International Journal of Cancer最新文献

{"title":"Deficient Mismatch Repair Represents a Distinct Molecular Feature of Early-Onset Colorectal Cancer in Chinese Single-Center Cohort","authors":"Deng Tang,&nbsp;Zhigang Mao,&nbsp;Siqi Lan,&nbsp;Yali Song,&nbsp;Si Chen,&nbsp;Yuemei Chen,&nbsp;Mi Su,&nbsp;Yufei Tang,&nbsp;Chengyi Zhu,&nbsp;Ruiting Yan,&nbsp;Ji Zhang,&nbsp;Yufang Wang","doi":"10.1002/ijc.70667","DOIUrl":"10.1002/ijc.70667","url":null,"abstract":"<div>\u0000 \u0000 <p>Early-onset colorectal cancer (EOCRC), defined as colorectal cancer diagnosed before the age of 50 years, is increasing worldwide, with a similar trend emerging in China. However, the clinicopathological and mismatch repair features of EOCRC in Chinese patients remain insufficiently characterized. We retrospectively reviewed 23,414 colorectal neoplasia cases diagnosed at West China Hospital between November 2008 and June 2023. Among these, 4,159 colorectal cancer cases with complete immunohistochemical assessment of MLH1, PMS2, MSH2, and MSH6 were included in the primary analysis. Clinicopathological characteristics and mismatch repair status were compared between EOCRC and late-onset colorectal cancer (LOCRC), with additional stratification by documented family history. Multivariable logistic regression was used to evaluate the independent association between early-onset status and deficient mismatch repair (dMMR). Compared with LOCRC, EOCRC showed less favorable clinicopathological features, including higher proportions of poor differentiation, T4 tumors, nodal involvement, and advanced TNM stage. EOCRC also had a significantly higher prevalence of dMMR. In multivariable analysis, early-onset status was independently associated with dMMR in the overall cohort (adjusted OR, 2.27; 95% CI, 1.60–3.22; <i>p</i> &lt; 0.001), and among patients without documented family history (adjusted OR, 1.95; 95% CI, 1.33–2.86; <i>p</i> &lt; 0.001). Patterns of MMR protein loss differed according to documented family history status. In conclusion, EOCRC in this Chinese MMR-tested cohort was associated with more advanced clinicopathological features and a higher prevalence of dMMR, supporting routine MMR assessment in young patients with colorectal cancer.</p>\u0000 </div>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2473-2484"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148648048","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":"De-Escalation of Neoadjuvant Treatment for HER2-Positive Breast Cancer","authors":"Yiyin Ma,&nbsp;Dedian Chen,&nbsp;Sheng Huang","doi":"10.1002/ijc.70614","DOIUrl":"10.1002/ijc.70614","url":null,"abstract":"<p>With improved prognosis in early HER2-positive breast cancer, safely de-escalating treatment is increasingly investigated to minimize overtreatment. This article focuses on neoadjuvant de-escalation strategies for HER2-positive breast cancer. There have been initiatives to shorten the duration of anti-HER2 therapy or to reduce the use of chemotherapy agents. Predictive or prognostic biomarkers and imaging techniques might help to identify subsets of patients within HER2-positive cancer with the best chance of responding to treatment and benefiting from de-escalated treatment.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2393-2402"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70614","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148596928","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":"The Circulating Cholangiocarcinoma Protein Biomarkers CRP and MASP2 Also Predict Gallbladder Cancer Risk","authors":"Linda Zollner,&nbsp;Jeroen Krijgsveld,&nbsp;Dominique Scherer,&nbsp;Justo Lorenzo Bermejo,&nbsp;the EULAT Eradicate GBC Consortium","doi":"10.1002/ijc.70661","DOIUrl":"10.1002/ijc.70661","url":null,"abstract":"<p>In a recent publication, Lapitz et al. reported differences in serum levels that predict the development of cholangiocarcinoma (CCA) in patients with primary sclerosing cholangitis prior to clinical manifestation. We examined whether these biomarkers also predict the risk of gallbladder cancer (GBC) in European prospective plasma samples from 24 GBC cases and 90 control individuals. After logarithmic transformation and quantile normalisation of individual protein levels measured with a timsTOF PRO mass spectrometer, we fitted univariate logistic regression models and applied backward model selection to identify the optimal model for GBC risk prediction. CRP and MASP2, previously reported markers of CCA, were found to be predictive for GBC risk as well (<i>p</i> value &lt; 0.05), and complemented by age at blood sampling, provided an area under the receiver operating characteristic curve of 0.80 (95% confidence interval 0.69–0.92) when combined in a prediction model for GBC risk. We further examined the mRNA expression of CRP and MASP2 in serum samples from 82 GBC cases and 79 control subjects from Chile. CRP mRNA levels were elevated in Chilean GBC cases, but MASP2 showed an opposite trend. While there are considerable differences in the design of the discovery study and ours, the finding that circulating levels of CRP and MASP2 are associated with the risk of both CCA and GBC in Europeans highlights the need for further research into potential shared mechanisms and strategies for the prevention of these two aggressive biliary tumours.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2403-2407"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70661","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148519678","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":"Obesity-Driven Early-Onset Colorectal Cancer: Mechanistic Insights and Emerging Clinical Implications","authors":"Jian Liu,&nbsp;Jia Lu,&nbsp;Cuihong Dai,&nbsp;Yingyu Zhou","doi":"10.1002/ijc.70609","DOIUrl":"10.1002/ijc.70609","url":null,"abstract":"<div>\u0000 \u0000 <p>Early-onset colorectal cancer (EOCRC), defined as colorectal cancer diagnosed before 50 years of age, has increased markedly over the past decades, especially in high-income settings. In parallel, obesity and related metabolic disturbances have become more common in both adults and younger populations, raising the possibility that excess adiposity contributes to the changing EOCRC burden. Epidemiological studies increasingly support this association, particularly for early-life adiposity and persistent metabolic dysfunction. Most EOCRC cases are sporadic, indicating that environmental and lifestyle-related exposures likely play a major role. Among these, obesity may be especially important because it links systemic metabolic stress with intestinal inflammation, microbial imbalance, and epigenetic change. However, the mechanisms through which obesity promotes early colorectal carcinogenesis are still not fully defined. In this review, we examine how obesity may shape EOCRC development across four interacting domains: chronic inflammation, metabolic reprogramming, gut microbiota dysbiosis, and epigenetic remodeling. We also discuss how these pathways may converge during early-life windows of susceptibility and consider their implications for risk identification, prevention, and early intervention in younger populations.</p>\u0000 </div>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2381-2392"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337086","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":"Herpes Zoster as a Marker of Occult Malignancy in Older Adults: A Real-World Cohort Study","authors":"Shih-Wei Lai,&nbsp;Kuan-Fu Liao","doi":"10.1002/ijc.70612","DOIUrl":"10.1002/ijc.70612","url":null,"abstract":"<div>\u0000 \u0000 <p>This study aimed to evaluate whether herpes zoster (HZ) is associated with an increased short-term probability of newly diagnosed cancer in older adults, and to determine whether HZ may serve as an early clinical marker of occult cancer. We conducted a retrospective cohort study using de-identified electronic health record data from the TriNetX Research Network (2006–2024). Adults aged 65–84 years with newly diagnosed HZ were compared with matched controls without HZ. Propensity score matching (1:1) was performed based on demographics and comorbidities. A 1-month lag period was applied to minimize detection bias. The primary outcome was any newly diagnosed cancer. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models within the TriNetX platform. After propensity score matching and applying a 1-month lag period, 182,104 adults in the HZ group and 182,463 controls were included. During the 1-year follow-up, 4527 adults with HZ and 667 controls developed cancer, corresponding to cumulative incidences of 2.49% and 0.37%, respectively. HZ was associated with a higher probability of cancer diagnosis (HR 5.81; 95% CI, 5.35–6.30). In adults aged 65–84 years, HZ is associated with a higher likelihood of a new diagnosis of cancer within 1 year. These findings suggest that HZ may serve as a clinical marker of occult cancer. Further research is warranted to clarify underlying mechanisms and to evaluate whether targeted cancer surveillance following HZ could improve early cancer detection.</p>\u0000 </div>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2431-2436"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337016","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":"DPYD and UGT1A1 Genotype-Based Dosing for Fluoropyrimidines and Irinotecan Chemotherapy: Variant-Specific Impact on Treatment Intensity and Toxicity","authors":"Martina Gambron,&nbsp;Elena Peruzzi,&nbsp;Samantha Perfler,&nbsp;Marcella Montico,&nbsp;Riccardo Cecchin,&nbsp;Elena De Mattia,&nbsp;Michele Spina,&nbsp;Camilla Lisanti,&nbsp;Serena Corsetti,&nbsp;Luisa Foltran,&nbsp;Fabio Puglisi,&nbsp;Rossana Roncato,&nbsp;Erika Cecchin","doi":"10.1002/ijc.70580","DOIUrl":"10.1002/ijc.70580","url":null,"abstract":"<p><i>DPYD</i> and <i>UGT1A1</i> variants significantly affect fluoropyrimidines and irinotecan safety. While genotype-driven dosing reduces severe toxicity, the impact of individual variants remains incompletely investigated. This retrospective cohort study includes 178 cancer patients with a matched actionable <i>DPYD</i> and/or <i>UGT1A1</i> genotypes, defined by the presence of guideline-recommended variants (<i>DPYD</i>: rs3918290, <i>DPYD</i>*2A, c.1905+1G&gt;A; rs55886062, <i>DPYD</i>*13, c.1679T&gt;G; rs67376798, c.2846A&gt;T; rs56038477, c.1236G&gt;A (HapB3); <i>UGT1A1</i>: rs8175347, <i>UGT1A1</i>*28/*37 and rs4148323, <i>UGT1A1</i>*6, c.211G&gt;A), and treated with fluoropyrimidines and/or irinotecan. Patients were classified into standard-of-care (posttreatment genotyping; <i>n</i> = 97) or genotype-driven group (pretreatment genotyping with DPWG-driven dosing; <i>n</i> = 81). Clinically relevant toxicity and relative dose intensity (RDI), a proxy for drug exposure, were evaluated by genotype. Genotype-driven dosing significantly reduced overall clinically relevant toxicity (16.0% vs. 43.3%; <i>p</i> &lt; 0.001). Among <i>DPYD</i> c.1905+1G&gt;A heterozygous carriers, clinically relevant toxicities occurred only within standard-of-care (61.5% vs. 0%, <i>p</i> = 0.007), with lower RDI despite full starting dose (41% [IQR 13–62] vs. 48% [IQR 46–50], <i>p</i> = 0.425). In <i>DPYD</i> c.2846A&gt;T heterozygous carriers, standard-of-care had slightly higher RDI (63% [IQR 54–80] vs. 50% [IQR 43–50], <i>p</i> = 0.007) but doubled toxicity rate (27% vs. 67%, <i>p</i> = 0.092). Conversely, <i>DPYD</i> c.1236G&gt;A (HapB3) heterozygous carriers experienced similarly low toxicity rates (23.7 vs. 13.2, <i>p</i> = 0.375), but genotype-driven dosing markedly reduced RDI (50% [IQR 43–55] vs. 82% [IQR 63–92], <i>p</i> &lt; 0.001). In <i>UGT1A1</i>*28 homozygous carriers, genotype-driven dosing reduced toxicity (21.1% vs. 45.7%, <i>p</i> = 0.086) while preserving comparable RDI (58% [IQR 50–69] vs. 61% [IQR 41–76], <i>p</i> = 0.906). These findings suggest uniform genotype-based strategies may not fully capture variant-specific effects, particularly for <i>DPYD</i> c.1236G&gt;A (HapB3), supporting more flexible dosing approaches.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2512-2524"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70580","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209455","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 Implementation and Oncological Relevance of Molecular Profiling in Brain Metastases Patients—A Multicenter Retrospective Cohort Study","authors":"Maria Nikolaeva,&nbsp;Jacopo Bellomo,&nbsp;Meltem Gönel,&nbsp;Vittorio Stumpo,&nbsp;Victor Egon Staartjes,&nbsp;Flavio Vasella,&nbsp;Kevin Akeret,&nbsp;André Sagerer,&nbsp;Anna Maria Zeitlberger,&nbsp;David Wasilewski,&nbsp;Christopher Krämer,&nbsp;Sven König,&nbsp;Julia Onken,&nbsp;Tareq Juratli,&nbsp;Alexander Köpp,&nbsp;Regina Reimann,&nbsp;Marcus Czabanka,&nbsp;Peter Vajkoczy,&nbsp;Ilker Y. Eyüpoglu,&nbsp;Oliver Bozinov,&nbsp;Michael Weller,&nbsp;Emilie Le Rhun,&nbsp;Luca Regli,&nbsp;Carlo Serra,&nbsp;Marian C. Neidert,&nbsp;Stefanos Voglis","doi":"10.1002/ijc.70611","DOIUrl":"10.1002/ijc.70611","url":null,"abstract":"<p>Brain metastases (BM) require a multidisciplinary treatment approach combining surgery, radiotherapy, and systemic therapy. While current guidelines recommend the analysis of established cancer driver genes in BM tissue, little is known about its real-life implementation and relevance on oncological treatment strategies. This retrospective multicenter study includes patients with BM from melanoma, lung and breast cancer operated between 2010 and 2022. Clinical records were evaluated for BM molecular analyses of predefined cancer drivers and their discordance to extracranial tumor sites, that is, ALK, BRAF, EGFR, KRAS, NTRK for lung, HER2, estrogen/progesterone receptor, BRCA1/2 for breast cancer and BRAF, KIT, NRAS among others for melanoma. Adjustment of systemic therapies based on BM molecular profiles was analyzed. Among 1431 BMs screened for availability of molecular analysis, molecular profiling was performed at least partially in 723 BMs (51%). In cases with matched extracranial tumor samples (<i>n</i> = 276), discordant alterations were found in 18% of lung, 4.7% of melanoma and 45% of breast cancer BMs. Molecular BM analyses informed systemic therapy adjustments in 13%–27% of patients depending on the primary tumor. Overall survival was significantly better in patients who underwent BM profiling, especially when operated in recensst years (median 19.3 vs. 9.9 months; <i>p</i> &lt; 0.0001) and in patients with breast cancer who had a change in systemic therapies upon BM profiling (<i>p</i> = 0.0085). In conclusion, molecular profiling of BM allows selecting available treatment options for a substantial subset of patients. This study underscores the need for more systematic molecular testing in BM patients to guide systemic treatment decisions.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2562-2574"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70611","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148269417","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":"Total Neoadjuvant Treatment for Esophageal Adenocarcinoma With Oligometastases: TNT-OES-1 Trial","authors":"Charlène J. van der Zijden,&nbsp;Tamara J. Huizer,&nbsp;Ben M. Eyck,&nbsp;Ate van der Gaast,&nbsp;Leni van Doorn,&nbsp;Marjolein Y. V. Homs,&nbsp;J. Jan B. van Lanschot,&nbsp;Joost J. M. E. Nuyttens,&nbsp;Lindsey Oudijk,&nbsp;Manon C. W. Spaander,&nbsp;Bas P. L. Wijnhoven,&nbsp;Bianca Mostert,&nbsp;Sjoerd M. Lagarde","doi":"10.1002/ijc.70594","DOIUrl":"10.1002/ijc.70594","url":null,"abstract":"<p>Chemotherapy (FLOT) and chemoradiotherapy (CROSS) are both effective as neoadjuvant regimens for esophageal/junctional cancer. Total Neoadjuvant Therapy (TNT) aims to increase efficacy by combining chemotherapy with chemoradiotherapy. This study aimed to evaluate the feasibility and safety of TNT FLOT-CROSS. Patients with histologically proven esophageal/junctional adenocarcinoma with oligometastases (maximum four lesions in maximum two organs) were included. Treatment consisted of four cycles of FLOT followed by response evaluation (CT-scan). Patients without disease progression proceeded to CROSS, followed by response evaluation (CT-scan, endoscopy with biopsies and endoscopic ultrasonography with fine-needle aspiration on indication). Primary endpoint was the safety and tolerability of TNT FLOT-CROSS. Secondary endpoints included progression-free survival (PFS), disease control rate (DCR), quality of life (QoL) using QLQ-C30 and QLQ-OG25, toxicity and the proportion of patients proceeding to local therapy. Twenty patients were included of whom 16 (80%) had a single metastatic lesion. Median follow-up was 47.9 months (95% CI 32.8–63.1). Fifteen patients (75%) completed TNT FLOT-CROSS. FLOT came with manageable, expected toxicity, and all patients without progression were able to start and complete CROSS. No grade 3–5 toxicities occurred during CROSS. After TNT FLOT-CROSS, two patients underwent surgery. The 1- and 2-year PFS were 40% and 13%, respectively. Three months after TNT FLOT-CROSS completion, DCR was 55%. Dysphagia scores significantly decreased over time, while fatigue significantly increased. Sequencing TNT FLOT-CROSS in patients with oligometastatic esophageal adenocarcinoma is feasible and comes with manageable toxicity and promising efficacy, with a 1-year progression free survival of 40%.</p><p><b>Trial Registration:</b> Dutch trial register, NL9269</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2552-2561"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70594","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148269477","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":"Changing the History of Science—An Editorial Perspective on Critical Developments in Current Citation Practice, “Forgetting” the Pioneers of Scientific Discoveries","authors":"Heike Allgayer,&nbsp;Petra Boukamp","doi":"10.1002/ijc.70685","DOIUrl":"10.1002/ijc.70685","url":null,"abstract":"&lt;p&gt;Sixty years have passed since the &lt;i&gt;International Journal of Cancer&lt;/i&gt; launched its first publication in 1966, and we would like to take this opportunity to congratulate the Journal on this jubilee. Tremendous developments in science and medicine have been seen and reported during the history that passed since then, and many changes have taken place in the way how we observe, conduct, publish, and rank the importance of science. Many of these changes have increased our knowledge immensely and led to iconic changes and improvements for humankind, for example for the diagnosis, treatment, or the prevention of cancer.&lt;/p&gt;&lt;p&gt;However, some developments in the more and more professionalized world of publishing and selling research have also given rise to concern. In this Editorial, we would like to bring attention to a particular development in publication practice that we consider worrisome, which seems to become an increasing trend within habits of acknowledging and citing, or rather not citing, earlier pioneering references within scientific original publications and reviews. Specifically, during the last years it has become evident that a growing number of publications tend to cite mainly recent publications in the field and particularly recent reviews that, themselves, frequently rely on citations of the latest previous reviews. Thereby, they tend to ignore and miss seminal papers that have been published in the past by the scientific pioneers in the respective field.&lt;/p&gt;&lt;p&gt;As an example, in a pioneering phase starting at the end of the 1980s and lasting through the 1990s, many pioneers in the field discovered, and described in utmost detail, the essential molecular function of tumor-associated proteases in all major steps of the metastatic cascade of cancer cells. Certainly, also the &lt;i&gt;International Journal of Cancer&lt;/i&gt; took its part in the early publications on this topic. Some of the proteases, especially the urokinase (u-PA) system with u-PA, the receptor u-PAR, and the inhibitor PAI-1, were shown at this time to be highly relevant, not only for migration, invasion, metastasis, and associated molecular signaling, but also for patient survival, prognosis, minimal residual disease, or tumor recurrence. This knowledge was driven by many protagonists in Europe, for example, the Finsen Laboratory Denmark, basic, translational and clinical research groups in Germany, Italy, the Netherlands, and further European countries, as well as groups in the United States (e.g., [&lt;span&gt;1-26&lt;/span&gt;], and briefly reviewed again recently in [&lt;span&gt;27&lt;/span&gt;]). This list of publications is by far not complete and many further publications by these and further groups were published at these early times. While the u-PA/u-PA-R system seems to regain international attention at present, in many recent publications on this topic (e.g., [&lt;span&gt;28, 29&lt;/span&gt;]), however, the many pioneering pieces of work of the early phase mentioned above are rather ignored, and acc","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2377-2380"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70685","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663004","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":"Impact of Reimbursement on the Utilisation of Gene Expression Profiles and Chemotherapy Decision-Making in Dutch Breast Cancer Patients: A Population-Based Study","authors":"Joyce Meijer,&nbsp;Nienke Hermanns,&nbsp;Rhodé Bijlsma,&nbsp;Hedwig M. Blommestein,&nbsp;Desiree H. J. G. van den Bongard,&nbsp;Thijs van Dalen,&nbsp;Paul J. van Diest,&nbsp;Caroline A. Drukker,&nbsp;Cristina Guerrero Paez,&nbsp;Aafke H. Honkoop,&nbsp;Agnes Jager,&nbsp;Linetta B. Koppert,&nbsp;Sabine C. Linn,&nbsp;Marissa C. van Maaren,&nbsp;Ester J. Siemerink,&nbsp;Laura J. van ’t,&nbsp;José H. Volders,&nbsp;Marie Jeanne Vrancken Peeters,&nbsp;Sabine Siesling","doi":"10.1002/ijc.70571","DOIUrl":"10.1002/ijc.70571","url":null,"abstract":"<p>This study examined gene expression profile (GEP) use in relation to reimbursement policies and chemotherapy administration, both for patients with and without GEP indication. Women aged ≥ 18–69 years and diagnosed with early-stage breast cancer between January 2011 and June 2024 were selected from the Netherlands Cancer Registry. GEP use in relation to reimbursement policies and GEP result in relation to chemotherapy administration was analysed using flowcharts and a trend line. For patients with GEP indication, logistic regression analyses were conducted to determine if the reimbursement periods influenced the GEP use, and GEP use was analysed per region in the Netherlands and incidence year using trend lines. In total, 138,765 patients were included. Among 17,525 patients with GEP indication, proportions of patients who received a GEP were higher during retrospective reimbursement (25%) and publicly known reimbursement (37%) compared with no reimbursement (9%) and differed across regions in the Netherlands. Proportions of patients who did not receive chemotherapy were higher for patients who had a low-risk MammaPrint (93%) or Oncotype DX (97%) result compared with patients who had a high-risk MammaPrint (17%) or Oncotype DX (15%) result. Among 13,003 patients with GEP indication who did not receive GEP, 52% did receive chemotherapy. Approximately one-third of patients who met GEP criteria and were eligible for publicly known reimbursement received a GEP. Appropriate follow-up steps and further research seem required to analyse reasons for not ordering a GEP in times of reimbursement, since GEP results help chemotherapy decision-making.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 10","pages":"2485-2497"},"PeriodicalIF":4.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70571","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161057","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}