International Journal of Cancer最新文献_第3页

Metabolome analysis identified exogenous cholesterol within lipid rafts that activate the Akt/mTOR signaling pathway in epithelial ovarian cancer. 代谢组学分析发现，在上皮性卵巢癌中，脂筏内的外源性胆固醇激活Akt/mTOR信号通路。

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-07-01 Epub Date: 2026-02-26 DOI: 10.1002/ijc.70401

Hitomi Sakaguchi-Mukaida, Kosuke Hiramatsu, Tatsuo Masuda, Mamoru Kakuda, Satoshi Nakagawa, Tadashi Iwamiya, Shinya Matsuzaki, Tetsuji Naka, Yutaka Ueda, Tadashi Kimura, Michiko Kodama

{"title":"Metabolome analysis identified exogenous cholesterol within lipid rafts that activate the Akt/mTOR signaling pathway in epithelial ovarian cancer.","authors":"Hitomi Sakaguchi-Mukaida, Kosuke Hiramatsu, Tatsuo Masuda, Mamoru Kakuda, Satoshi Nakagawa, Tadashi Iwamiya, Shinya Matsuzaki, Tetsuji Naka, Yutaka Ueda, Tadashi Kimura, Michiko Kodama","doi":"10.1002/ijc.70401","DOIUrl":"10.1002/ijc.70401","url":null,"abstract":"Epithelial ovarian cancer (EOC) is a highly aggressive malignancy with poor prognosis. Thus, new treatment options are needed. Recently, lipid metabolism in EOC has been highlighted. However, the specific lipid molecules activating lipid metabolism remain unclear. This study aimed to elucidate lipid metabolism in EOC and evaluate the potential of its inhibition as a therapeutic approach. We obtained high-fat diet (HFD)-fed mouse serum and performed metabolome analysis to identify lipid molecules contributing to cell proliferation of EOC. We also analyzed which signaling pathway was activated by the lipid molecule. Finally, we demonstrated the inhibition of lipid metabolism in EOC cells. HFD significantly promoted tumor growth of EOC cells in vivo, and HFD-fed mouse serum promoted EOC cell proliferation in vitro. Metabolome analysis identified cholesterol (C27H46O) as a key molecule in HFD-fed mouse serum. Cholesterol (C27H46O) activated the Akt/mTOR signaling pathway in vitro. Cholesterol (C27H46O) is an important component of lipid rafts, and its inhibitor, which extracts cholesterol (C27H46O) from lipid rafts, inactivated the Akt/mTOR signaling pathway and suppressed subsequent EOC cell proliferation. Exogenous cholesterol (C27H46O) contributed to cell proliferation of EOC via the lipid rafts-Akt/mTOR signaling pathway, and its inhibition undoubtedly presents a novel therapeutic strategy for EOC.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"257-268"},"PeriodicalIF":4.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147300433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PVT1 lincRNA signals an androgen-dependent transcriptional activation program of oncogenes in prostate cancer cells. PVT1 lincRNA是前列腺癌细胞中雄激素依赖性癌基因转录激活程序的信号。

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-07-01 Epub Date: 2026-03-06 DOI: 10.1002/ijc.70417

Maria Gabriela Berzoti-Coelho, Fabio Nunes de Mello, Ana Carolina Tahira, Gabriel Nakanishi Fortes, Agatha Fischer-Carvalho, Pedro Jardim Poli, Murilo Sena Amaral, Sergio Verjovski-Almeida

{"title":"PVT1 lincRNA signals an androgen-dependent transcriptional activation program of oncogenes in prostate cancer cells.","authors":"Maria Gabriela Berzoti-Coelho, Fabio Nunes de Mello, Ana Carolina Tahira, Gabriel Nakanishi Fortes, Agatha Fischer-Carvalho, Pedro Jardim Poli, Murilo Sena Amaral, Sergio Verjovski-Almeida","doi":"10.1002/ijc.70417","DOIUrl":"10.1002/ijc.70417","url":null,"abstract":"Prostate cancer is the most prevalent malignancy among men and is driven by multiple factors, including androgen signaling and its receptor. Long non-coding RNAs, such as PVT1, play key roles in cancer, particularly by regulating gene expression. PVT1 is upregulated in several cancer types and has been shown to interact with the androgen receptor in prostate cells. This study investigates how PVT1 contributes to the prostate cancer phenotype under androgen stimulation. Knockdown of PVT1 was achieved using CRISPR-Cas13d in LNCaP prostate cancer cells subjected to androgen (R1881) or vehicle treatment. Cellular proliferation, invasion, and apoptosis rates were assessed, alongside RNA sequencing (RNA-seq) to analyze genome-wide transcriptomic changes. Six epigenetic marks-AR, EZH2, H3K4me1, H3K4me3, H3K27me3, and H3K27ac-were examined using CUT&RUN. PVT1 knockdown led to a significant reduction in cell proliferation and an increase in apoptosis signaling. Oncogenes such as MYC, AKT1, AKT2, cyclins CCNA2, CCNB1, CCNB2, CCNE1, CCNE2 and cyclin-dependent kinases CDK1 and CDK4, which were upregulated under androgen treatment, exhibited a significantly reduced expression following PVT1 knockdown, thereby modulating cancer-associated oncogenic pathways. Epigenetically, PVT1 knockdown markedly decreased the occupancy of transcriptionally activating epigenetic marks-H3K4me1, H3K4me3, and H3K27ac-on oncogenes, regardless of androgen presence. Analysis of enriched transcription factors associated with the altered genes revealed a regulatory network linked to prostate cancer pathogenesis. PVT1 drives a genome-wide epigenetic reprogramming in prostate cells, underscoring the role of PVT1 as a positive regulator of oncogenic pathways in prostate cancer and highlighting PVT1's potential as a therapeutic target.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"144-158"},"PeriodicalIF":4.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147369047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reprogramming innate immunity to overcome endocrine resistance in estrogen receptor-positive breast cancer. 重编程先天免疫克服雌激素受体阳性乳腺癌的内分泌抵抗。

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-07-01 Epub Date: 2026-03-07 DOI: 10.1002/ijc.70421

Siti Nur Hasyila Muhammad, Maryam Azlan, Agustine Nengsih Fauzi

{"title":"Reprogramming innate immunity to overcome endocrine resistance in estrogen receptor-positive breast cancer.","authors":"Siti Nur Hasyila Muhammad, Maryam Azlan, Agustine Nengsih Fauzi","doi":"10.1002/ijc.70421","DOIUrl":"10.1002/ijc.70421","url":null,"abstract":"Estrogen receptor-positive (ER+) breast cancer accounts for the majority of breast cancer cases worldwide, yet the long-term efficacy of endocrine therapy is limited by resistance and recurrence. While tumor-intrinsic mechanisms of endocrine resistance are well established, growing evidence highlights the contributions of innate immune cells and the tumor microenvironment (TME) in shaping therapeutic outcomes. This review synthesizes recent advances into how tumor-associated macrophages (TAMs), natural killer (NK) cells, myeloid-derived suppressor cells (MDSCs), and tumor-associated neutrophils (TANs) collectively foster an immunosuppressive TME that undermines endocrine responsiveness. Central to this crosstalk is the STAT3 signaling pathway, which integrates inflammatory and metabolic stress signals to drive immune reprogramming, promotes tumor progression, and facilitates therapy resistance. By activating tolerogenic pathways and inhibiting anti-tumor immunity, STAT3 provides a mechanistic link between innate immune dysregulation and endocrine resistance. Preclinical studies demonstrate that STAT3 inhibition can restore tamoxifen sensitivity in resistant ER+ breast cancer models, highlighting its therapeutic potential. These insights reveal the immunological complexity of endocrine resistance and provide rationale for combinatorial strategies integrating endocrine therapy with immunomodulation. Future approaches that incorporate STAT3 inhibitor, immune checkpoint blockade, and biomarker-guided patient selection may transform the management of ER+ breast cancer, offering more durable and clinically meaningful outcomes by acknowledging the emerging interactions between immune dysregulation and metabolic stress in resistant ER+ breast cancer.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"54-66"},"PeriodicalIF":4.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147371906","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}

引用次数: 0

Clinical implications of PD-L1 expression in oncogene-driven NSCLC: Differential responses to targeted agents and immune checkpoint inhibitors. PD-L1表达在癌基因驱动的非小细胞肺癌中的临床意义：对靶向药物和免疫检查点抑制剂的差异反应

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-07-01 Epub Date: 2026-03-23 DOI: 10.1002/ijc.70413

Xiaoxiao Fan, Chenxi Wei, Minjun Rong, Shengnan Wang, Jiaying Wang, Xiaohan Wang, Xiao Han, Xue Meng

{"title":"Clinical implications of PD-L1 expression in oncogene-driven NSCLC: Differential responses to targeted agents and immune checkpoint inhibitors.","authors":"Xiaoxiao Fan, Chenxi Wei, Minjun Rong, Shengnan Wang, Jiaying Wang, Xiaohan Wang, Xiao Han, Xue Meng","doi":"10.1002/ijc.70413","DOIUrl":"10.1002/ijc.70413","url":null,"abstract":"PD-L1 is a reliable biomarker for predicting immunotherapy efficacy in NSCLC patients without driver gene mutations. However, its significance in patients with driver gene-positive tumors remains unclear. This study analyzed 273 patients with stage IV non-small cell lung cancer harboring driver gene mutations. All patients had PD-L1 expression levels ≥10%. The effect of PD-L1 expression on progression-free survival (PFS) and overall survival (OS) was assessed. Among the 273 patients with driver gene-positive NSCLC, 127 had a PD-L1 tumor proportion score (TPS) of 10-49%, and 146 had TPS ≥50%. Patients in the TPS 10%-49% group had significantly better median PFS and OS compared to those in the TPS ≥50% group (p = 0.0008 and p = 0.0009, respectively). In the realm of targeted therapy, patients who received first-line tyrosine kinase inhibitors (TKIs) showed superior outcomes in the TPS 10-49% group compared to the TPS ≥50% group in terms of both median PFS (30.8 months vs. 13.9 months, p = .0001) and OS (44.8 months vs. 26.3 months, p = .0006). Regarding immunotherapy, PD-L1 expression level was not significantly associated with treatment efficacy. However, in patients with KRAS mutations, those who received first-line immunotherapy exhibited better median PFS and OS (p <.0001 for both). Notably, among patients with high PD-L1 expression, no statistically significant clinical benefit was observed. In NSCLC patients with driver gene mutations, PD-L1 expression is associated with the efficacy of targeted therapy but is not predictive of response to immunotherapy.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"269-279"},"PeriodicalIF":4.7,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147502740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The value of nasopharyngeal brush versus plasma EBV DNA detection in diagnosing local recurrence of nasopharyngeal carcinoma. 鼻咽刷与血浆EBV DNA检测在鼻咽癌局部复发诊断中的价值。

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-06-15 Epub Date: 2026-02-03 DOI: 10.1002/ijc.70357

Yan-Feng Ouyang, Jiong-Lin Liang, Ruo-Qi Xie, You-Ping Liu, Rui You, Tian-Liang Xia, Ming-Yuan Chen

{"title":"The value of nasopharyngeal brush versus plasma EBV DNA detection in diagnosing local recurrence of nasopharyngeal carcinoma.","authors":"Yan-Feng Ouyang, Jiong-Lin Liang, Ruo-Qi Xie, You-Ping Liu, Rui You, Tian-Liang Xia, Ming-Yuan Chen","doi":"10.1002/ijc.70357","DOIUrl":"10.1002/ijc.70357","url":null,"abstract":"Nasopharyngeal carcinoma (NPC) remains a major challenge due to the high incidence of recurrence, often leading to therapeutic failure. Early detection of recurrence is critical, yet effective surveillance methods are limited. This study aims to evaluate the utility of Epstein-Barr virus (EBV) DNA detection in nasopharyngeal brush samples for identifying recurrent NPC. A total of 187 NPC patients who had undergone radical radiotherapy with or without chemotherapy were included. EBV DNA levels in both nasopharyngeal brush and plasma samples were analyzed using real-time quantitative PCR. Head and neck MRI, sinus endoscopy examination, and biopsy of suspicious lesions were used as the gold standard to confirm recurrence. Patients without recurrence after more than 1 year of follow-up served as controls. Nasopharyngeal brush EBV DNA detection demonstrated significantly higher sensitivity (95.7%) for detecting recurrence compared to plasma EBV DNA testing (61.4%), with comparable specificity (94.0% vs. 96.6%). The positive predictive value was similar between methods, whereas the negative predictive value was markedly higher for the nasopharyngeal brush group (97.3% vs. 80.7%). These findings suggest that EBV DNA detection in nasopharyngeal brush samples is a highly sensitive and minimally invasive supplementary tool for monitoring NPC recurrence. This approach offers superior sensitivity and an improved negative predictive value compared to plasma EBV DNA testing, and may enhance early surveillance and clinical management of NPC recurrence.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"3279-3287"},"PeriodicalIF":4.7,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111574","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}

引用次数: 0

ID3 deficiency alters chromatin accessibility at DSB sites and enhances vulnerability to HDAC inhibition. ID3缺陷改变了DSB位点染色质的可及性，增强了对HDAC抑制的易感性。

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-06-15 Epub Date: 2026-02-24 DOI: 10.1002/ijc.70400

Giuditta Della Corte, Hossam Eldesouky, Julia Puchan, Sercan Öz, Elena Everatt, Ashish Goyal, Gianluca Sigismondo, Udo Oppermann, Christoph Plass, Dieter Weichenhan, Ali Bakr

{"title":"ID3 deficiency alters chromatin accessibility at DSB sites and enhances vulnerability to HDAC inhibition.","authors":"Giuditta Della Corte, Hossam Eldesouky, Julia Puchan, Sercan Öz, Elena Everatt, Ashish Goyal, Gianluca Sigismondo, Udo Oppermann, Christoph Plass, Dieter Weichenhan, Ali Bakr","doi":"10.1002/ijc.70400","DOIUrl":"10.1002/ijc.70400","url":null,"abstract":"The inhibitor of DNA-binding 3 (ID3) plays a crucial role in DNA double-strand break (DSB) repair. We previously reported that ID3 loss reduced chromatin accessibility at DNA repair gene promoters, yet its exact role in DNA repair via chromatin regulation remains elusive. Using the AID-DIvA cell system with inducible DSBs, we show that ID3 directly regulates chromatin accessibility at DSB sites, as demonstrated by reduced chromatin accessibility and lower H3K27ac levels in ID3-knockout (KO) cells. Loss of ID3 renders cells susceptible to histone deacetylase (HDAC) inhibition, particularly to the Class I HDAC inhibitor, leading to the accumulation of unrepaired DSBs and delayed cell cycle progression. Transcriptome and proteome analyses revealed that HDAC inhibition in ID3-KO cells results in the downregulation of gene sets involved in the regulation of cell cycle and cell division. The synthetic lethality observed between ID3 loss and Class I HDAC inhibition underscores a novel therapeutic vulnerability in ID3-deficient cancers, driven by compounded defects in chromatin remodeling, cell cycle, and DNA repair. Our study provides new insights into the relationship between chromatin regulation and genome stability, with implications for targeted cancer therapies.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"3173-3186"},"PeriodicalIF":4.7,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106931/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147281513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lymphoma, multiple myeloma and leukaemia incidence in regions of Belarus most heavily contaminated by the Chernobyl accident. 白俄罗斯受切尔诺贝利事故污染最严重地区的淋巴瘤、多发性骨髓瘤和白血病发病率。

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-06-15 Epub Date: 2026-01-23 DOI: 10.1002/ijc.70346

Ljubica Zupunski, Alesia Yaumenenka, Ilya Veyalkin, Victor Minenko, Pavel Moiseyev, Joachim Schüz, Tatiana Kukhta, Sergey Trofimik, Richard Harbron, Vladimir Drozdovitch, Evgenia Ostroumova

{"title":"Lymphoma, multiple myeloma and leukaemia incidence in regions of Belarus most heavily contaminated by the Chernobyl accident.","authors":"Ljubica Zupunski, Alesia Yaumenenka, Ilya Veyalkin, Victor Minenko, Pavel Moiseyev, Joachim Schüz, Tatiana Kukhta, Sergey Trofimik, Richard Harbron, Vladimir Drozdovitch, Evgenia Ostroumova","doi":"10.1002/ijc.70346","DOIUrl":"10.1002/ijc.70346","url":null,"abstract":"There is little information on non-thyroid cancer risks, including haematological malignancies (HM), among the residents of most contaminated regions after the Chernobyl (Chornobyl) nuclear power plant accident. We studied the incidence of lymphoma, multiple myeloma and leukaemia in relation to the raion-average age-specific cumulative absorbed red bone marrow (RBM) dose among the residents of Gomel and Mogilev oblasts in Belarus, which were highly contaminated. The follow-up period was 40 years (1978-2018). HM cases and population size data were received from the Belarusian national cancer registry and the state department of statistics. Our ecological study included 7328 lymphoma, 9476 leukaemia and 2003 multiple myeloma incident cases and 90.8 million person-years in people who were born before the accident and have attained age <80 years old. The mean (median) RBM dose accumulated by December 31, 2018 was 14.2 (6.4) mGy. We found no evidence of increased risks of Hodgkin and non-Hodgkin lymphoma, multiple myeloma or total leukaemia associated with two-year lagged raion-average cumulative RBM dose after adjustment for sex, attained age, urban/rural status and calendar period effects. There was a suggestion of an elevated relative risk of myeloid leukaemia per 100 mGy after exclusion of Gomel and Mogilev cities. Little evidence was found on interaction between selected factors, except sex, and RBM dose for each study outcome. Studies with individually reconstructed cumulative absorbed RBM doses are warranted to provide more insight on dose-effect relationships between HM risk, specifically leukaemia, and protracted environmental exposure at a low dose range.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"3161-3172"},"PeriodicalIF":4.7,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146027953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Changes in 1-year relative survival of patients with cancer during the COVID-19 pandemic in Denmark, Finland, Iceland, Norway, and Sweden: A population-based cohort study. 在丹麦、芬兰、冰岛、挪威和瑞典，COVID-19大流行期间癌症患者1年相对生存率的变化：一项基于人群的队列研究

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-06-15 Epub Date: 2026-01-21 DOI: 10.1002/ijc.70336

Fernando Gonzalez Yli-Mäyry, Tomas Tanskanen, Karri Seppä, Anna L V Johansson, Charlotte Wessel Skovlund, Lina Steinrud Mørch, Søren Friis, Simon Mathis Kønig, Tom Børge Johannesen, Tor Åge Myklebust, Sasha Pejicic, David Pettersson, Eva María Guðmundsdóttir, Sirpa Heinävaara, Nea Malila, Joonas Miettinen, Johan Ahlgren, Giske Ursin, Janne Pitkäniemi

{"title":"Changes in 1-year relative survival of patients with cancer during the COVID-19 pandemic in Denmark, Finland, Iceland, Norway, and Sweden: A population-based cohort study.","authors":"Fernando Gonzalez Yli-Mäyry, Tomas Tanskanen, Karri Seppä, Anna L V Johansson, Charlotte Wessel Skovlund, Lina Steinrud Mørch, Søren Friis, Simon Mathis Kønig, Tom Børge Johannesen, Tor Åge Myklebust, Sasha Pejicic, David Pettersson, Eva María Guðmundsdóttir, Sirpa Heinävaara, Nea Malila, Joonas Miettinen, Johan Ahlgren, Giske Ursin, Janne Pitkäniemi","doi":"10.1002/ijc.70336","DOIUrl":"10.1002/ijc.70336","url":null,"abstract":"During the first year of the COVID-19 pandemic, reported cancer cases declined in the Nordic countries, potentially reflecting delays in cancer diagnosis. We compared 1-year relative survival (RS) and excess mortality of patients diagnosed with cancer in the Nordic countries in March-December 2020 with that expected based on patients diagnosed in 2011-2019. We used flexible parametric RS models, defining excess mortality as the difference in total mortality between patients with cancer and the national population without cancer. We report the ratio between the observed and expected excess mortality (EMR) and the difference in 1-year RS in percentage points (pp) by country, age, sex, and cancer site. Excess mortality of patients diagnosed during the pandemic was increased in all Nordic countries except Iceland. Swedish men had the highest EMR of 1.12 (95% CI 1.06, 1.17), corresponding to a 1.4 pp reduction in 1-year RS (87.1%-85.8%). In women, the highest EMR was 1.10 (95% CI 1.03, 1.18) in Norway, corresponding to a 1-year RS decrease of 1.2 pp (86.6%-85.5%). The largest site-specific decreases in 1-year RS were observed for liver cancer in Finnish and Swedish men, with decreases of 10.2 pp (45.3%-35.1%) and 7.2 pp (55.7%-48.5%), respectively. We found reduced 1-year RS among Nordic patients diagnosed with cancer during the COVID-19 pandemic in 2020, especially in older patients and those with aggressive cancers. These reductions coincided with restrictions and potential delays in seeking healthcare.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"3121-3131"},"PeriodicalIF":4.7,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Stereoscopic epidemiology of global cancer: Complementary lenses from GBD 2023 and GLOBOCAN 2022. 全球癌症的立体流行病学：来自GBD 2023和GLOBOCAN 2022的互补透镜。

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-06-15 Epub Date: 2026-02-07 DOI: 10.1002/ijc.70378

Fang Li, Liqun Zhang

引用次数: 0

Cohort study of standardized treatment pathways by multidisciplinary tumor board decision making in patients with salivary gland malignancies. 涎腺恶性肿瘤患者多学科肿瘤委员会决策标准化治疗途径的队列研究。

IF 4.7 2区医学

International Journal of Cancer Pub Date : 2026-06-15 Epub Date: 2026-02-14 DOI: 10.1002/ijc.70382

Nils Feldmann, Gunnar Wichmann, Andreas Dietz, Markus Pirlich

{"title":"Cohort study of standardized treatment pathways by multidisciplinary tumor board decision making in patients with salivary gland malignancies.","authors":"Nils Feldmann, Gunnar Wichmann, Andreas Dietz, Markus Pirlich","doi":"10.1002/ijc.70382","DOIUrl":"10.1002/ijc.70382","url":null,"abstract":"Salivary gland malignancies (SGM) are heterogeneous regarding origin, biology and prognosis. We investigated patterns of clinical and pathological features and outcome differences attributable to standardized decision making for treatment pathways before and after establishing our multidisciplinary tumor board (MDTB) in 2007. We retrospectively analyzed data of electronic health records, the Saxon cancer registry and the clinic's tumor database (1990-2024). Statistical analysis included contingency tables, Pearson's chi-squared tests for categorical, Student's t test for numerical data, Kaplan-Meier cumulative survival plots and log-rank tests for time-dependent outcome measures. Among 200 patients, 83 were diagnosed before and 117 since 2007. Treatment modalities included surgery in 93% of cases, with 33.5% receiving adjuvant radiotherapy and 12.5% receiving adjuvant chemo-radiotherapy. We observed disease progression in 50% of patients. Locoregional free survival was superior since 2007 (p = .035). Distant metastasis-free survival (DMFS) decreased related to earlier detection of distant metastasis (M1) linked to prevention of deaths from the index cancer in patients with M1 at diagnosis or relapse (rM1) since 2007 (p = .120). Moreover, conditional OS was not affected for patients with M1/rM1 diagnosis by numerically increased detection of distant metastasis since 2007 (p = .574). MDTB decision making at a certified cancer center is accompanied by increasing numbers of diagnosis of SGM and better locoregional control but not DMFS due to higher metastasis detection rate and treatment. Despite excellent and numerically improved disease-specific survival, 10-years OS remained similar.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"3241-3251"},"PeriodicalIF":4.7,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146193881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0