Cancer Medicine最新文献

{"title":"Occupational Disparities in Cancer Survival Among the Working Population in Japan: 10-Year Survival Analysis Using the Kanagawa Cancer Registry","authors":"Kazuhiko Watanabe,&nbsp;Ichiro Kawachi,&nbsp;Masayoshi Zaitsu","doi":"10.1002/cam4.71020","DOIUrl":"https://doi.org/10.1002/cam4.71020","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Limited data exist on occupational disparities in long-term cancer mortality among the working-age population in Japan. We examined occupational disparities in long-term cancer survival, focusing on 10-year survival outcomes among working-age populations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This retrospective observational study used data from the Kanagawa Cancer Registry of 41,632 patients with cancer aged 20–65 years who were diagnosed between 1992 and 2015, with a 10-year follow-up. Patients were classified into four occupational classes based on their longest-held occupations (upper nonmanual, lower nonmanual, manual, and primary industry). The primary outcome was all-cause mortality, and cancer-specific mortality was the secondary outcome. Poisson regression was used to estimate the mortality rate ratios (MRRs) and 95% confidence intervals (CIs) for each occupational class, adjusted for sex, age, and year of diagnosis. Additional analyses were performed for common cancer sites (stomach, lung, colorectal, and breast).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>MRRs for all-cause mortality were higher in lower nonmanual (MRR = 1.14, 95% CI 1.10–1.18), manual (MRR = 1.38, 95% CI 1.32–1.43), and primary industry workers (MRR = 1.19, 95% CI 1.09–1.31) than in upper nonmanual workers (professional and managerial occupations). Similar patterns were observed across common cancer sites and cancer-specific mortality. Adjusting for cancer stage and treatment attenuated these disparities but did not eliminate them, particularly among manual workers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We observed occupational disparities in long-term cancer mortality among working-age populations in Japan, with manual workers experiencing worse survival outcomes. Promoting targeted interventions, healthy lifestyles, and early cancer detection for cancer survivors in the workplace are crucial for mitigating these disparities.</p>\u0000 </section>\u0000 </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144537032","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":"Incidence, Outcomes and Risk Factors for Atrial Fibrillation in Patients With JAK2V617F-Positive Myeloproliferative Neoplasms","authors":"Guangshuai Teng,&nbsp;Ke Shang,&nbsp;Yuhui Zhang,&nbsp;Yifan Duan,&nbsp;Chenxiao Du,&nbsp;Yan Wang,&nbsp;Yanqi Li,&nbsp;Huiqin Zhang,&nbsp;Lan Peng,&nbsp;Xiaojing Wei,&nbsp;Gary Tse,&nbsp;Yuan Zhou,&nbsp;Gregory Y. H. Lip,&nbsp;Tong Liu,&nbsp;Wei Yang,&nbsp;Minghui Duan,&nbsp;Jie Bai","doi":"10.1002/cam4.71015","DOIUrl":"https://doi.org/10.1002/cam4.71015","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The incidence, outcomes and risk factors for AF in the <i>JAK2</i>^<i>V617F</i>-positive MPN patients are still unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The clinical profiles of patients with <i>JAK2</i>^<i>V617F</i>-positive MPN were retrospectively analyzed. Multivariable Cox regression analysis was performed to identify risk factors of AF, thereby developing a risk prediction model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 439 patients were included (age 57 [12–87] years; 51.3% male). AF was associated with higher risks of stroke (<i>p</i> = 0.036, HR = 1.987, 95% CI 1.047–3.772) and mortality (<i>p</i> &lt; 0.001, HR = 3.857, 95% CI 1.836–8.103). Multivariable Cox regression showed that <i>TET2</i> mutation (<i>p</i> = 0.042, HR = 4.361, 95% CI 1.053–18.056) and increased IL-1β (<i>p</i> = 0.012, HR = 5.476, 95% CI 1.547–28.123) were significant risk factors for AF in patients with <i>JAK2</i>^<i>V617F</i>-positive MPN. Nomograms were constructed, allowing patients to be categorized into high- and low-risk groups. The 10-year AF-free survival rate was significantly lower in the high-risk group (62% vs. 91.7%; log-rank test: <i>p</i> = 0.002). The validation cohort confirmed that the survival without AF in the high-risk group was significantly worse than that in the low-risk group. The use of either interferon-α or ruxolitinib, was associated with longer AF-free survival in the high-risk group (<i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>AF was significantly associated with higher risks of stroke and mortality. <i>TET2</i> mutation and increased IL-1β were independent risk factors of AF in patients with <i>JAK2</i>^<i>V617F</i>-positive MPN.</p>\u0000 </section>\u0000 </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144537031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Iron Chelation Therapy in Colorectal Cancer: A Systematic Review on Its Mechanisms and Therapeutic Potential","authors":"Gihani Vidanapathirana,&nbsp;Md Sajedul Islam,&nbsp;Sujani Gamage,&nbsp;Alfred K. Lam,&nbsp;Vinod Gopalan","doi":"10.1002/cam4.71019","DOIUrl":"https://doi.org/10.1002/cam4.71019","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Despite significant therapeutic advancements in recent decades, colorectal cancer (CRC) continues to exhibit high rates of mortality and morbidity. Chemoresistance and cancer recurrence remain substantial challenges, underscoring the need for novel treatment approaches. Iron chelation therapy has gained profound interest over the years as a potential cancer treatment, leveraging the increased iron demand by tumors. This review evaluates the effects of iron chelation therapy on CRC progression and the underlying mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>A comprehensive review of in vivo and in vitro studies was conducted to assess the effectiveness of iron chelation therapy in CRC. The literature search covered PubMed, Scopus, Medline (via Web of Science), and EMBASE between January 1995 and March 2024.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Several in vitro and in vivo studies have investigated the impact of iron chelators, such as deferoxamine, deferasirox, thiosemicarbazone-based chelators, quilamine-based chelators, and other novel compounds on CRC. Natural plant extracts with iron-chelating properties have also been explored as potential treatments. Most studies indicate that iron chelation can inhibit the proliferation of colon cancer cells, though some studies suggest cancer-promoting effects. Mechanistically, iron chelation affects several hallmarks of CRC by modulating histone methylation, upregulating NDRG1, and influencing the Wnt/β-catenin and p53 signaling pathways. However, certain iron chelators may inhibit TRAIL-mediated apoptosis and activate the hypoxia-inducible factor (HIF), potentially accelerating CRC progression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Future exploration of iron chelation therapy in CRC should focus on extensive in vitro, in vivo, and clinical studies to elucidate the precise mechanisms involved. A deeper understanding of the genetic and cellular alterations induced by iron chelation will enhance the development of effective therapeutic strategies for CRC.</p>\u0000 </section>\u0000 </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144537033","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":"Identification of Crucial Genes Associated With MYCN-Driven Neuroblastoma Based on Single-Cell Analysis and Machine Learning","authors":"Jiasi Zhang,&nbsp;Yichen Lei,&nbsp;Yaqin Wang,&nbsp;Wen Yu,&nbsp;Xiaoyan Zhao,&nbsp;Yongbing Zhu,&nbsp;Dedong Zhang,&nbsp;Siying Liu,&nbsp;Aiguo Liu","doi":"10.1002/cam4.71008","DOIUrl":"https://doi.org/10.1002/cam4.71008","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Neuroblastoma (NB) with MYCN amplification is strongly correlated with high-risk stratification and poor prognosis. However, the underlying mechanisms remain incompletely understood. Elucidating these pathways is critical for advancing personalized treatments for MYCN-driven NB.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We performed single-cell transcriptomic analysis comparing NB samples with and without MYCN. Key genes were then identified using machine learning based random survival forest (RSF) and nomogram analyses. The influence of key genes on immune infiltration and molecular mechanisms driving NB progression were further investigated. Finally, we visualized the expression levels and global function of these genes in single-cell datasets and validated their expression in patient samples through RT-qPCR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Single-cell transcriptome analysis of GSE218450 identified marker genes specific to NB cells. RSF and nomogram analyses revealed that overexpression of CKB, PCSK1N, OTUB1, and VGF is associated with poor prognosis, whereas upregulation of NTRK3 indicates a favorable prognosis. These genes are significantly associated with immune cell infiltration and play an important role in modulating the immune microenvironment. Pathway analysis further showed that these genes influence critical signaling pathways, including the Wnt pathway, and interact with tumor-related genes. Additionally, we confirmed that CKB and PCSK1N are positively correlated with MYCN in NB cell lines and are significantly overexpressed in MYCN-amplified NB patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our results provide molecular insights into the transcriptional changes associated with MYCN amplification in NB. In particular, the identification of CKB and PCSK1N suggests their potential role in driving tumor progression, making them promising targets for novel treatments in MYCN-driven NB.</p>\u0000 </section>\u0000 </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144524638","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":"Correction to Role of Exosome in Solid Cancer Progression and Its Potential Therapeutics in Cancer Treatment","authors":"","doi":"10.1002/cam4.71029","DOIUrl":"https://doi.org/10.1002/cam4.71029","url":null,"abstract":"<p>Aakel N, Mohammed R, Fathima A, Kerzabi R, Abdallah A, Ibrahim WN. Role of Exosome in Solid Cancer Progression and Its Potential Therapeutics in Cancer Treatment. Cancer Medicine. 2025 May;14(9):e70941. doi: 10.1002/cam4.70941. PMID: 40344389; PMCID: PMC12063069.</p><p>The first name of the third author was misspelled. The author's name should read Aseela Fathima.</p><p>We apologize for this error.</p>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144524722","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":"Correction to “SPARC Promotes Aerobic Glycolysis and 5-Fluorouracil Resistance in Colorectal Cancer Through the STAT3/HK2 Axis”","authors":"","doi":"10.1002/cam4.70998","DOIUrl":"https://doi.org/10.1002/cam4.70998","url":null,"abstract":"<p>Xiang J, et al. SPARC Promotes Aerobic Glycolysis and 5-Fluorouracil Resistance in Colorectal Cancer Through the STAT3/HK2 Axis. Cancer Med. 2025 Jun;14(11):e70972.</p><p>We apologize for this error.</p>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.70998","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144519629","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":"PRDX6 Drives Breast Cancer Progression Through Mitochondrial Biosynthesis and Oxidative Phosphorylation","authors":"Mei Dai,&nbsp;Danhua Zhang","doi":"10.1002/cam4.71005","DOIUrl":"https://doi.org/10.1002/cam4.71005","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Peroxiredoxin 6 (PRDX6) scavenges reactive oxygen species (ROS) and plays a key role in antioxidant defense. Although PRDX6 is involved in various cancers, its role in breast cancer (BRCA) remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Cell proliferation was assessed using CCK-8, EdU staining, and colony formation assays. Migration and invasion were evaluated via wound-healing and transwell assays. ROS levels and mitochondrial membrane potential were measured by fluorescence microscopy or flow cytometry. Oxidative phosphorylation (OXPHOS) activity was determined by ATP production and NAD⁺/NADH ratio. Mitochondria were visualized by TEM, and mitochondrial complex subunits were detected by quantitative real-time PCR and Western blotting. In vivo effects were evaluated using a xenograft tumor model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Although PRDX6 was downregulated in BRCA overall, it showed elevated expression in aggressive subtypes and advanced-stage tumors, correlating with poor prognosis. Overexpression of PRDX6 enhanced BRCA cell proliferation, migration, and invasion. PRDX6 reduced ROS levels, upregulated mitochondrial transcription factor A (TFAM) expression, and promoted mitochondrial complex subunit expression and OXPHOS. Inhibition of TFAM led to a decrease in the expression of some of the mitochondrial complex subunits, which reversed the pro-carcinogenic phenotype of the tumor. PRDX6 also promoted tumor growth in vivo.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>PRDX6 maintains intracellular homeostasis by reducing ROS and promotes mitochondrial biogenesis and OXPHOS through TFAM-dependent and -independent pathways, driving BRCA progression.</p>\u0000 </section>\u0000 </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144515053","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":"MMRN1 Facilitates Renal Cell Carcinoma by Activating AMPK/MMPs Axis","authors":"Mingji Ye,&nbsp;Jian Cao,&nbsp;Zhihao Ming,&nbsp;Yu Xie","doi":"10.1002/cam4.71013","DOIUrl":"https://doi.org/10.1002/cam4.71013","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>MMRN1 is a metastasis-associated gene that is abnormally expressed in a variety of tumors. The present study aimed to explore the role of MMRN1 in renal cell carcinoma (RCC) and its related molecular mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>RNA sequencing was used to detect differential gene expression in RCC. Immunohistochemical (IHC) analysis identified the expression of MMRN1 in RCC. Statistical evaluations and the GEPIA database were conducted to examine the association between MMRN1 expression and the prognosis of RCC patients. The MTT assay was employed to assess cellular proliferative capacity, while the Transwell assay was used to evaluate metastasis. Additionally, subcutaneous tumor transplantation and lung metastasis assays in nude mice were performed to investigate the growth and metastasis of RCC cells in vivo.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>MMRN1 was significantly upregulated in RCC. The GEPIA database revealed an association between MMRN1 and distal metastasis, as well as poor prognosis in RCC patients. The overexpression of MMRN1 was found to enhance the proliferation and metastasis of RCC cells, whereas MMRN1 knockout was opposite. Additionally, MMRN1 overexpression facilitated the growth and metastasis of transplanted tumors in nude mice models. Mechanistically, MMRN1 overexpression activated the AMPK signaling pathway in RCC, and inhibition of this pathway mitigated the observed effects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>MMRN1 is an oncogene in RCC. MMRN1 activates MMPs through the AMPK pathway to promote the proliferation and invasion of RCC.</p>\u0000 </section>\u0000 </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144515059","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":"Identification of the Oncogenic Role of MSH2 in the Stemness and Progression of Glioma Through Regulating Wnt Signaling Pathway","authors":"Jun Liu,&nbsp;Jiayu Chen,&nbsp;Lianglei Jiang","doi":"10.1002/cam4.70993","DOIUrl":"https://doi.org/10.1002/cam4.70993","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Glioma is one of the most aggressive brain tumors, and its progression is often associated with stemness maintenance and therapy resistance. The role of MSH2 in glioma remains largely unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analyzed public datasets and clinical samples to assess MSH2 expression and its clinical relevance. Functional assays in vitro and in vivo were performed to investigate the effects of MSH2 knockdown on glioma cell behavior. Mechanistic studies were conducted to explore downstream signaling pathways and stemness regulation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>MSH2 was found to be significantly upregulated in glioma tissues and cell lines, and its high expression correlated with poor prognosis. Silencing MSH2 inhibited cell proliferation, migration, and tumor growth, while promoting apoptosis and G2 cell cycle arrest. Mechanistically, phospho-kinase screening and rescue experiments suggested that MSH2 promotes glioma progression via activation of the Wnt/β-catenin signaling pathway. Furthermore, MSH2 knockdown suppressed the expression of stemness markers, impaired sphere formation, and sensitized glioma cells to cisplatin treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our study identifies MSH2 as an oncogenic factor in glioma, which drives stemness and progression through regulation of the Wnt/β-catenin pathway, and may serve as a potential therapeutic target.</p>\u0000 </section>\u0000 </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.70993","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144520232","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":"RETRACTION: MiRNA-545 Negatively Regulates the Oncogenic Activity of EMS1 in Gastric Cancer","authors":"","doi":"10.1002/cam4.71011","DOIUrl":"https://doi.org/10.1002/cam4.71011","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;p&gt;\u0000 &lt;b&gt;RETRACTION&lt;/b&gt;: &lt;span&gt;M. Ma&lt;/span&gt;, &lt;span&gt;J. Zhao&lt;/span&gt;, &lt;span&gt;Q. Wu&lt;/span&gt;, &lt;span&gt;K. Xiao&lt;/span&gt;, &lt;span&gt;S. Li&lt;/span&gt;, &lt;span&gt;H. Zhu&lt;/span&gt;, &lt;span&gt;C. Liu&lt;/span&gt;, &lt;span&gt;H. Xie&lt;/span&gt;, and &lt;span&gt;C. Zuo&lt;/span&gt;, “ &lt;span&gt;MiRNA-545 Negatively Regulates the Oncogenic Activity of EMS1 in Gastric Cancer&lt;/span&gt;,” &lt;i&gt;Cancer Medicine&lt;/i&gt; &lt;span&gt;7&lt;/span&gt;, no. &lt;span&gt;6&lt;/span&gt; (&lt;span&gt;2018&lt;/span&gt;): &lt;span&gt;2452&lt;/span&gt;–&lt;span&gt;2462&lt;/span&gt;, https://doi.org/10.1002/cam4.1520.\u0000 &lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;p&gt;The above article, published online on 07 May 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Stephen Tait; and John Wiley &amp; Sons Ltd.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;p&gt;The retraction has been agreed due to the use of contaminated cell lines in this article. Both the cell lines used to demonstrate the regulatory role of miR-545 in EMS1 expression (SGC-7901 &amp; BGC-823) have been reported to be contaminated with HeLa [1, 2], as has cell line MGC-803 [3, 4]. Thus, the editors consider the conclusions of this article to be invalid.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;p&gt;We did not find any evidence of misconduct by the authors.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; References&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;\u0000 [1] &lt;span&gt;F. Ye&lt;/span&gt;, &lt;span&gt;C. Chen&lt;/span&gt;, &lt;span&gt;J. Qin&lt;/span&gt;, &lt;span&gt;J. Liu&lt;/span&gt;, and &lt;span&gt;C. Zheng&lt;/span&gt;, “ &lt;span&gt;Genetic Profiling Reveals an Alarming Rate of Cross-Contamination Among Human Cell Lines Used in China&lt;/span&gt;,” &lt;i&gt;The FASEB Journal&lt;/i&gt; &lt;span&gt;29&lt;/span&gt;, no. &lt;span&gt;10&lt;/span&gt; (&lt;span&gt;2015&lt;/span&gt;): &lt;span&gt;4268&lt;/span&gt;–&lt;span&gt;4272&lt;/span&gt;, https://doi.org/10.1096/fj.14-266718.\u0000 &lt;/p&gt;\u0000 \u0000 &lt;p&gt;\u0000 [2] &lt;span&gt;X. Bian&lt;/span&gt;, &lt;span&gt;Z. Yang&lt;/span&gt;, &lt;span&gt;H. Feng&lt;/span&gt;, &lt;span&gt;H. Sun&lt;/span&gt;, and &lt;span&gt;Y. Liu&lt;/span&gt;, “ &lt;span&gt;A Combination of Species Identification and STR Profiling Identifies Cross-contaminated Cells from 482 Human Tumor Cell Lines&lt;/span&gt;,” &lt;i&gt;Scientific Reports&lt;/i&gt; &lt;span&gt;7&lt;/span&gt; (&lt;span&gt;2017&lt;/span&gt;): &lt;span&gt;9774&lt;/span&gt;, https://doi.org/10.1038/s41598-017-09660-w.\u0000 &lt;/p&gt;\u0000 \u0000 &lt;p&gt;\u0000 [3] &lt;span&gt;F. Cao&lt;/span&gt;, &lt;span&gt;H. Sun&lt;/span&gt;, &lt;span&gt;Z. Yang&lt;/span&gt;, &lt;span&gt;Y. Bai&lt;/span&gt;, &lt;span&gt;X. Hu&lt;/span&gt;, &lt;span&gt;Y. Hou&lt;/span&gt;, &lt;span&gt;X. Bian&lt;/span&gt;, and &lt;span&gt;Y. Liu&lt;/span&gt;, “ &lt;span&gt;Multiple Approaches Revealed MGc80-3 as a Somatic Hybrid with HeLa Cells Rather than a Gastric Cancer Cell Line&lt;/span&gt;,” &lt;i&gt;International Journal of Cancer&lt;/i&gt; &lt;span&gt;154&lt;/span&gt;, no. &lt;span&gt;1&lt;/span&gt; (&lt;span&gt;2024&lt;/span&gt;): &lt;span&gt;155&lt;/span&gt;–&lt;span&gt;168&lt;/span&gt;, https://doi.org","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 13","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144515052","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}