International Journal of Cancer最新文献

{"title":"Long-term risk of major cardiac events in breast cancer patients treated with intensity-modulated and 3-dimensional conformal radiotherapy: Secondary analysis of a randomized clinical trial.","authors":"Nam Kyu Kang, Kyu Hye Choi, Jae Uk Jeong, Sung Ja Ahn, Mina Yu, Jin Hee Kim, Bae Kwon Jeong, Han Byul Kang, Hyo Chun Lee, Jong Hoon Lee","doi":"10.1002/ijc.35476","DOIUrl":"10.1002/ijc.35476","url":null,"abstract":"<p><p>We assess the relationship between radiation dose to the heart and cardiac disease within the context of modern radiotherapy techniques of 3-dimensional and intensity-modulated radiotherapy (IMRT). The KROG 15-03 study was a multicenter phase III trial involving 693 breast cancer patients who underwent breast-conserving surgery (BCS). Patients were randomly assigned to receive either IMRT or 3D-CRT following BCS. Major cardiac event (MCE), defined as the occurrence of angina pectoris or myocardial infarction requiring coronary angiography, and admission for cardiac arrhythmia related to the irradiation of the heart. The primary outcome of the study was to investigate the incidence of MCE and factors associated with MCEs. At a median follow-up of 6.5 years, the incidence of MCEs at 6.5 years was 1.8%. The mean heart dose (MHD) for the entire cohort of 647 patients was 2.1 (±2.3) Gy. The cumulative incidence of MCEs at 6.5 years was 1.1% for the subgroup of MHD <2.9 Gy and 3.3% for the subgroup of MHD >2.9 Gy (p = 0.010), and 0.9% for the subgroup of age ≤55 years and 3.3% for the subgroup of age >55 years (p = 0.006), respectively. Multivariate analyses confirmed that MHD (p = 0.044; hazard ratio [HR], 1.21 per 1 Gy; 95% confidence interval [CI], 1.09-1.46) and age (p = 0.034; HR, 1.07 per 1 year; 95% CI, 1.03-1.14) were significant factors of MCEs. The incidence of MCE increased by 21% per 1-Gy increase in MHD within 6.5 years after radiotherapy.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"1395-1404"},"PeriodicalIF":4.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954222","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":"Characterization of bridging therapies in clinical trials leading to FDA approval of CAR-T cell therapies.","authors":"Victoria Kaestner, Alyson Haslam, Vinay Prasad","doi":"10.1002/ijc.35473","DOIUrl":"10.1002/ijc.35473","url":null,"abstract":"<p><p>During the time of chimeric antigen receptor T-cell (CAR-T) manufacturing, bridging therapy is often used to control disease. Because it often involves systemic treatment, the bridging therapies can induce responses and/or adverse events. We sought to assess bridging therapies used in CAR-T trials in a cross-sectional study. We reviewed FDA drug labels and peer-reviewed registration trial reports (including supplemental data) to evaluate the characteristics of bridging therapy used in trials testing CAR-T therapies. We looked at which bridging therapies were used, whether multiple therapies were combined, the response rates, and the reported adverse events associated with bridging therapy. Of the 11 studies testing CAR-T therapies, 10 reported the bridging therapies that were used in the study. Of those that reported the types of bridging therapies (n = 10), the most commonly used bridging therapy was dexamethasone (10/10, 100%), rituximab (6/10, 60%), gemcitabine (5/10, 50%), and etoposide (5/10, 50%). Of the trials, one of 11 (9%) clearly reported whether patients had responses to bridging therapy, six of 11 (55%) vaguely reported responses, and four of 11 (36%) trials did not report or mention any response information regarding bridging therapy. Although patients are often refractory to first-line therapies, which share considerable overlap with bridging therapies, these therapies may induce responses. Despite this possibility, the reporting of bridging therapy combinations and their subsequent response rates and adverse event rates are highly variable. These findings highlight the need for greater transparency in the reporting of bridging therapy to more reliably assess the efficacy of CAR-T therapies.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"1376-1385"},"PeriodicalIF":4.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109317","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":"Cigarette smoke induces expression of senescence markers and pro-inflammatory SASP in oral mucosa: Potential implications for early carcinogenic processes.","authors":"Martín Pérez-Leal, Cristina Estornut, Lourdes Alfaro-Ochoa, Germán Sánchez-Herrera, Inés Roger, Paula Montero, Santiago Arias-Herrera, Nicla Flacco","doi":"10.1002/ijc.70178","DOIUrl":"https://doi.org/10.1002/ijc.70178","url":null,"abstract":"<p><p>Oral squamous cell carcinoma, a leading global cause of cancer-related morbidity, is strongly associated with tobacco cigarette use. This study investigates the role of cigarette smoke in inducing cellular senescence and inflammation in oral mucosa, which may contribute to the development of oral cancer through mechanisms such as the senescence-associated secretory phenotype (SASP). Biopsies from smokers and non-smokers were analyzed using quantitative polymerase chain reaction to assess the expression of senescence markers p21, p16, and laminB1. Immunohistochemistry was performed to evaluate p21 and p16 expression in the tissues. In vitro experiments were conducted using primary oral keratinocytes (human oral keratinocytes [hOK]) and fibroblasts (human oral fibroblast [hOF]) exposed to increasing concentrations of cigarette smoke extract (CSE) for 72 h. Additionally, a three-dimensional (3D) reconstituted oral mucosa model was exposed to 5% CSE for 72 h, and senescence markers were analyzed by real-time quantitative polymerase chain reaction. Flow cytometry was performed in hOF after 72 h at 2% CSE to assess senescence-associated beta-galactosidase (SA-β-gal) activity. Smokers' biopsies showed a significant increase in p21 and p16 expression and a decrease in laminB1 compared with non-smokers. Immunohistochemistry confirmed increased p21 and p16 in smokers. In vitro, ≥2% CSE induced similar senescence patterns in hOK and hOF, with dose-dependent interleukin (IL)-6 and IL-8 secretion. The 3D oral mucosa model showed comparable changes in all three senescence markers. Exposure to 2% CSE increased SA-β-gal activity in hOF. Taken together, cigarette smoke exposure induces cellular senescence and inflammation in the oral mucosa. The pro-inflammatory response associated with SASP may contribute to the development of a pro-tumoral microenvironment in the oral cavity, promoting early oral carcinogenesis.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145190508","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":"Novel therapeutic strategy targeting STMN1 using chlorambucil-conjugated pyrrole-imidazole polyamide in small cell lung cancer.","authors":"Ryohei Yoshikawa, Takayoshi Watanabe, Yoichi Ohtaki, Toshikazu Bando, Hiroshi Sugiyama, Takuya Araki, Hideaki Yashima, Bilguun Erkhem-Ochir, Haruka Okami, Gendensuren Dorjkhorloo, Ikuma Shioi, Toshiteru Nagashima, Natsuko Kawatani, Tomohiro Yazawa, Eiji Narusawa, Takayuki Kosaka, Osamu Kawashima, Mitsuhiro Kamiyoshihara, John D Minna, Luc Girard, Ken Shirabe, Hiroki Nagase, Kimihiro Shimizu, Takehiko Yokobori","doi":"10.1002/ijc.70179","DOIUrl":"https://doi.org/10.1002/ijc.70179","url":null,"abstract":"<p><p>Small cell lung cancer (SCLC) is aggressive, with limited treatment progress for decades. Stathmin 1 (STMN1) is a cytoplasmic phosphorylated protein that is specific to cancerous tissues including SCLC and is associated with malignancy. Pyrrole-imidazole polyamide (PIP) compounds decrease gene expression by binding to specific DNA sites and disturbing RNA transcription. In this study, we synthesized a novel chlorambucil-conjugated PIP compound targeting both the STMN1 promoter and STMN1 DNA sequences (Chb-STMN1 PIP) to evaluate its therapeutic efficacy against SCLC. We examined the expression of STMN1 in surgically resected tissues and cell line database. Suppression of STMN1 by Chb-STMN1 PIP was analyzed using RT-PCR, WB, and CAGE-seq in vitro. The anti-tumor effects of Chb-STMN1 PIP were evaluated in vitro and in vivo. STMN1 mRNA expression was higher in cell lines with more STMN1 copy number alterations. In vitro studies showed that Chb-STMN1 PIP treatment resulted in significant STMN1 suppression and cell viability reduction compared to the control groups. Administration of Chb-STMN1 PIP to an SCLC xenograft mouse model also showed a tumor reduction effect and significantly suppressed angiogenesis, proliferation potency, and cell viability of SCLC. CAGE analysis indicated that the expression of STMN1 was suppressed in Chb-STMN1 PIP-treated cells compared to that in control cells. A novel compound, Chb-STMN1 PIP, induced significant anti-tumor effects and suppressed STMN1 expression in SCLC cell lines. Furthermore, SCLC xenograft mouse models showed tumor shrinkage and reduced malignant properties. Targeting STMN1 with our developed PIP compound appears to be a novel strategy and promising in SCLC.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145190564","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":"Solute carrier family 2 member 3: A central mediator in aerobic glycolysis contributing to tumor malignant progression.","authors":"Yuan Li, Jinlong Tang, Xiujing Wu, Honghe Zhang","doi":"10.1002/ijc.70180","DOIUrl":"https://doi.org/10.1002/ijc.70180","url":null,"abstract":"<p><p>The solute carrier family 2 member 3 (SLC2A3) gene, located on human chromosome 12p3.3, encodes the glucose transporter 3 protein, which exhibits a notably high affinity for glucose and a substantial capacity to ferry glucose from extracellular fluid into the cytoplasm across the plasma membrane. SLC2A3 is frequently upregulated in various tumors, playing a pivotal role in aerobic glycolysis and thereby furnishing vital energy for tumor sustenance and malignant advancement, particularly in adverse conditions. Importantly, SLC2A3 exerts influence on multiple signaling pathways, particularly through the establishment of several positive feedback loops that amplify oncogenic effects, solidifying its status as a key oncogene in numerous malignancies. Such upregulation contributes significantly to uncontrolled proliferation, migration, invasion, distant metastasis, poor prognosis, and chemoresistance. Encouraging research has pinpointed certain potent and synergistic treatment effects via novel small molecules, including microRNAs directly targeting SLC2A3 or impacting associated signaling pathways in some tumors, particularly in tumors exhibiting chemoresistance. Therefore, disrupting the SLC2A3-mediated aerobic glycolysis appears to be a practical and feasible strategy to augment chemotherapeutic efficacy and potentially reverse chemoresistance.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145190535","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":"Incidence patterns and temporal trends of childhood cancer in Germany, 1980-2019: Forty years of childhood cancer registration in Germany.","authors":"Friederike Erdmann, Maike Wellbrock, Claudia Trübenbach, Desiree Grabow, Martin Schrappe, Peter Kaatsch, Claudia Spix, Joachim Schüz, Cécile M Ronckers","doi":"10.1002/ijc.70167","DOIUrl":"https://doi.org/10.1002/ijc.70167","url":null,"abstract":"<p><p>Comparing incidence patterns over time and between populations stimulates aetiological research and informs health policy. With this report, we provide the first comprehensive assessment and interpretation of 40 years of childhood cancer registration data and observed incidence patterns and time trends in Germany. We identified all incident childhood cancer cases diagnosed before the age of 15 years between 1980 and 2019 from the German Childhood Cancer Registry (N = 65,163) and examined incidence patterns and temporal trends. Over the entire period (1980-2019), boys were more frequently diagnosed than girls, children aged <5 years had the highest age-specific incidence rates and age-standardised incidence rates (ASR) were highest for leukaemias and CNS tumours. Trend analyses indicated a statistically significant increase in ASRs for childhood cancer overall (from 122.8/million in 1980-1989 to 173.4/million in 2010-2019) as well as across diagnostic groups and age groups. The steepest increase (on average 4.9% per annum for all cancer diagnoses combined) occurred in the initial years of registration (1980-1987), mostly driven by the sharp increase in the reporting of CNS tumours diagnoses, soft tissue sarcoma and germ cell tumours. Since the 1990s, temporal patterns were more heterogeneous across diagnostic groups; yet overall, less pronounced than during the build-up phase of the registry. Various factors have influenced the observed incidence patterns in Germany over the 40-year registration period. The steep increase in ASRs during the early years is primarily attributable to improvements in case reporting and registration. Explanations for the more recent temporal patterns remain speculative.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184227","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":"Metastatic osteosarcoma, patterns of care and outcomes of patients in a real-life national setting over a decade.","authors":"Mathilde Reich, Derek Dinart, Hélène Bellio, Juliane Berchoud, Myriam Jean-Denis, Maeva Bonneau, Sarah Winter, Maxime Brunet, Romain Duong, Simon Nannini, Justine Gantzer, Berengère Narciso, Sophie Piperno-Neumann, Thibaud Valentin, Perrine Marec-Berard, Mehdi Brahmi, Emmanuelle Bompas, Philippe Anract, François Goldwasser, Raul Perret, Axel Le Cesne, Nathalie Gaspar, Pascaline Boudou-Rouquette, Carine Bellera, Maud Toulmonde","doi":"10.1002/ijc.70157","DOIUrl":"https://doi.org/10.1002/ijc.70157","url":null,"abstract":"<p><p>Metastatic osteosarcoma (MOS) has a poor prognosis, and few treatment options. This multicentre observational study provides real-world data on treatment patterns of patients with MOS in France. The primary objective was to describe treatment modalities of patients with MOS aged ≥12 years treated in 11 reference network centers. Secondary objectives were to assess time to next treatment (TTNT), overall survival (OS) and prognostic factors for TTNT and OS. From 2008 to 2018, 262 patients with MOS were included; 88 patients were metastatic at diagnosis, and 174 patients had a metastatic relapse. Median age at diagnosis was 26 (12-86). A total of 227 (86.6%) patients received systemic treatment in the metastatic setting, and 75 (28.6%) patients received more than two lines. Overall, 153 (58.4%) patients underwent at least a loco-regional procedure, and 50 patients (19.1%) participated in a clinical trial in the metastatic setting. Median OS from metastasis diagnosis was 21.5 months [95% CI 18.9-27.0], 23.0 months [95% CI 15.0-31.1] in the synchronous cohort, and 21.4 months [95% CI 18.7-29.7] in the metachronous cohort. Median TTNT was 8.2 months [95% CI 6.7-9.9], 5.7 months [95% CI 4.2-7.2], 3.7 months [95% CI 3.0-4.3], and 2.9 months [95% CI 1.8-3.9] in first, second, third, and fourth line. It was 7.6 months [95% CI 5.1-12.5], 6 months [95% CI 3.6-8.7], and 4.8 months [95% CI 2.9-7.5] for tyrosine kinase inhibitors such as regorafenib or cabozantinib in first, second, and third line. In MOS, the benefit of chemotherapy after first line is limited. TKIs show encouraging activity from first line. Inclusion in clinical trials should be prioritized.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184292","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":"Linkage disequilibrium score regression identifies genetic correlations between hepatocellular carcinoma and clinically relevant traits.","authors":"Younghun Han, Vikram R Shaw, Jinyoung Byun, Aaron P Thrift, Catherine Zhu, Donghui Li, Rikita I Hatia, Robin Kate Kelley, Sean P Cleary, Anna S Lok, Paige M Bracci, Jennifer B Permuth, Roxana Bucur, Jennifer Knox, Jian-Min Yuan, Amit G Singal, Prasun K Jalal, R Mark Ghobrial, Yuko Kono, Dimpy P Shah, Mindie H Nguyen, Neehar D Parikh, Richard Kim, Hui-Chen Wu, Hashem El-Serag, Ping Chang, Yun Shin Chun, Jian Gu, Chad Huff, Asif Rashid, Lu-Yu Hwang, Alison P Klein, Saira A Khaderi, Ahmed O Kaseb, Kathrine A McGlynn, Lewis R Roberts, Manal M Hassan, Christopher I Amos","doi":"10.1002/ijc.70136","DOIUrl":"https://doi.org/10.1002/ijc.70136","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) mortality is increasing globally, partly due to the growing prevalence of nonviral liver diseases. Genome-wide association studies (GWAS) have identified genetic variants associated with HCC development. Leveraging GWAS summary statistics and linkage disequilibrium score regression (LDSR), we investigated disease co-development with hepatitis C virus-negative (HCV-negative) HCC to provide unique insights into HCC etiology and prioritize relationships for further causal inquiry. We utilized the LDSR statistical framework to estimate the genetic correlation and heritability between HCV-negative HCC with 901 epidemiologic, behavioral, and clinical traits from the United Kingdom Biobank (UKBB). First, we set the threshold for observed scale heritability of each trait at 0.02 to ensure reliable inferences with adequate study power. Next, we observed significant positive genetic correlations between HCV-negative HCC and blood-based biomarkers of liver injury (ALT, GGT) and allostatic load (including glycated hemoglobin, blood pressure, and total albumin). We also identified a positive genetic correlation between HCV-negative HCC and diseases associated with metabolic dysfunction-associated steatotic liver disease (MASLD), including diabetes, hypertension, chronic ischemic heart disease, and others. Taken together, our results help to identify polygenic and pleiotropic signals related to different phenotypic traits associated with HCC and support further exploration of the predictive power of blood-based biomarkers identified in this study for inferring HCC development among HCV-negative individuals.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172177","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":"New cell lines expanding the diversity of Ewing sarcoma models.","authors":"Maximilian Kerkhoff, Christiane Schaefer, Wilhelm G Dirks, Dawid Krzeciesa, Maximilian Bretschneider, Pauline R Plaumann, Wiebke K Guder, Arne Streitbürger, Sonja Herter, Heike Peterziel, Ina Oehme, Felina Zahnow, Thomas G P Grünewald, Uta Dirksen","doi":"10.1002/ijc.70172","DOIUrl":"https://doi.org/10.1002/ijc.70172","url":null,"abstract":"<p><p>Ewing sarcoma (EwS) is a highly aggressive, malignant, solid tumor of childhood, and adolescence. Most EwS develop in bone, while it originates from connective, adipose, or muscle tissue less frequently. We report the establishment of new human EwS cell lines, all of which carry a t(11;22)(q24;q12) translocation generating the oncogenic transcription factor EWSR1::FLI1. Sequencing of the chimeric mRNAs indicated genomic DNA breakpoints localized in intron 8 of the EWSR1 gene and three different introns of the translocation partner gene FLI1. While three EwS cell lines carry the EWSR1::FLI1 fusions of ex7/ex6 (type I) or ex7/ex5 (type II), the EWSR1::FLI1 fusion variant ex7/ex7 (type IV) is described for the first time in a continuous EwS model. The cell lines presented genomic, epigenomic, and transcriptomic stability over a period of 6 months, though some variations in the chromosomal aberrations were observed in one cell line. TP53, STAG2, and CDKN2A/B mutations were the most frequent and most relevant mutations in our cell line panel. The TP53 mutational status seemed to have the biggest impact on drug sensitivity profiles. The new EwS models presented here may help to identify small molecule inhibitors that act directly on EWSR1::FLI1 fusion proteins or uncover other genetic vulnerabilities of the altered epigenome and transcriptome in EwS, which would contribute to a better understanding of Ewing sarcoma tumorigenesis.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147058","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":"Prospective inter-individual analysis of quality-adjusted life years (QALYs) in brain tumor patients: A comprehensive assessment of health preferences.","authors":"Lisa S Hönikl, Anna Kelm, Sandro M Krieg, Bernhard Meyer, Vicki M Butenschoen","doi":"10.1002/ijc.70171","DOIUrl":"https://doi.org/10.1002/ijc.70171","url":null,"abstract":"<p><p>Eloquent intracranial tumors, whether primary or secondary, are located in brain regions critical for language, motor, or sensory function. In neuro-oncology, evaluating treatment outcomes requires more than survival analysis alone. Quality-adjusted life years combine survival and quality of life, based on numerical health preference values reflecting how patients perceive specific health states. However, such data are lacking for patients with eloquent tumors. In this prospective, single-center cohort study (2016-2019), patients with eloquent brain tumors underwent standardized assessments at four time points: preoperative, postoperative, and at 3- and 6-month follow-ups. Instruments included Time Trade-Off (TTO), Standard Gamble, EuroQol 5 Dimensions (EQ-5D), and the Beck Depression Inventory (BDI). Patients indicated how many years from a 10-year life span they would trade to live in perfect health, including for hypothetical deficits like hemiparesis, aphasia, or dependency. The resulting values (range 0-1) were calculated and analyzed using Mann-Whitney U-tests. Preoperatively, 78 patients reported high quality of life (TTO median 0.9). EQ-5D index declined significantly after surgery (p < .05), while TTO and BDI scores remained stable, reflecting a deterioration in health. At 3 months (n = 23), dependency was rated as less severe compared to preoperative (p = .055; TTO 0.2 vs. 0.5), suggesting psychological adaptation. By 6 months (n = 8), health perceptions improved, indicating resilience (TTO 0.7 vs. 0.6 at 3 months). This is the first study to quantify health preferences in patients with eloquent brain tumors. While postoperative health status initially declines, resilience and adaptation occur over time, emphasizing the need for tailored postoperative care.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136052","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}