International Journal of Cancer最新文献

{"title":"Cell Line Authentication Reveals HeLa-Derived Contamination of SACC-83 and SACC-LM in Adenoid Cystic Carcinoma Research.","authors":"Cuijie Chen, Xiankun Zhao, Xuekun Chen, Yuzhen Gao","doi":"10.1002/ijc.70771","DOIUrl":"https://doi.org/10.1002/ijc.70771","url":null,"abstract":"<p><p>SACC-83 was established in 1990 from a patient with adenoid cystic carcinoma, with SACC-LM as its lung-metastatic subline derived through in vivo selection in nude mice. Although several other purported ACC cell lines have already been reported as cross-contaminated, the true origin of SACC-83 and SACC-LM has remained unclear despite their wide use in the field. To address this, we carried out short tandem repeat (STR) profiling on 10 SACC-83 and SACC-LM samples submitted from six independent laboratories across China during our routine authentication work. Statistical analysis using the classic Tanabe comparison algorithm on the CLASTR website returned matches to multiple common cell line contaminants. Among these, comparison with HeLa yielded a random match probability (RMP) of 1.29 × 10^-19 and a likelihood ratio (LR) of 7.75 × 10¹⁸. These findings provide direct evidence that both SACC-83 and SACC-LM are HeLa-derived contaminants rather than authentic SACC models. We therefore recommend that researchers suspend further use of these two lines and highlight the broader role that independent authentication platforms, by virtue of their direct access to cell line data, can play as an effective early-warning system against misidentification in the scientific community.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147254","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":"Neonatal Dried Blood Spot Metabolomics Reveals Signatures of Early-Onset Myeloproliferative Neoplasms.","authors":"Domenica Berardi, Caroline H Johnson, Andrew T DeWan, Rong Wang, Abhishek Jain, Joseph L Wiemels, Catherine Metayer, Nikolai A Podoltsev, Xiaomei Ma","doi":"10.1002/ijc.70784","DOIUrl":"https://doi.org/10.1002/ijc.70784","url":null,"abstract":"<p><p>The etiology of myeloproliferative neoplasms (MPN) is poorly understood. We investigated the possible role of early-life exposures in the pathogenesis of MPN diagnosed among children and young adults in a population-based case-control study in California. Untargeted metabolomics analysis was conducted using archived neonatal dried blood spots. Data reduction methodologies revealed subtle metabolic differences between cases and controls, particularly when stratifying by age at diagnosis. Key differences were observed in fatty acids, amino acids, and metabolites in redox pathways. This study suggests that moderate metabolic changes in early life may contribute to the development of MPN in children and young adults. It also provides a foundation for future investigations aimed at a deeper exploration of the identified metabolites as potential biomarkers in early-onset MPN.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147122","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":"Stability of GLOBOCAN Estimates Across Consecutive Releases: A Quantitative Benchmark for Global Cancer Epidemiology.","authors":"Mehmet Zafer Sabuncuoğlu, İsmail Zihni, Bilal Turan, Serdar Acar, İsa Karaca","doi":"10.1002/ijc.70773","DOIUrl":"https://doi.org/10.1002/ijc.70773","url":null,"abstract":"<p><p>GLOBOCAN is the most widely used source of national cancer statistics, yet users routinely treat the difference between two releases as real epidemiological change. We quantified how far estimates move between the 2022 and 2024 cycles and whether this depends on development level. Age-standardised incidence and mortality rates for eight cancers were paired between GLOBOCAN 2022 and 2024 for 185 countries common to both cycles. Agreement was assessed by Bland-Altman analysis and Lin's concordance correlation coefficient (CCC); per-country revision magnitude was related to the Human Development Index (HDI) using rank and robust regression, with partial correlation adjusting for baseline incidence. Pooled concordance was high (CCC 0.97 for incidence, 0.95 for mortality) with negligible mean bias, but limits of agreement were wide and the tail heavy: 62.4%, 40.3%, 28.1% and 13.4% of country-cancer-sex cells were revised by more than 10%, 20%, 30% and 50%. Revision magnitude was inversely related to HDI (Spearman ρ = -0.62 for incidence and -0.62 for mortality; both p < 0.001), falling from 23.3% in low-HDI to 8.1% in very-high-HDI countries and persisted after adjustment for baseline incidence (partial ρ = -0.36); the development gradient is thus only partly explained by lower, more volatile baseline rates. Thyroid cancer showed the largest revisions. These findings provide, to our knowledge, the first quantitative benchmark for interpreting apparent differences between successive GLOBOCAN releases and support more cautious interpretation of single-cycle estimates from lower-HDI settings.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101602","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":"Optimal Sequencing of First-Line Immune Checkpoint Inhibitors With Definitive Chemoradiotherapy: A Multicenter Real-World Cohort Study Comparing Induction, Concurrent, and Consolidation Strategies for Unresectable Locally Advanced Esophageal Squamous Cell Carcinoma.","authors":"Xiaohan Zhao, Shiwang Wen, Chunyang Song, Jie Wang, Yaowen Zhang, Chenyu Wang, Yatian Liu, Pudong Qian, Jianzhong Cao, Qing Hou, Yuanji Xu, Zhongmei Lin, Xianghua Ye, Min Hou, Yan Gui, Lulu Wang, Wei Zhou, Zhimin Zeng, Yaqi Song, Honglei Luo, Jiahua Lv, Shuchai Zhu, Wenbin Shen","doi":"10.1002/ijc.70740","DOIUrl":"https://doi.org/10.1002/ijc.70740","url":null,"abstract":"<p><p>While first-line immune checkpoint inhibitors (ICIs) combined with chemoradiotherapy (CRT) represent a crucial advancement for unresectable locally advanced esophageal squamous cell carcinoma (ESCC), the optimal sequencing of these modalities remains unresolved. To evaluate the efficacy and safety of induction, concurrent, and consolidation ICI strategies, this multicenter real-world cohort study enrolled 662 patients with Stage II-IVA unresectable ESCC across 12 cancer centers. Patients were categorized into induction (IC-CRT), concurrent (ICRT), and consolidation (CRT-IC) groups, with inverse probability of treatment weighting (IPTW) applied to balance baseline characteristics. Following IPTW adjustment, the median overall survival (OS) in the IC-CRT, ICRT, and CRT-IC groups was 34.7 months, not reached, and 23.1 months, respectively (p = 0.016), while the corresponding median progression-free survival (PFS) times were 20.1, 25.3, and 12.9 months, respectively (p = 0.014). Among the three sequencing strategies, ICRT achieved the most favorable survival outcomes, followed by IC-CRT and CRT-IC. Multivariable Cox regression confirmed that ICRT was associated with a significantly reduced risk of mortality compared with IC-CRT (HR = 0.71, p = 0.046) and CRT-IC (HR = 0.53, adjusted p < 0.001). Safety profiles indicated that ICRT carried the highest burden of Grade 3-4 treatment-related pneumonitis (7.7%). In conclusion, ICRT as a first-line treatment for locally advanced ESCC showed the most favorable survival profile compared with induction or consolidation sequencing, although its higher toxicity profile necessitates careful patient selection and proactive clinical management. In contrast, the CRT-IC strategy exhibited the best tolerability but the least favorable survival outcome.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101582","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":"Physical Activity and Risk of Liver Cancer: A Competing Risk Analysis.","authors":"Frances E M Albers, S Ghazaleh Dashti, Charles E Matthews, Lin Yang, Darren R Brenner, Linda M Liao, Roger L Milne, Dallas R English, Katherine A McGlynn, Brigid M Lynch","doi":"10.1002/ijc.70741","DOIUrl":"https://doi.org/10.1002/ijc.70741","url":null,"abstract":"<p><p>Physical activity is associated with lower risk of liver cancer, but obtaining an unbiased estimate of the causal effect is challenging due to the competing risk of death due to any other cause. We performed a causal competing risk analysis to estimate the total effect of physical activity on risk of liver cancer in the presence of competing deaths. Data were included for 263,184 participants (870 liver cancers) in the NIH-AARP Diet and Health Study. Total effects in the presence of competing deaths were estimated on the risk difference (RD) scale as the differences, by age, in standardised cause-specific cumulative incidence functions of liver cancer had all participants engaged in ≥ 4 h/week of moderate- to vigorous-intensity physical activity (MVPA) versus < 4 h/week. There were an estimated 18 per 100,000 fewer liver cancer cases for ≥ 4 h/week of MVPA versus < 4 h/week (95% confidence interval [CI]: 6.2, 29.9) by age 67 years (average age of diagnosis in the United States), and an estimated 58 per 100,000 fewer cases (95% CI: 21.1, 95.8) by age 78 years (average US life expectancy). Estimated RDs were larger in older than younger age groups (e.g., RD per 100,000 at age 85 years = -79.0, 95% CI: -133.4, -24.7; at age 55 years = -2.0, 95% CI: -4.5, 0.6). Our findings strengthen the evidence for physical activity reducing risk of liver cancer. Increasing physical activity at the population level may reduce the growing, global burden of liver cancer.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101528","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":"Neoadjuvant Dual Immunotherapy in T4 Locally Advanced Deficient Mismatch Repair Gastric or Esophagogastric Junction (EGJ) Adenocarcinoma.","authors":"Qiancheng Hu, Haiyan Luo, Ming Liu, Yuan Yin, Xiaolong Chen, Mojin Wang, Bo Zhang, Wen Zhuang, Chaoyong Shen, Pengfei Zhang, Shuming Ji, Kun Yang, Jiankun Hu, Hongfeng Gou","doi":"10.1002/ijc.70763","DOIUrl":"https://doi.org/10.1002/ijc.70763","url":null,"abstract":"<p><p>Although combining programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) inhibitors in neoadjuvant therapy is effective for deficient mismatch repair (dMMR) or microsatellite instability-high (MSI-H) gastric or esophagogastric junction (EGJ) adenocarcinoma, few T4 stage patients have been studied. The effectiveness and safety of this dual immunotherapy for T4 locally advanced dMMR/MSI-H gastric/EGJ adenocarcinoma is largely unknown. Patients with T4 locally advanced dMMR/MSI-H gastric/EGJ adenocarcinoma treated with dual immune checkpoint inhibitors as neoadjuvant therapy were identified from a prospectively maintained gastric/EGJ adenocarcinoma database. The primary endpoint was the pathological complete response (pCR) rate. Twenty-three patients were included in this study. Of these, 22 (95.7%) completed dual immunotherapy before surgery, while one missed a dose due to immune-related hypophysitis. Sixteen patients (69.6%) underwent surgery, achieving a 100% R0 resection rate. The pCR rate was 81.3% (95% confidence interval (CI): 57.0%-93.4%) and the major pathological response (MPR) rate was 93.8%. Seven patients did not have surgery; five of them, with complete clinical response, opted for a \"watch-and-wait\" strategy. The event-free survival rate was 95.5% at a median follow-up of 22.1 months, with manageable adverse events. Dual immunotherapy shows promise for T4 locally advanced dMMR/MSI-H gastric/EGJ adenocarcinoma, and the \"watch-and-wait\" strategy deserves further study in dMMR/MSI-H cases. Larger studies are needed to confirm these results and optimize treatment.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101569","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-Onset Type 2 Diabetes Mellitus and Cancer Risk: A Matched Cohort Study in China Kadoorie Biobank","authors":"Mengying Wang,&nbsp;Owen Tipping,&nbsp;Bowen Liu,&nbsp;Derrick A. Bennett,&nbsp;Baiyong Shen,&nbsp;Siyi Zou,&nbsp;Shulin Zhao,&nbsp;Richard M. Martin,&nbsp;Matthew Sperrin,&nbsp;Andrew G. Renehan","doi":"10.1002/ijc.70638","DOIUrl":"10.1002/ijc.70638","url":null,"abstract":"<p>The prevalence of type 2 diabetes mellitus (T2DM) is rising rapidly in China and is linked to increased cancer risk, but causality remains unclear due to biases. We examined the causal effect of T2DM on cancer risk using bias-minimizing methods. We conducted a matched cohort study within China Kadoorie Biobank (median follow-up 49 months in men and 53 months in women). To minimize bias, we included only new-onset T2DM, applied sequential longitudinal matching, used pre-diagnosis BMI, and accounted for detection time bias. Stratified Cox models estimated sex-specific time-split hazard ratios (tsHRs). Results were triangulated with two-sample Mendelian Randomization (MR) in East Asians. After 1:3 matching, 8657 men and 13,680 women with T2DM were matched to unexposed individuals. T2DM was associated with increased risk of total cancers in men (tsHR 1.57, 95% CI 1.38–1.78) and women (tsHR 1.29, 95% CI 1.14–1.46). Site-specifically, T2DM was associated with liver cancer (men: 68 cases, tsHR 2.12, 95% CI 1.42–3.15; women: 43 cases, tsHR 2.39, 95% CI 1.42–4.04) and pancreatic cancer (men: 36 cases, tsHR 2.57, 95% CI 1.35–4.92; women: 33 cases, tsHR 3.95, 95% CI 1.92–8.13). No significant associations were observed for colorectal, lung, stomach, or breast cancers. In multivariable MR, genetic liability to T2DM was associated with pancreatic cancer after adjusting for BMI (OR 1.07, 95% CI 1.01–1.14, p = 0.03). In this large Chinese population, we found evidence for causal associations between T2DM and pancreatic cancer only, whereas evidence for other cancers was weak or discordant.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 11","pages":"2705-2719"},"PeriodicalIF":4.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70638","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148409688","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":"Asymptomatic Cardiotoxicity After High-Dose Anthracycline Treatment in Sarcoma Patients Assessed by Biomarkers and Echocardiography","authors":"Elissa A. S. Polomski,&nbsp;Frank M. Speetjens,&nbsp;J. Wouter Jukema,&nbsp;Julius C. Heemelaar,&nbsp;Michiel A. J. van de Sande,&nbsp;Hans Gelderblom,&nbsp;M. Louisa Antoni","doi":"10.1002/ijc.70620","DOIUrl":"10.1002/ijc.70620","url":null,"abstract":"<p>Treatment of sarcoma includes high-dose anthracyclines, which can cause cardiotoxicity. This study assesses the correlation of cardiac biomarkers and echocardiographic parameters on asymptomatic cardiotoxicity in sarcoma patients treated with anthracyclines. Consecutive patients diagnosed with sarcoma and treated with anthracyclines were included in this retrospective cohort study using registry data. Echocardiography was performed before start of anthracycline chemotherapy (baseline), after completing treatment (short-term follow-up), and 6–12 months after termination of treatment (long-term follow-up). The primary endpoint was the occurrence of asymptomatic cardiotoxicity at short-term follow-up. We included 44 patients (29.6% female) with a median age of 28.9 [22.2–38.7] years. Baseline left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) decreased significantly from 58.4% ± 5.0% to 54.2% ± 9.3% (<i>p</i> = 0.013) and −19.1% ± 2.2% to −17.2% ± 3.5% at short-term follow-up (<i>p</i> = 0.002), respectively. After Cycle 1, 86.5% of the patients showed NT-proBNP ≥ 125 ng/L compared to 3.9% at baseline (<i>p</i> &lt; 0.001), and after completion of therapy, 65.5% had elevated cardiac Troponin T (cTnT) ≥ 14 ng/L compared to 11.5% at baseline (<i>p</i> = 0.003). Asymptomatic cardiotoxicity was observed in 30 patients (68.2%). Mean follow-up was 2.4 [1.5–2.9] years. cTnT ≥ 14 ng/L after Cycle 4 was associated with cardiotoxicity (HR: 3.75 [1.28–11.0], <i>p</i> = 0.016), and NT-proBNP per 100 units increase after Cycle 1 was associated with an increased risk of mortality (HR: 1.36 [1.004–1.85], <i>p</i> = 0.047). Sarcoma patients treated with high-dose anthracyclines are at increased risk of developing cardiac dysfunction as assessed by LVEF and GLS. cTnT and NT-proBNP levels increase significantly during treatment and can be valuable markers to improve the risk stratification of patients treated with high-dose anthracyclines.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 11","pages":"2755-2765"},"PeriodicalIF":4.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70620","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148358687","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":"Lung Cancer Risk Assessment Beyond Smoking History","authors":"Sam Hanash","doi":"10.1002/ijc.70713","DOIUrl":"10.1002/ijc.70713","url":null,"abstract":"&lt;p&gt;Lung cancer remains the top cancer killer worldwide. Currently in the United States, annual screening for lung cancer with low-dose computed tomography, based on the USPSTF criteria, is recommended for adults aged 50–80 years with a 20 or more pack-year smoking history, who currently smoke or who quit within the past 15 years [&lt;span&gt;1&lt;/span&gt;]. However, current screening eligibility misses a large proportion of lung cancers diagnosed among never-smoker or light-smoker individuals or outside the recommended age range, due in part to a continued decrease in smoking rates [&lt;span&gt;2, 3&lt;/span&gt;]. Thus, there is a pressing need for lung cancer risk assessment beyond smoking history. Multiple factors may contribute to lung cancer risk in addition to smoking history. They include genetic predisposition and environmental exposure to secondhand smoke, radon, air pollutants, and forever chemicals [&lt;span&gt;4&lt;/span&gt;]. Given the multitude of factors that contribute to risk, there is increased interest in the application of artificial intelligence (AI) to large sets of data to derive and integrate cancer risk features into algorithms. This is exemplified in a study that relied on machine learning to develop a 3-year lung cancer risk prediction model using large real-world data [&lt;span&gt;5&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;One contributor to risk that has received much attention consists of polygenic risk scores (PRS). There have been numerous studies of PRS and lung cancer risk. A systematic review of their performance was undertaken based on the UK Biobank (UKB) cohort that included gender, ethnicity, and smoking status [&lt;span&gt;6&lt;/span&gt;]. In most studies PRS exhibited better performance among smokers, whereas in some others PRS exhibited the reverse. PRS may provide an estimate of life-time risk. However, risk may change over time. Blood-based biomarkers together with subject characteristics have the potential to assess lung cancer risk in real time. An example of how biomarkers may inform about cancer risk is a 4-marker protein panel predictive of lung cancer risk including among individuals not eligible for screening [&lt;span&gt;7&lt;/span&gt;]. The panel has been validated using the longitudinal Prostate, Lung, Colorectal, and Ovarian cohort, demonstrating the potential of a mortality benefit stemming from this marker panel [&lt;span&gt;8&lt;/span&gt;]. Also, importantly, an algorithm based on repeated measurements of this 4-marker panel over time for lung cancer risk assessment resulted in improved performance over a single time measurement, thus allowing for the monitoring of change in risk over time [&lt;span&gt;9&lt;/span&gt;]. Besides proteins, there are a multitude of sources of potential biomarkers that may be relevant for risk assessment of lung cancer. They include various biological fluids, notably blood, urine, saliva, or sputum. Another source is exhaled breath, which has also been explored as a source of biomarkers as well airway brushing [&lt;span&gt;10&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;A study in this issue of the journal by ","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 11","pages":"2631-2632"},"PeriodicalIF":4.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70713","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148904581","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":"Geographical Pattern of Testicular Cancer Points to Maternal Exposures Behind Increasing Incidence","authors":"Antti Kaipia,&nbsp;Karri Seppä,&nbsp;Elli Hirvonen,&nbsp;Eetu Mäkinen,&nbsp;Nea Malila,&nbsp;Janne Pitkäniemi,&nbsp;Jorma Toppari,&nbsp;Peter Boström,&nbsp;Heikki Seikkula","doi":"10.1002/ijc.70636","DOIUrl":"10.1002/ijc.70636","url":null,"abstract":"<p>Evidence suggests that testicular cancer (TC) originates from germ cell neoplasia in situ arising during fetal development, implying that prenatal environmental exposures may influence disease risk. We investigated whether maternal place of residence during pregnancy is associated with regional variation in TC incidence. We conducted a nationwide cohort study including 1,342,996 men born in Finland between 1960 and 1999. Participants were followed from birth until diagnosis of TC, death, emigration, or the end of follow-up (2021). A total of 2976 TC cases were identified. Information on municipality of birth was used as a proxy for maternal residence during pregnancy. Incidence rates and cumulative incidence were estimated by birth cohort and age at diagnosis. To examine regional variation, cumulative TC incidence by birth cohort and municipality was modeled using Bayesian hierarchical binomial regression allowing incidence to vary across municipalities. TC incidence increased across birth cohorts, peaking among men born in 1975–1979 (16.8 per 100,000). Cumulative incidence rose in all municipalities, ranging from 67.9 to 132.5 per 100,000 among men born in 1960–1969 and from 283.2 to 327.6 among those born in 1980–1989. Marked geographic clustering was observed. Incidence was consistently elevated among men born in southwestern Finland and remained high throughout the study period. Over successive birth cohorts, an eastward shift in higher incidence was observed. Although direct cohort evidence linking specific environmental exposures to TC remains limited, these findings support the hypothesis that prenatal environmental factors contribute to the pathogenesis of TC and may partly explain regional differences in incidence.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"159 11","pages":"2688-2693"},"PeriodicalIF":4.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.70636","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387146","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}