Cancer最新文献

{"title":"Racial differences in multiple myeloma survival: Associations with stem cell transplantation, insurance, and Medicaid expansion","authors":"F. Lennie Wong PhD,&nbsp;Scott R. Goldsmith MD,&nbsp;Kimlin Ashing PhD,&nbsp;Amrita Krishnan MD,&nbsp;Michael A. Rosenzweig MD,&nbsp;Saro H. Armenian DO, MPH","doi":"10.1002/cncr.70596","DOIUrl":"10.1002/cncr.70596","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>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).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>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).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 17","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cncr.70596","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838671","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}

{"title":"Cancer statistics for Asian American, Native Hawaiian, and Pacific Islander people, 2026","authors":"Nikita Sandeep Wagle PhD, MBBS, MHA,&nbsp;Angela N. Giaquinto MSPH,&nbsp;Mandi Yu PhD,&nbsp;Hyuna Sung PhD,&nbsp;Tyler B. Kratzer MPH,&nbsp;Kekoa Taparra MD, PhD, MPH,&nbsp;Jessica Star MA, MPH,&nbsp;Ahmedin Jemal DVM, PhD,&nbsp;Rebecca L. Siegel MPH","doi":"10.1002/cncr.70584","DOIUrl":"10.1002/cncr.70584","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 17","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cncr.70584","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148823580","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}

{"title":"Vimseltinib for patients with tenosynovial giant cell tumor: A multicenter, open-label, phase 2 trial","authors":"Silvia Stacchiotti MD,&nbsp;Jean-Yves Blay MD, PhD,&nbsp;Piotr Rutkowski MD, PhD,&nbsp;Hans Gelderblom MD, PhD,&nbsp;Alejandro Falcón MD, PhD,&nbsp;Axel Le Cesne MD,&nbsp;Jayesh Desai MBBS, FRACP,&nbsp;Emanuela Palmerini MD, PhD,&nbsp;César Serrano MD, PhD,&nbsp;Kristen N. Ganjoo MD,&nbsp;Gina Z. D’Amato MD,&nbsp;Christopher W. Ryan MD,&nbsp;Breelyn A. Wilky MD,&nbsp;Virginia Ferraresi MD,&nbsp;Ramy Saleh MD, MSc, FRCPC,&nbsp;Vinod Ravi MD, MS, MBA,&nbsp;Albiruni Abdul Razak MB BCh, BM BCh,&nbsp;Antonio Casado Herráez MD, PhD,&nbsp;Mahbubl Ahmed MBBS, PhD,&nbsp;Nicholas M. Bernthal MD,&nbsp;Michiel van de Sande MD, PhD,&nbsp;Mehdi Brahmi MD, PhD,&nbsp;Bartlomiej Szostakowski MD, PhD,&nbsp;Jasmine Sen MS,&nbsp;Nicholas A. Zeringo PhD,&nbsp;Brooke Harrow PhD,&nbsp;Supraja Narasimhan PhD,&nbsp;Amanda Saunders DO,&nbsp;Maitreyi G. Sharma MD,&nbsp;Matthew L. Sherman MD,&nbsp;Andrew J. Wagner MD, PhD,&nbsp;William D. Tap MD","doi":"10.1002/cncr.70564","DOIUrl":"10.1002/cncr.70564","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Tenosynovial giant cell tumor (TGCT) is a locally aggressive neoplasm caused by dysregulation of the colony-stimulating factor 1 (<i>CSF1</i>) 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 (<i>n</i> = 46; prior imatinib/nilotinib allowed), and cohort B included patients who received prior specific agents (<i>n</i> = 20).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 17","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13507761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148816887","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}

{"title":"Gynecologic cancers in low- and middle-income countries: Bridging the survival gap","authors":"Dewi Setiawati SpOG,&nbsp;Wachyudi Muchsin SKed, SH, MKes, CMed,&nbsp;Alfi Sophan SSi, MSi","doi":"10.1002/cncr.70518","DOIUrl":"10.1002/cncr.70518","url":null,"abstract":"<p>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.</p>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 17","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond risk factors: A capacity framework for cancer survivorship research","authors":"Keith M. Bellizzi PhD, MPH","doi":"10.1002/cncr.70582","DOIUrl":"https://doi.org/10.1002/cncr.70582","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 17","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blinatumomab administration in the outpatient setting: Safety and health care utilization","authors":"Yannis K. Valtis MD,&nbsp;Benjamin F. Frost MD,&nbsp;David Nemirovsky MA,&nbsp;Andriy Derkach PhD,&nbsp;Kuo-Kai Chin MD,&nbsp;Meira Yisraeli Salman MD,&nbsp;Leora Boussi MD,&nbsp;Natalia Tijaro Ovalle MD,&nbsp;Emilie Baxter BA,&nbsp;Ann Mercurio MD,&nbsp;Eytan M. Stein MD,&nbsp;Mark B. Geyer MD,&nbsp;Deborah Schrag MD, MPH,&nbsp;Amar H. Kelkar MD,&nbsp;Daniel J. DeAngelo MD,&nbsp;Marlise R. Luskin MD,&nbsp;Jae H. Park MD,&nbsp;Evan C. Chen MD","doi":"10.1002/cncr.70566","DOIUrl":"https://doi.org/10.1002/cncr.70566","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>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).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>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%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>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.</p>\u0000 </section>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 16","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"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}

{"title":"Clinical trial skepticism influenced by political ideology","authors":"Leah Lawrence","doi":"10.1002/cncr.70514","DOIUrl":"https://doi.org/10.1002/cncr.70514","url":null,"abstract":"&lt;p&gt;Approximately 1 in 4 people believe that clinical trials should be approached with suspicion according to data recently published in &lt;i&gt;JAMA Network Open&lt;/i&gt;, with political ideology appearing to influence levels of skepticism.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;“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.”&lt;/p&gt;&lt;p&gt;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).&lt;/p&gt;&lt;p&gt;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).&lt;/p&gt;&lt;p&gt;Similar trends were seen among respondents who were cancer survivors.&lt;/p&gt;&lt;p&gt;The study researchers called the implications of these data both “pragmatic and urgent.”&lt;/p&gt;&lt;p&gt;“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.”&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;“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.”&lt;/p&gt;&lt;p&gt;Instead, Dr O’Regan suggests that clinicians focus on tactics for enrolling patie","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.70514","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784368","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}

{"title":"PSA monitoring alone proves inadequate for detecting prostate cancer progression","authors":"Leah Lawrence","doi":"10.1002/cncr.70512","DOIUrl":"https://doi.org/10.1002/cncr.70512","url":null,"abstract":"&lt;p&gt;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.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;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.&lt;span&gt;&lt;sup&gt;2, 3&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;The results revealed a discordance between imaging-based progression and PSA changes during enzalutamide treatment.&lt;/p&gt;&lt;p&gt;“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.”&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;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.”&lt;/p&gt;&lt;p&gt;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","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.70512","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784137","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}

{"title":"Estradiol patches noninferior to LHRH agonists in locally advanced prostate cancer","authors":"Leah Lawrence","doi":"10.1002/cncr.70511","DOIUrl":"https://doi.org/10.1002/cncr.70511","url":null,"abstract":"&lt;p&gt;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 &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;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.&lt;/p&gt;&lt;p&gt;“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.”&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;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).&lt;/p&gt;&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;“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.&lt;/p&gt;&lt;p&gt;“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.&lt;/p&gt;&lt;p&gt;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","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.70511","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784369","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}