{"title":"RETRACTION: MAEL Expression Links Epithelial-Mesenchymal Transition and Stem Cell Properties in Colorectal Cancer.","authors":"","doi":"10.1002/ijc.70739","DOIUrl":"10.1002/ijc.70739","url":null,"abstract":"<p><strong>Retraction: </strong>Q. Li, P. Wei, B. Huang, Y. Xu, X. Li, Y. Li, S. Cai, and D. Li, \"MAEL Expression Links Epithelial-Mesenchymal Transition and Stem Cell Properties in Colorectal Cancer,\" International Journal of Cancer 139, no. 11 (2016): 2502-2511, https://doi.org/10.1002/ijc.30388. The above article, published online on 30 July 2025 in Wiley Online Library (wileyonlinelibrary.com), and its erratum (https://doi.org/10.1002/ijc.33194), have been retracted by agreement between the journal Editor-in-Chief, Christoph Plass; the Union for International Cancer Control; and John Wiley & Sons Ltd. A third party reported on PubPeer [1] that images in Figure 3 were later published in another article by different authors [Jiang et al. 2018 (https://doi.org/10.1111/jcmm.13732)] and that Figure 1c(2) was also published in a separate article by different authors [Wu et al. 2018 (https://doi.org/10.7150/jca.26359)]. Further investigation by the publisher found that several lanes of the GAPDH bands in Figure 4a had been re-used and labeled as beta-actin in another article by some of the same authors [Li et al. 2018 (https://doi.org/10.7150/ijbs.24505)] and that there was evidence of duplication and splicing in Figures 2a and 3a. Additionally review by the editors found concerns about data handling that were not adequately addressed during peer review. Additionally, upon re-investigation, the authors' previous explanation for the erratum which replaced images in Figures 2d, 2g, and 2h was not considered satisfactory by either the editors or the publisher. The authors did not respond to an inquiry by the publisher. The retraction has been agreed to because the concerns over data handling, coupled with evidence that the authors have re-used data in a later article, fundamentally compromises the editors' confidence in the results in this article. The authors were informed of the retraction. REFERENCE: [1] Reese Richardson. Comments on \"MAEL expression links epithelial-mesenchymal transition and stem cell properties in colorectal cancer,\" PubPeer, July 2025. https://pubpeer.com/publications/E5633F92CB80ECA22A7893E2D6F840.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"220"},"PeriodicalIF":4.9,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149011716","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":"Correction to \"Design and Initial Findings of a Natural History Study of Anal HPV and Associated Lesions Among Young Adult Women in Costa Rica\".","authors":"","doi":"10.1002/ijc.70757","DOIUrl":"10.1002/ijc.70757","url":null,"abstract":"","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"219"},"PeriodicalIF":4.9,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079116","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":"Reply to: Comment on \"The Prognostic Potential of RNA in Stage II Colon Cancer: Insights From a Screened Multicenter Population-Based Cohort Study\".","authors":"Lasse S Kristensen, Ulrik Korsgaard, Henrik Hager","doi":"10.1002/ijc.70701","DOIUrl":"10.1002/ijc.70701","url":null,"abstract":"","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"3051-3052"},"PeriodicalIF":4.9,"publicationDate":"2026-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148786274","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":"Correction to \"Health-Related Quality of Life in Chinese Children and Adolescents With Cancer: A Systematic Review and Meta-Analysis\".","authors":"","doi":"10.1002/ijc.70696","DOIUrl":"10.1002/ijc.70696","url":null,"abstract":"","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"2850"},"PeriodicalIF":4.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808039","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":"Reply to: Comments on \"Survival by Detection Pathway in Patients With Lung Cancer-A Nationwide Descriptive Epidemiological Study in Japan\".","authors":"Ryo Koto, Atsuki Yamamoto, Ikumi Takashima, Chikako Iwao, Jung-Ho Shin, Yuko Hayashi, Hiroshi Kitagawa, Yoshiharu Horie","doi":"10.1002/ijc.70678","DOIUrl":"10.1002/ijc.70678","url":null,"abstract":"","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"2621-2622"},"PeriodicalIF":4.9,"publicationDate":"2026-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148672843","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}
Alexander Quaas, Hanna Schiemann, Su Ir Lyu, Thomas Zander, Axel Hillmer, Hans Schlößer, Christiane J Bruns, Reinhard Büttner, Bastian Grothey
{"title":"Sex-Specific Proteomic Profiling Identifies Pregnancy Zone Protein as a Complement-Linked Marker of Adverse Prognosis in Esophageal Adenocarcinoma.","authors":"Alexander Quaas, Hanna Schiemann, Su Ir Lyu, Thomas Zander, Axel Hillmer, Hans Schlößer, Christiane J Bruns, Reinhard Büttner, Bastian Grothey","doi":"10.1002/ijc.70687","DOIUrl":"10.1002/ijc.70687","url":null,"abstract":"<p><p>Esophageal adenocarcinoma (EAC) exhibits marked male predominance with male-to-female ratios reaching 8.5:1, yet the molecular basis underlying this sex disparity remains poorly characterized. We analyzed 92 EAC specimens using mass spectrometry-based proteomics, comprising 47 female and 45 male tumors from treatment-naïve patients. Differential expression, pathway enrichment, immunohistochemical, and survival analyses were used to identify sex-associated proteomic features and prognostic signatures. Proteomic profiling revealed focal yet biologically meaningful sex differences in EAC. After multiple testing correction, three proteins were differentially expressed: the autosomal protein pregnancy zone protein (PZP), enriched in female tumors, and the Y-chromosome-encoded proteins DDX3Y and RPS4Y1, which were overexpressed in male tumors. At nominal significance, proteins upregulated in female tumors showed marked enrichment of immune-related pathways. Proteins correlated with PZP expression formed a network dominated by complement cascade. Clinically, elevated PZP expression was associated with significantly poorer overall survival specifically in male patients, with no significant association detected in the combined or female-only cohort. Proteome-wide survival analyses further demonstrated distinct sex-specific prognostic landscapes. Our study provides the first comprehensive characterization of sex-associated proteomic differences in EAC. Sex shapes immune-related pathways, prognostic proteomic signatures, and survival associations. PZP emerges as a sex-differential, complement-associated protein with adverse prognostic significance in male patients, highlighting sex as a biologically and clinically relevant variable in EAC.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"2595-2605"},"PeriodicalIF":4.9,"publicationDate":"2026-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148710708","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}
Youmi Shin, Dong Keon Kim, Yoojeong Seo, Hyeon Hee Lee, Jihye Park, Soo Jung Park, Jae Jun Park, Jae Hee Cheon, Jongwon Oh, Sanghoo Lee, Tae Il Kim
{"title":"Evaluation of Mutation Risk Using Patient-Derived Organoids in Patients With Lynch Syndrome.","authors":"Youmi Shin, Dong Keon Kim, Yoojeong Seo, Hyeon Hee Lee, Jihye Park, Soo Jung Park, Jae Jun Park, Jae Hee Cheon, Jongwon Oh, Sanghoo Lee, Tae Il Kim","doi":"10.1002/ijc.70646","DOIUrl":"10.1002/ijc.70646","url":null,"abstract":"<p><p>Lynch syndrome (LS) is a hereditary cancer predisposition syndrome caused by germline mutation of DNA mismatch repair (MMR) genes, most notably associated with colorectal cancer. Although LS patients face high risk of CRC, risk can vary even among those with the same pathogenic MMR germline mutations. We suggest a functional assay platform for assessing mutation risk using patient-derived organoid (PDOs). We measured organoid response to the cytotoxic effects of a methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) based on DNA damage-induced apoptosis. When normal (non-LS) colon organoids were used, treatment with MNNG and four passages of organoid culture led to decreased total growth (organoid area), but there was no significant change in number. To increase the effect of MNNG and induce apoptosis in normal colon organoids, we added O<sup>6</sup>BG (an MGMT inhibitor) and an ATR inhibitor. The cytotoxic effects of combined treatment with MNNG, O<sup>6</sup>BG and ATR inhibitor on non-LS-PDOs were significantly higher than in PDOs of LS patients. To detect the difference at an earlier phase, we examined DNA damage response by analyzing γH2AX expression after treatment with MNNG and O6BG for 24 h. Then, we found higher expression of γH2AX in non-LS-PDOs than in PDOs of LS patients, suggesting continued cell survival with mutation accumulation in LS-PDOs. In conclusion, treatment with MNNG and O6BG using PDOs and measurement of resulting DNA damage response could be used as a preclinical platform for risk stratification in LS patients.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"2585-2594"},"PeriodicalIF":4.9,"publicationDate":"2026-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595499/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148417193","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}
Tillmann Bedau, Thomas Zander, Hans Anton Schlößer, Hakan Alakus, Onur Mustafov, Reinhard Büttner, Christiane Bruns, Alexander Quaas
{"title":"MET Expression in Upper Gastrointestinal Adenocarcinoma: Prevalence, Prognostic Impact, and Implications for Anti-MET Antibody-Drug Conjugate Therapy.","authors":"Tillmann Bedau, Thomas Zander, Hans Anton Schlößer, Hakan Alakus, Onur Mustafov, Reinhard Büttner, Christiane Bruns, Alexander Quaas","doi":"10.1002/ijc.70634","DOIUrl":"10.1002/ijc.70634","url":null,"abstract":"<p><p>MET is an actionable receptor tyrosine kinase, and MET-directed antibody-drug conjugates (ADCs) have recently entered clinical practice with FDA approval in non-small cell lung cancer and are now being evaluated across gastrointestinal malignancies, with patient selection based on MET immunohistochemistry (IHC) 3+ membranous staining at varying percentage thresholds. However, robust real-world data on MET protein expression and clinically relevant ADC-aligned thresholds in upper GI adenocarcinomas remain limited. We profiled 1532 upper GI adenocarcinomas using the clinically validated VENTANA MET (SP44) IHC assay. MET was stratified by (i) 3+ membranous staining fractions (any, ≥ 10%, ≥ 50%) reflecting contemporary ADC eligibility concepts and (ii) H-score (0-300; high ≥ 150). Overall survival analyses and multivariable Cox regression analyses were performed. High MET expression was uncommon (H-score ≥ 150: 2.3%; any 3+: 1.6%; ≥ 10% 3+: 1.3%; ≥ 50% 3+: 1.0%) and enriched in advanced T stage. MET IHC strongly predicted MET amplification (H-score ≥ 150: 63.6% amplified vs. 2.4% in negatives; any 3+: 75.0% vs. 2.6%; all p < 0.001). Any MET 3+ staining was independently associated with inferior overall survival (adjusted HR 2.22, 95% CI 1.29-3.83). Most MET 3+ tumors lacked concurrent HER2 positivity, Claudin-18.2 expression, or dMMR/MSI. In the largest real-world cohort to date, MET overexpression identifies a rare, biologically aggressive subset with poor outcomes. By applying the latest MET-ADC-relevant IHC criteria (including the ≥ 10% 3+ threshold), this study provides clinically translatable prevalence estimates and supports standardized MET testing to inform prospective MET-directed ADC trials in upper GI adenocarcinoma.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"2606-2618"},"PeriodicalIF":4.9,"publicationDate":"2026-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148373990","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":"Comments on 'Survival by Detection Pathway in Patients With Lung Cancer: A Nationwide Descriptive Epidemiological Study in Japan'.","authors":"Masashi Matsuzaka, Rina Tanaka","doi":"10.1002/ijc.70677","DOIUrl":"10.1002/ijc.70677","url":null,"abstract":"","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":"2619-2620"},"PeriodicalIF":4.9,"publicationDate":"2026-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148672808","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 Epithelial Epigenome: A Unified Platform for Cancer Risk Prediction and Prevention Monitoring.","authors":"Martin Widschwendter","doi":"10.1002/ijc.70800","DOIUrl":"https://doi.org/10.1002/ijc.70800","url":null,"abstract":"<p><p>Intrinsic biological processes and carcinogenic exposures leave cumulative DNA methylation (DNAme) imprints in epithelial cells. These changes reflect cellular composition, replicative/mitotic age and impaired differentiation capacity, and arise long before clinically detectable cancer, consistent with the concept of field cancerisation. Importantly, such epigenetic alterations are not confined to the tissue of origin but extend to anatomically distant epithelia that share developmental lineage and/or carcinogen exposure/susceptibility, thereby serving as field defect indicators. Notably, these signatures are dynamic and responsive to preventive interventions, enabling both risk assessment and real-time monitoring of prevention efficacy. The epithelial epigenome is thus emerging as a unified, minimally invasive platform for personalised, multi-cancer prevention.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149340010","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}