and Drug Administration (FDA) announced that it has permitted expanded access to daraxonrasib for patients with previously treated mPDAC.<span><sup>2</sup></span></p><p>“This is a great avenue for access to this drug or any effective drug before it goes to market,” says Dr Florou. “The ca
根据RASolute 302在2026年美国临床肿瘤学会年会上发表并同时发表在《新英格兰医学杂志》上的研究结果,与化疗相比,daraxonrasib治疗之前治疗过的转移性胰腺导管腺癌(mPDAC)患者的总生存期(OS)和无进展生存期(PFS)增加了一倍以上。盐湖城犹他大学亨茨曼癌症研究所肿瘤科副教授Vaia Florou医学博士解释道。先前批准的KRAS抑制剂sotorasib和adagrasib都靶向KRAS G12C突变,这在胰腺癌中并不常见。“Daraxonrasib是一种泛RAS抑制剂,覆盖多种不同的RAS突变。”RASolute 302试验招募了500名先前接受过mPDAC治疗的患者,并随机分配给他们daraxonrasib或研究者选择的化疗方案。该试验在RAS G12突变患者亚群中有OS和PFS的双重主要终点,占研究患者的91.8%。Daraxonrasib使RAS G12突变患者和整个研究人群的进展或死亡风险降低了60%(风险比[HR], 0.40; p < .001)。RAS G12突变患者分配给daraxonrasib的中位生存期为13.2个月,分配给化疗的患者为6.6个月。对于整个研究人群,daraxonrasib组的中位OS为13.2个月,化疗组为3.6个月。同样,PFS在两个人群中都得到了显著改善。在RAS G12突变患者中,daraxonrasib的中位PFS为7.3个月,化疗为3.5个月(HR, 0.45; p < .001),而在整个人群中,daraxonrasib的中位PFS为7.2个月,化疗为3.6个月(HR, 0.49; p < .001)。1.2%接受daraxonrasib治疗的患者和11.2%接受化疗的患者因不良事件而停止治疗。Florou博士说:“这是一项具有里程碑意义的研究,在某种程度上将成为我们治疗这种疾病的范式转变。”正在进行的试验正在评估daraxonrasib在新诊断的mPDAC (RASolute 303)和局部环境(RASolute 304)中的作用。此外,针对G12D和G12V突变的其他RAS抑制剂正在临床试验中进行研究,这是PDAC中最常见的RAS G12变体。在这些结果发表之前,美国食品和药物管理局(FDA)宣布,它已经允许扩大daraxonrasib用于先前治疗过的mPDAC患者。Florou博士说:“这是在这种药物或任何有效药物上市之前获得它的一个很好的途径。”“需要注意的是,扩大访问范围在后勤上并不容易。可能还需要几周或几个月的时间才能获得准入,但这仍然比等待FDA的最终批准要好。”Daraxonrasib的制造商宣布,它打算根据FDA专员的国家优先凭证试点计划提交新药申请
{"title":"Daraxonrasib doubles survival in patients with metastatic pancreatic cancer","authors":"Leah Lawrence","doi":"10.1002/cncr.70513","DOIUrl":"https://doi.org/10.1002/cncr.70513","url":null,"abstract":"&lt;p&gt;Compared with chemotherapy, treatment with daraxonrasib more than doubled overall survival (OS) and progression-free survival (PFS) for patients with previously treated metastatic pancreatic ductal adenocarcinoma (mPDAC) according to results from RASolute 302 presented at the 2026 annual meeting of the American Society of Clinical Oncology and published simultaneously in &lt;i&gt;The New England Journal of Medicine&lt;/i&gt;.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;“About 90% of pancreatic cancers harbor mutations in KRAS,” explains Vaia Florou, MD, an associate professor in the Division of Oncology at Huntsman Cancer Institute at the University of Utah in Salt Lake City. Previously approved &lt;i&gt;KRAS&lt;/i&gt; inhibitors sotorasib and adagrasib both target &lt;i&gt;KRAS&lt;/i&gt; G12C mutations, which are uncommon in pancreatic cancer. “Daraxonrasib is a pan-RAS inhibitor, covering multiple different RAS mutations.”&lt;/p&gt;&lt;p&gt;The RASolute 302 trial enrolled 500 patients with previously treated mPDAC and randomly assigned them to daraxonrasib or the investigator’s choice of chemotherapy. The trial had dual primary endpoints of OS and PFS in the subpopulation of patients with &lt;i&gt;RAS&lt;/i&gt; G12 mutations, who composed 91.8% of the study patients.&lt;/p&gt;&lt;p&gt;Daraxonrasib yielded a 60% reduction in the risk for progression or death in patients with &lt;i&gt;RAS&lt;/i&gt; G12 mutations and in the entire study population (hazard ratio [HR], 0.40; p &lt; .001). The median OS was 13.2 months for patients with &lt;i&gt;RAS&lt;/i&gt; G12 mutations who were assigned to daraxonrasib and 6.6 months for patients who were assigned to chemotherapy. For the entire study population, the median OS was 13.2 months with daraxonrasib and 3.6 months with chemotherapy.&lt;/p&gt;&lt;p&gt;Similarly, PFS was significantly improved in both populations. In patients with RAS G12 mutations, the median PFS was 7.3 months with daraxonrasib and 3.5 months with chemotherapy (HR, 0.45; &lt;i&gt;p&lt;/i&gt; &lt; .001), and in the entire population, the median PFS was 7.2 months with daraxonrasib and 3.6 months with chemotherapy (HR, 0.49; &lt;i&gt;p&lt;/i&gt; &lt; .001).&lt;/p&gt;&lt;p&gt;Treatment was discontinued because of adverse events in 1.2% of patients assigned to daraxonrasib and in 11.2% of patients assigned to chemotherapy.&lt;/p&gt;&lt;p&gt;“This is a landmark study in a way that is going to be a paradigm shift in how we treat this disease,” Dr Florou says.&lt;/p&gt;&lt;p&gt;Ongoing trials are evaluating daraxonrasib in newly diagnosed mPDAC (RASolute 303) and in the localized setting (RASolute 304). Additionally, other RAS inhibitors are being investigated in clinical trials targeting the G12D and G12V mutations, which are the most common &lt;i&gt;RAS&lt;/i&gt; G12 variants in PDAC.&lt;/p&gt;&lt;p&gt;Before the publication of these results, the US Food and Drug Administration (FDA) announced that it has permitted expanded access to daraxonrasib for patients with previously treated mPDAC.&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;“This is a great avenue for access to this drug or any effective drug before it goes to market,” says Dr Florou. “The ca","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 16","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cncr.70513","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Clinical trial skepticism influenced by political ideology 受政治意识形态影响的临床试验怀疑主义
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-18 DOI: 10.1002/cncr.70514
Leah Lawrence
<p>Approximately 1 in 4 people believe that clinical trials should be approached with suspicion according to data recently published in <i>JAMA Network Open</i>, with political ideology appearing to influence levels of skepticism.<span><sup>1</sup></span></p><p>Onyema G. Chido-Amajuoyi, MD, MPH, a hematology/oncology fellow at the University of Washington in Seattle, and his colleagues published data from a cross-sectional study evaluating associations between political ideology and clinical trial skepticism.</p><p>Data were taken from the National Cancer Institute’s publicly available Health Information National Trends Survey 7, which included 6377 responders, 1009 of whom were cancer survivors. Participants used a Likert scale to respond to the statement “People should be suspicious of clinical trials,” and 27.2% agreed.</p><p>Ruth O’Regan, MD, chair of the Department of Medicine at the University of Rochester in New York, says that she was not surprised that more than one fourth of responders expressed skepticism.</p><p>“Across therapeutic cancer clinical trials, only 10% or fewer patients enroll,” Dr O’Regan says. “The reasons are multifactorial, but some is skepticism from the patients and their families. We as physicians should do a better job communicating the benefit of clinical trials to patients.”</p><p>Among the respondents, 37.6% identified as moderate, 30.5% identified as liberal, and 31.9% identified as conservative. Compared with those who neither agreed nor disagreed with the study statement, those who identified as conservative were more likely to agree that people should be suspicious of clinical trials than liberals (adjusted odds ratio [aOR], 1.30; 95% CI, 1.10–1.54) or moderates (aOR, 1.43; 95% CI, 1.22–1.67).</p><p>In addition, those who identified as liberal were more likely than moderates to disagree that people should be suspicious of clinical trials (aOR, 1.98; 95% CI; 1.70–2.31).</p><p>Similar trends were seen among respondents who were cancer survivors.</p><p>The study researchers called the implications of these data both “pragmatic and urgent.”</p><p>“If political ideology influences receptivity to clinical trials, recruitment strategies that overlook ideological diversity risk biased enrollment and underrepresentation,” Dr Chido-Amajuoyi and his colleagues wrote. “Prior research demonstrates disparities in clinical trial participation by political orientation. Recognizing political ideology as a factor in medical mistrust may help reduce participation barriers and improve representativeness.”</p><p>Although Dr O’Regan says that the trends related to political ideology in this study were also not surprising, she is not sure how this information could be used in the clinic.</p><p>“How do you determine if someone is liberal or conservative?” Dr O’Regan says. “In fact, we tend to steer away from talking about politics in the clinic.”</p><p>Instead, Dr O’Regan suggests that clinicians focus on tactics for enrolling patie
根据最近发表在JAMA Network Open上的数据,大约四分之一的人认为应该对临床试验持怀疑态度,政治意识形态似乎影响了怀疑的程度。onyema G. Chido-Amajuoyi,医学博士,公共卫生硕士,西雅图华盛顿大学血液学/肿瘤学研究员,和他的同事发表了一项横断面研究的数据,评估政治意识形态和临床试验怀疑之间的联系。数据来自国家癌症研究所公开的健康信息国家趋势调查7,其中包括6377名应答者,其中1009名是癌症幸存者。参与者使用李克特量表来回答“人们应该对临床试验持怀疑态度”,27.2%的人同意这一说法。纽约罗彻斯特大学医学系主任Ruth O 'Regan医学博士说,她对超过四分之一的应答者表示怀疑并不感到惊讶。“在整个治疗性癌症临床试验中,只有10%或更少的患者参加,”奥雷根博士说。“原因是多方面的,但一些是来自患者及其家属的怀疑。作为医生,我们应该更好地向患者宣传临床试验的好处。”在被调查者中,37.6%的人认为是温和派,30.5%的人认为是自由派,31.9%的人认为是保守派。与那些既不同意也不反对研究声明的人相比,那些被认定为保守派的人比自由派(调整优势比[aOR], 1.30; 95% CI, 1.10-1.54)或温和派(aOR, 1.43; 95% CI, 1.22-1.67)更有可能同意人们应该对临床试验持怀疑态度。此外,那些自认为是自由派的人比温和派更有可能不同意人们应该怀疑临床试验(aOR, 1.98; 95% CI; 1.70-2.31)。癌症幸存者的受访者也有类似的趋势。研究人员称这些数据的含义既“实用又紧迫”。Chido-Amajuoyi博士和他的同事写道:“如果政治意识形态影响临床试验的接受程度,那么忽视意识形态多样性的招聘策略可能会导致入学偏见和代表性不足。”“先前的研究表明,政治取向在临床试验参与方面存在差异。认识到政治意识形态是医疗不信任的一个因素,可能有助于减少参与障碍,提高代表性。”虽然奥雷根博士说,这项研究中与政治意识形态相关的趋势也并不令人惊讶,但她不确定这些信息如何在临床中使用。“你如何判断一个人是自由派还是保守派?”奥雷根博士说。“事实上,我们倾向于避免在诊所里谈论政治。”相反,奥雷根博士建议临床医生把重点放在招募患者参加临床试验的策略上,以解决任何程度的怀疑。“我通常发现,你可以很早就知道病人是否对临床试验持怀疑态度,”奥雷根博士说。“如果他们是这样,你可以花更多的时间了解试验细节,让他们放心,他们至少会得到标准的治疗,他们可以随时决定退出试验。”
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引用次数: 0
PSA monitoring alone proves inadequate for detecting prostate cancer progression 单靠PSA监测不足以检测前列腺癌的进展
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-18 DOI: 10.1002/cncr.70512
Leah Lawrence
<p>Prostate-specific antigen (PSA) monitoring should not be used alone to monitor patients with metastatic hormone-sensitive prostate cancer (HSPC) or nonmetastatic castration-resistant prostate cancer (CRPC) who are being treated with androgen receptor inhibitors according to the results of a recent analysis.<span><sup>1</sup></span></p><p>Researchers led by Andrew J. Armstrong, MD, FACP, a professor of medicine at the Duke Cancer Institute Center for Prostate and Urologic Cancers in Durham, North Carolina, conducted a post hoc analysis using data from two phase 3 clinical trials—ARCHES and PROSPER—to evaluate the development of radiographic progression occurring without PSA levels rising or progressing.<span><sup>2, 3</sup></span></p><p>ARCHES included patients with metastatic HSPC treated with enzalutamide plus androgen deprivation therapy (ADT); PROSPER included patients with nonmetastatic CRPC treated with enzalutamide plus ADT.</p><p>The results revealed a discordance between imaging-based progression and PSA changes during enzalutamide treatment.</p><p>“We clearly found that patients were often developing radiographic progression without meeting PSA progression or without even having a rise in PSA,” Dr Armstrong says. “At radiographic progression, about a quarter of all patients had no rise in PSA at all.”</p><p>In ARCHES, 23.2% of patients developed radiographic progression. Among patients treated with enzalutamide plus ADT, 3.5% had no PSA rise, and 8.5% did not meet the parameters of PSA progression at radiographic progression. Among patients with radiographic progression who received enzalutamide plus ADT, 25.3% showed no rise in PSA, and 62.0% did not experience PSA progression; in contrast, the corresponding values were 7.4% and 38.3% for those treated with ADT alone. In PROSPER, 29.3% of patients developed radiographic progression. Among those treated with enzalutamide plus ADT, 4.4% experienced no PSA rise, and 10.3% showed no PSA progression, at the time of radiographic progression. Among patients with radiographic progression, 21.9% had no PSA rise, and 51.3% did not experience PSA progression; in contrast, the corresponding values were 3.6% and 18.8% for patients assigned to the ADT-alone group.</p><p>Commenting on the results, Rana R. McKay, MD, a medical oncologist and professor of medicine and urology at the University of California, San Diego, says, “These data highlight that PSA alone is not going to provide the full story for how someone is doing clinically and should serve as one data point out of other data points. The results reinforce a need for periodic surveillance imaging, even in the metastatic hormone-sensitive and nonmetastatic castration resistant setting.”</p><p>Dr Armstrong agrees. “We are not saying that clinicians have to do imaging as rigorously as we did in the ARCHES study, which was every 3 months. I would do it every 6 months for the first 2 to 3 years; then over time, if the patient is doing well, I mi
根据最近的一项分析结果,前列腺特异性抗原(PSA)监测不应单独用于监测转移性激素敏感前列腺癌(HSPC)或非转移性去雄抵抗前列腺癌(CRPC)患者,这些患者正在接受雄激素受体抑制剂的治疗。由北卡罗莱纳州达勒姆市杜克癌症研究所前列腺和泌尿系统癌症中心医学教授Andrew J. Armstrong MD, FACP领导的研究人员进行了一项回顾性分析,使用了两个3期临床试验(arches和prosper)的数据,以评估在没有PSA水平上升或进展的情况下放射学进展的发展。2,3 arches包括接受恩杂鲁胺加雄激素剥夺治疗(ADT)的转移性HSPC患者;PROSPER纳入了用恩杂鲁胺加ADT治疗的非转移性CRPC患者。结果显示,在恩杂鲁胺治疗期间,影像学进展与PSA变化之间存在不一致。阿姆斯特朗博士说:“我们清楚地发现,患者通常在没有达到PSA进展或PSA甚至没有上升的情况下出现放射学进展。”“在放射学进展中,大约四分之一的患者PSA完全没有上升。”在arch中,23.2%的患者出现影像学进展。在enzalutamide + ADT治疗的患者中,3.5%的患者PSA未升高,8.5%的患者不符合影像学进展时PSA进展参数。在接受恩杂鲁胺加ADT治疗的放射学进展患者中,25.3%的患者PSA未升高,62.0%的患者PSA未进展;相比之下,单独使用ADT治疗组的相应值为7.4%和38.3%。在PROSPER中,29.3%的患者出现影像学进展。在enzalutamide + ADT治疗的患者中,4.4%的患者在放射学进展时没有PSA升高,10.3%的患者没有PSA进展。在影像学进展的患者中,21.9%的患者PSA未升高,51.3%的患者PSA未进展;相比之下,单独使用adt组的相应值分别为3.6%和18.8%。Rana R. McKay医学博士是加州大学圣地亚哥分校的肿瘤学家和医学和泌尿学教授,他在评论这些结果时说:“这些数据强调,PSA本身并不能提供一个人临床表现的全部情况,应该作为其他数据点中的一个数据点。结果强调了定期监测成像的必要性,即使在转移性激素敏感和非转移性去势抵抗的情况下也是如此。”阿姆斯特朗博士对此表示赞同。“我们并不是说临床医生必须像我们在arch研究中那样严格地进行成像,每3个月进行一次。在最初的2到3年里,我会每6个月做一次;然后随着时间的推移,如果病人做得很好,我可能会每6到12个月继续做一次成像。”阿姆斯特朗博士强调,在他们的分析中,不协调的进展事件与症状的出现无关。“我们不能依靠病人告诉我们什么时候做成像;这些都不是由疼痛或任何症状变化引起的,”阿姆斯特朗博士说。“这必须成为他们日常医疗护理的一部分。”
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引用次数: 0
Estradiol patches noninferior to LHRH agonists in locally advanced prostate cancer 雌二醇贴剂治疗局部晚期前列腺癌优于LHRH激动剂
IF 5.6 2区 医学 Q1 ONCOLOGY Pub Date : 2026-08-18 DOI: 10.1002/cncr.70511
Leah Lawrence
<p>Transdermal estradiol (tE2) patches were noninferior to luteinizing hormone–releasing hormone (LHRH) agonists as a form of androgen deprivation therapy (ADT) in patients with locally advanced prostate cancer according to a study published in <i>The New England Journal of Medicine</i>.<span><sup>1</sup></span></p><p>Ruth E. Langley, FRCP, PhD, professor of oncology and clinical trials at University College London in the United Kingdom, and her colleagues conducted a phase 3 noninferiority trial comparing 3-year metastasis-free survival in 1360 patients with locally advanced prostate cancer who were randomly assigned to receive tE2 patches or LHRH agonists. Patients were recruited through the PATCH or STAMPEDE-1 trial networks.</p><p>“In prostate cancer, lowering testosterone is a key part of treatment; for the last 30-40 years, that has been done mainly with LHRH agonists,” says Dr Langley. “When you do this, you get two types of side effects, those from low testosterone and those from low estrogen, which causes symptoms like weakened bones and hot flashes.”</p><p>Previous research into tE2 patches showed that their use did not increase cardiovascular risk and improved quality of life and preservation of bone mineral density in comparison with LHRH agonists, Dr Langley says. With this phase 3 study, Dr Langley and her colleagues wanted to specifically evaluate prostate cancer outcomes and see if similar outcomes could be achieved with fewer side effects with tE2 versus LHRH agonists.</p><p>The observed 3-year metastasis-free survival rate was noninferior with tE2 at 87.1% versus 85.9% with LHRH agonists (hazard ratio [HR] for confirmed metastasis or death, 0.96). The observed 5-year overall survival rates were also similar: 81.1% with tE2 and 79.2% with LHRH agonists (HR for death, 0.90).</p><p>The side-effect profile for each treatment approach varied. Among patients assigned to tE2 only, 44% experienced hot flashes, whereas 89% of patients assigned to LHRH agonists did. In contrast, gynecomastia occurred in 85% of patients assigned to tE2 versus 42% of patients assigned to LHRH agonists.</p><p>“I interpret these data to say that tE2 patches could theoretically be used in lieu of LHRH agonists for people with nonmetastatic hormone-sensitive prostate cancer as long as there is an understanding of the risks and the benefits,” says Rana R. McKay, MD, a medical oncologist and professor of medicine and urology at the University of California, San Diego.</p><p>“Another thing for patients to consider, but this wasn’t quantified in this trial, is that tE2 therapy could potentially have a protective bone effect,” Dr McKay mentions.</p><p>Dr Langley agrees that choosing between these two therapies will be very personal. “Younger men who are going to the gym every day, as an example, may be more concerned with their physical appearance and will not want gynecomastia,” Dr Langley says. “But some men who have experienced the hot flashes and disturbed sleep
根据发表在《新英格兰医学杂志》上的一项研究,在局部晚期前列腺癌患者中,经皮雌二醇(tE2)贴片作为雄激素剥夺治疗(ADT)的一种形式,并不亚于促黄体生成素释放激素(LHRH)激动剂。和她的同事进行了一项3期非劣效性试验,比较了1360名局部晚期前列腺癌患者3年无转移生存率,这些患者被随机分配接受tE2贴片或LHRH激动剂。患者通过PATCH或STAMPEDE-1试验网络招募。“对于前列腺癌,降低睾丸激素是治疗的关键部分;在过去的30-40年里,这主要是用LHRH激动剂进行的,”Langley博士说。“当你这样做的时候,你会有两种副作用,一种是睾丸激素水平低,另一种是雌激素水平低,这会导致骨骼变弱和潮热等症状。”Langley博士说,先前对tE2贴片的研究表明,与LHRH激动剂相比,使用tE2贴片不会增加心血管风险,也不会改善生活质量和保存骨密度。在这项三期研究中,Langley博士和她的同事想要专门评估前列腺癌的结果,看看tE2和LHRH激动剂是否可以在副作用更小的情况下达到相似的结果。观察到的3年无转移生存率,tE2组为87.1%,而LHRH激动剂组为85.9%(确诊转移或死亡的危险比[HR]为0.96)。观察到的5年总生存率也相似:tE2组为81.1%,LHRH激动剂组为79.2%(死亡风险比为0.90)。每种治疗方法的副作用情况各不相同。在仅接受tE2治疗的患者中,44%的患者出现潮热,而接受LHRH激动剂治疗的患者中有89%出现潮热。相比之下,使用tE2的患者中有85%发生了男性乳房发育,而使用LHRH激动剂的患者中有42%发生了男性乳房发育。加州大学圣地亚哥分校医学肿瘤学家、医学和泌尿学教授Rana R. McKay博士说:“我对这些数据的解释是,理论上,tE2贴片可以代替LHRH激动剂用于非转移性激素敏感前列腺癌患者,只要了解其风险和益处。”麦凯博士提到:“患者需要考虑的另一件事是,tE2治疗可能具有保护骨骼的作用,但这在本试验中没有量化。”兰利博士也认为,在这两种疗法之间做出选择是非常个人化的。兰利博士说:“例如,每天都去健身房的年轻男性可能更关心自己的外表,不会想要男性乳房症。”“但一些经历过潮热和睡眠紊乱的男性感到疲惫,可能想要改变。”兰利博士说,要有这两种选择,就需要更公开地讨论患者在开始ADT治疗时的目标。总的来说,拥有这些选项反映了进步。兰利博士说:“如果你回到20年前,那时前列腺癌的治疗效果还不太好,那么人们就很少考虑15年后病人的骨骼健康状况。”“现在,由于结果得到了改善,这些讨论与我们的患者非常相关。”
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引用次数: 0
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Cancer
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