International Journal of Cancer最新文献

{"title":"Reply to comments on: \"International Anal Neoplasia Society's consensus guidelines for anal cancer screening\".","authors":"Elizabeth A Stier, Megan A Clarke, Ashish A Deshmukh, Nicolas Wentzensen, Yuxin Liu, I Mary Poynten, Eugenio Nelson Cavallari, Valeria Fink, Luis F Barroso, Tamzin Cuming, Stephen E Goldstone, Richard J Hillman, Isabela Rosa-Cunha, Luciana L A Rosa, Joel M Palefsky, Rosalyn Plotzker, Jennifer M Roberts, Naomi Jay","doi":"10.1002/ijc.35394","DOIUrl":"https://doi.org/10.1002/ijc.35394","url":null,"abstract":"","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603166","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":"Eye-sparing treatment for sinonasal tumors invading the orbit in the era of personalized therapy.","authors":"Jie Wang, Li Wang, Tian Wang, Tianci Tang, Yi Li, Qiang Li, Xinmao Song","doi":"10.1002/ijc.35395","DOIUrl":"https://doi.org/10.1002/ijc.35395","url":null,"abstract":"<p><p>Few studies investigated the eye-sparing treatment in patients with sinonasal carcinomas (SNCs) from the perspective of modern precision radiation, and the eye-sparing treatment in patients with grade III orbital invasion was rarely discussed. This retrospective study included patients with primary SNCs who accepted eye-sparing treatment from October 2000 to June 2022 at a single institution. Patients' clinical information and follow-up data (including visual data) were obtained. All patients underwent radio(chemo)therapy alone or with surgery. The primary outcomes were overall survival (OS) and progression-free survival (PFS) rates. Secondary outcomes included regional-failure-free survival (RFS) and distant metastasis-free survival (DMFS) rates. 42.7% of SNC patients (430/1006) had orbital invasion. Orbital invasion significantly decreased the 5-year OS (77.9% vs. 61.1%, p < .001), PFS (70.5% vs. 51.3%, p < .001), RFS (77.8% vs. 60.8%, p < .001), and DMFS (76.8% vs. 59.3%, p < .001), which worsened as the invasion grade increased. Stratified analysis by treatment indicated that surgery significantly improved the OS (p < .001) and PFS (p = .0031) in patients with grade I/II orbital invasion. In contrast, surgery conferred no benefits to OS (p = .14) and PFS (p = .16) in patients with grade III orbital invasion. Blindness occurred in 6.7% of patients with orbital involvement and 1.9% of patients without orbital involvement. There was no difference in the blindness ratio among different treatment modes (χ² = 2.35, p = .31). Orbital invasion predicted poor survival outcomes, which worsened as the invasion grade increased. Surgery combined with radio(chemo)therapy was preferred in patients with grade I/II orbital invasion; however, surgery may have a limited effect on the survival of patients with grade III orbital invasion.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613045","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":"Comments on \"International anal neoplasia society's consensus guidelines for anal cancer screening\".","authors":"Massimiliano Mistrangelo, Francesca Farnesi, Emanuel Cavazzoni, Mario Morino","doi":"10.1002/ijc.35393","DOIUrl":"https://doi.org/10.1002/ijc.35393","url":null,"abstract":"","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603158","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":"Balanced diet quality and risk of upper gastrointestinal cancers: Insights from a prospective cohort study in China.","authors":"Shanrui Ma, Yueying Zhang, Shuanghua Xie, Xinqing Li, Ru Chen, Shaoming Wang, Wenqiang Wei","doi":"10.1002/ijc.35402","DOIUrl":"https://doi.org/10.1002/ijc.35402","url":null,"abstract":"<p><p>Upper gastrointestinal (UGI) cancers are highly prevalent in China and have been linked to dietary factors, yet the impact of overall diet quality remains underexplored. This study aimed to assess the association between Chinese diet quality, as measured by the Chinese Diet Balance Index 2016 (DBI-16) and plant-based diet index (PDI), and UGI cancer risks in high-risk populations. We conducted a prospective cohort study from 2017 to 2019 in five high-risk regions of China. Diet quality was assessed using DBI-16 and PDI. Diet quality was evaluated using DBI-16, which includes higher bound scores (HBS), lower bound scores (LBS), and diet quality distance (DQD), alongside the PDI, which distinguishes between overall, healthy, and unhealthy PDI. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox regression analysis. Over a median follow-up of 55 months, 790 cases of UGI cancers were recorded. A high HBS (excessive intake) was associated with a lower risk of UGI cancers (HR = 0.57, 95% CI: 0.41-0.81) and esophageal cancer (HR = 0.51, 95% CI: 0.32-0.80). Conversely, significant dietary imbalance (high DQD) increased UGI cancer risk (HR = 1.59, 95% CI: 1.08-2.36), while severe inadequate intake (high LBS) was only associated with an increased risk of esophageal cancer (HR = 2.16, 95% CI: 1.00-4.65). A higher overall PDI was protective against UGI cancers (HR_Q4vs.Q1 = 0.69, 95% CI: 0.49-0.98), whereas an unhealthy PDI increased the risk (HR_Q4vs.Q1 = 1.92, 95% CI: 1.38-2.67). The study concludes that unbalanced diets elevate UGI cancer risk, while balanced, plant-based diets reduce it. Promoting healthier dietary habits may benefit high-risk populations.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143583882","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":"Integrative metabolomics and microbiomics analysis reveals distinctive microbiota-metabolites interactions in gastric carcinogenesis.","authors":"Xiao-Wen Jiang, Li Zhang, Zong-Chao Liu, Tong Zhou, Wen-Qing Li, Wei-Dong Liu, Lan-Fu Zhang, Wei-Cheng You, Yang Zhang, Kai-Feng Pan","doi":"10.1002/ijc.35392","DOIUrl":"https://doi.org/10.1002/ijc.35392","url":null,"abstract":"<p><p>Gastric microbiota and metabolites may interact and play collaborative roles in the carcinogenesis process. This study aims to investigate differential metabolites and microbes, as well as the possible roles of microbe-metabolite interactions in gastric cancer (GC) development. Targeted metabolomics assays and 16S rRNA sequencing were performed to compare metabolic and microbial profiles in gastric tissues from subjects with superficial gastritis/chronic atrophic gastritis (SG/CAG), intestinal metaplasia/low-grade intraepithelial neoplasia (IM/LGIN) and GC. Significant differences were found in metabolic and microbial profiles between the GC and SG/CAG or IM/LGIN groups, respectively (all p < .05). By comparing GC with the other lesions, 69 differential metabolites mainly comprised triglycerides and phosphatidylcholines, and 21 differential microbes included Peptostreptococcus, Lactobacillus, Dialister, Helicobacter pylori, and Streptococcus anginosus (all p < .05). The altered metabolites and microbes in GC were both significantly enriched in the glycerophospholipid metabolism pathway, in which the predicted down-regulation of phospholipase C (plc) and up-regulation of 1-acyl-sn-glycerol-3-phosphate acyltransferase (plsC) by microbiota may affect phosphatidylcholine hydrolysis and triglyceride biosynthesis modules. More and stronger microbe-metabolite correlations in GC compared to the other lesion group further supported the potential microbial regulations to the important metabolites in gastric carcinogenesis, such as Lactobacillus and phosphatidylcholines (.32 ≤ r ≤ .57, all p < .05), Peptostreptococcus (.36 ≤ r ≤ .60, all p < .05) or Dialister (.36 ≤ r ≤ .62, all p < .05) and triglycerides. We simultaneously identified differential metabolites and microbes and their altered correlations between GC and gastric lesions. The main GC-associated phosphatidylcholines and triglycerides may be affected by gastric microbes, which provides new perspectives on the microbiota-metabolite interactions during the development of GC.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595882","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":"DNA methylation signatures of cervical pre-invasive and invasive disease: An epigenome-wide association study.","authors":"Sarah J Bowden, Barbara Bodinier, Maria Paraskevaidi, Ilkka Kalliala, Maria Nasioutziki, Laura Burney Ellis, Ruben Colindres Zuehlke, James M Flanagan, Maria Kyrgiou, Marc Chadeau-Hyam","doi":"10.1002/ijc.35406","DOIUrl":"https://doi.org/10.1002/ijc.35406","url":null,"abstract":"<p><p>Epigenetic alterations are essential in the development of cancers, while epigenome-wide exploration in cervical cancer has been limited. In this epigenome-wide association study (EWAS) we explore differential DNA methylation signatures associated with CIN (cervical intraepithelial neoplasia) grade 3 and cervical cancer to better understand potential drivers and biomarkers of cervical carcinogenesis. 247 women were recruited between 2014 and 2020 (N = 119 benign, N = 74 CIN3/CGIN [cervical glandular intraepithelial neoplasia] and N = 54 cancer). Methylation signatures were obtained from exfoliated cervical cells and sequenced using the Illumina 850 k array. Logistic regression and conditional analyses were used to test for independent associations between Cytosine-phosphate-Guanine (CpG) sites and case-control status, with adjustment for batch, chip, age, and human papillomavirus (HPV) status. 409 CpG sites were strongly associated with CIN3/cancer (p-value <5 × 10^-8). Following conditional analysis, two CpG sites located in PAX1 (cg16767801) and NREP-AS1 genes (cg23642047) were independently associated with case status, yielding an area under the curve (AUC) of 0.92 (AUC = 0.97 for invasive disease). In a validation dataset (CIN3 only) PAX1/NREP-AS1 yielded a combined AUC of 0.77. Methylation markers offer promise for use in cervical screening, particularly as triage tests and self-sampling. We have identified a novel combined methylation marker that offers a high accuracy for the detection of CIN3 or worse.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595813","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":"The transcription factor RIP140 regulates interferon γ signaling in breast cancer.","authors":"Stéphan Jalaguier, Axel Kuehn, Chloé Petitpas, Arnaud Dulom, Rémy Jacquemont, Cindy Assi, Sophie Sixou, Udo Jeschke, Jacques Colinge, Vincent Cavaillès","doi":"10.1002/ijc.35405","DOIUrl":"https://doi.org/10.1002/ijc.35405","url":null,"abstract":"<p><p>RIP140 (receptor interacting protein of 140 kDa) is an important player in breast cancer (BC) by regulating key cellular pathways such as nuclear hormone receptor signaling. In order to identify additional genes specifically regulated by RIP140 in BC, we performed a transcriptomic analysis after silencing its expression in MCF-7 cells. We identified the interferon γ (IFNγ) signaling as being substantially repressed by RIP140 knockdown. Using the GBP1 (guanylate binding protein 1) gene as a reporter of IFNγ signaling, we demonstrated its robust induction by RIP140 through an ISRE motif, leading to a significant reduction of its induction upon IFNγ treatment. Furthermore, we showed that low levels of RIP140 amplified the IFNγ-dependent inhibition of BC cell proliferation. In line with these data, reanalysis of transcriptomic data obtained in human BC samples revealed that IFNγ levels were associated with good prognosis only for BC patients exhibiting tumors expressing low levels of RIP140, thus confirming its effect on the anti-tumor activity of IFNγ provided by our experimental data. Altogether, this study identifies RIP140 as a new regulator of IFNγ signaling in breast tumorigenesis.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595884","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":"Safe prescribing in cancer patients during the COVID-19 pandemic and outcomes following restart of cancer care following SARS-CoV-2 infection: The COV-SPOT initiative.","authors":"Nathan Appanna, Rosie Mew, Sophie Williams, Thomas Starkey, Grisma Patel, Laura Hudson, Emma Burke, Francesca Aquilina, Caroline Harnett, Harrison Boult, William Greig, Daisy Ubsdell, Shannon Crouch, Philippa Smith, Katerina Jiskrova, Grant Vallance, Susanna Nallamilli, Alex Burnett, James Clark, Sam Khan, Martin Little, Justin Liu, Hari Panneerselvam, Vijay Patel, James Platt, Michael Tilby, Isabella Watts, Catherine Harper Wynne, Lennard Lee","doi":"10.1002/ijc.35377","DOIUrl":"https://doi.org/10.1002/ijc.35377","url":null,"abstract":"<p><p>SARS-CoV-2 continues to spread across the world as a highly transmissible endemic disease. For many cancer patients, SARS-CoV-2 infection is unavoidable. It continues to disrupt cancer care, causing treatment delays and major psycho-socio-medical issues. At present, there is limited evidence on safe prescribing of anti-cancer therapy, and safe treatment restart following SARS-CoV-2 infection. We conducted a prospective cohort study involving 406 COVID-19-positive cancer patients across five UK cancer centres and collected data on delay durations, COVID-19 symptoms and mortality, to ascertain the effect of treatment interruptions. Patients were studied between May 2022 and March 2023, during which Omicron variants of SARS-CoV-2 were predominant. Mean treatment interruption was 12.7 days (standard deviation 47.3 days). Upon resuming anti-cancer therapy, 8.5% experienced COVID-19 symptom progression, and 1.2% succumbed to COVID-19-related mortality. Patients with haematological cancers had a 3.4-fold increased risk of severe symptoms at 4 weeks compared to solid tumour patients. Higher symptom burden at COVID-19 diagnosis was associated with a 3.0-fold increase in symptom severity at 4 weeks following treatment restart. At 8 weeks following restart, 2.1% had increased morbidity or mortality. We highlight the ongoing impact of COVID-19 on patients and cancer care, and the risk of resuming cancer treatments in patients with symptomatic COVID-19. Although the risk of mortality is relatively low upon treatment resumption, personalised approaches assessing cancer diagnosis and SARS-CoV-2 status are crucial. Treatments are also stopped due to other infectious conditions and our results could be reviewed in the context of yearly influenza pandemics.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143583897","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":"Eosinophil-induced adverse events induced by treatment with programmed cell death 1/ligand 1 inhibitors: A comprehensive disproportionality analysis of the FDA adverse event reporting system.","authors":"Lu Lyu, Sainan Bian, Kai Guan, Bin Zhao","doi":"10.1002/ijc.35398","DOIUrl":"https://doi.org/10.1002/ijc.35398","url":null,"abstract":"<p><p>Eosinophil-induced adverse events (Eo-irAEs) have been observed in patients treated with programmed cell death 1/ligand 1 (PD-1/PD-L1) inhibitors. Surprisingly, the clinical features and outcomes of Eo-irAEs induced by PD-1/PD-L1 inhibitors have not yet been elucidated. This study investigated the characteristics of and risk factors for Eo-irAEs induced by PD-1/PD-L1 inhibitors. We extracted data on Eo-irAEs related to PD-1/PD-L1 inhibitors from the FDA Adverse Event Reporting System (FAERS) from 2015 to 2023. Disproportionality and Bayesian analyses were applied for data mining and analysis. A total of 430 Eo-irAEs induced by PD-1/PD-L1 inhibitors were included in this study. Older male patients were found to be at a high risk of developing Eo-irAEs. Cemiplimab (ROR 2.66 [1.38, 5.13]), nivolumab (ROR 1.82 [1.61, 2.05]), and pembrolizumab (ROR 1.35 [1.13, 1.62]) showed stronger signals than the other drugs. Cemiplimab showed higher signals for Eo-irAEs than other PD-1/PD-L1 inhibitors, with an information component (IC) of 1.41 (IC 0.25:0.73). Patients experienced Eo-irAEs within the first 100 days, with a median onset time of 56 (interquartile range: 17.0-169.0) days. Eo-irAEs were more likely to occur in patients with lung (n = 147, 34.83%) and skin tumors (n = 145, 34.36%). Eosinophilia (n = 193, 44.88%), drug reactions with eosinophilia and systemic symptoms (DRESS) (n = 98, 22.79%), and eosinophilic fasciitis (n = 69, 16.05%) were the most common adverse events. Eo-irAEs that were life-threatening or resulted in death comprised 5.15% (n = 21) and 5.39% (n = 22) of the patients. PD-1/PD-L1 inhibitors used across a broad spectrum of cancers are associated with an increased risk of Eo-irAEs, which tend to occur early. Although these complications are rare, clinicians using PD-1/PD-L1 inhibitors should be aware of and monitor these potentially serious adverse events related to Eo-irAEs.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595880","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":"Cohesin mutations and chromatin changes in cancer.","authors":"Ariel D Swett, Zuzana Tothova","doi":"10.1002/ijc.35378","DOIUrl":"https://doi.org/10.1002/ijc.35378","url":null,"abstract":"<p><p>The identification of recurrent mutations in genes encoding the cohesin complex in cancer was among the most unexpected findings from cancer exome sequencing studies. Cohesin is a multi-subunit protein complex that is essential for sister chromatid cohesion, three-dimensional chromosome organization, DNA damage repair, and gene regulation. It forms a ring around DNA, with four structural subunits, SMC1A, SMC3, RAD21, and either STAG1 or STAG2. In particular, the cohesin subunit STAG2 is one of only 12 human genes to be significantly mutated in four or more distinct types of cancer. Cohesin mutations are typically heterozygous and result in haploinsufficiency and/or loss-of-function, and although they might be expected to cause defects in chromosome segregation, the sister chromatid cohesion function of the complex is unlikely the driving mechanism of tumorigenesis, given the lack of aneuploidy in cohesin-mutant cancers. In this review, we will focus on the prevalence of somatic mutations in cohesin subunits across different cancer types, the influence of these mutations on chromatin organization and gene regulation, the resulting cellular and disease phenotypes, and the therapeutic potential of targeting the mutant cohesin complex.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143583894","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}