World Journal of Oncology最新文献

{"title":"Hypoxia-Induced Exosomal miR-1225-5p Accelerates Colorectal Cancer Progression by Targeting Carboxypeptidase M.","authors":"Yue Hui Guo, Qing Yun Zhu, Shi Wei Chen, Yan Xiang Li, Chuan Chen, Cai Fang Ni","doi":"10.14740/wjon2766","DOIUrl":"10.14740/wjon2766","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) remains a considerable public health burden worldwide, with hypoxia emerging as a key driver of tumor aggressiveness. Within the hypoxic tumor microenvironment (TME), exosomes function as vital vehicles for intercellular communication, especially through their cargo of microRNAs (miRNAs). Despite the growing recognition of this phenomenon, the specific functions of hypoxia-induced exosomal miRNAs in CRC remain inadequately defined.</p><p><strong>Methods: </strong>Human CRC cell lines (SW620 and HCT116) were subjected to normoxic or hypoxic conditions. Exosomes were isolated via ultracentrifugation and rigorously characterized by transmission electron microscopy (TEM) and dynamic light scattering (DLS). Quantitative real-time PCR (qRT-PCR) profiling identified miR-1225-5p as significantly enriched under hypoxia. The uptake of Cy3-labeled miR-1225-5p-loaded and PKH67-labeled exosomes by CRC cells was confirmed. The impact of these phenomena on cell progression capabilities was subsequently evaluated through the implementation of cell counting kit-8, colony formation, Transwell invasion, and wound-healing assays. The validation of the miR-1225-5p-carboxypeptidase M (<i>CPM</i>) regulatory axis was conducted through a series of rigorous methods, including luciferase reporter assays, Western blot analysis, and siRNA-mediated knockdown. Bioinformatic assessments via UALCAN examined correlations between <i>CPM</i> expression and clinical CRC prognosis.</p><p><strong>Results: </strong>Hypoxic CRC cell-derived exosomes exhibited markedly increased miR-1225-5p content. These exosomes effectively transferred miR-1225-5p to recipient CRC cells, thereby enhancing their malignant behaviors. Mechanistically, miR-1225-5p directly suppressed <i>CPM</i> expression by interacting with its 3'UTR. Bioinformatics analysis demonstrated that lower CPM expression correlates with poor patient prognosis, indicating a tumor-suppressive role. The downregulation of <i>CPM</i> independently recapitulated the oncogenic phenotypes induced by miR-1225-5p, whereas the inhibition of miR-1225-5p reversed these effects, suppressing CRC cell malignancy.</p><p><strong>Conclusion: </strong>The present study identifies a novel hypoxia-driven exosome-mediated miRNA pathway, whereby miR-1225-5p promotes CRC progression through targeted inhibition of the tumor suppressor gene, <i>CPM</i>. These findings contribute to our expanded understanding of exosomal RNA signaling within a hypoxic TME, thus identifying potential therapeutic targets.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 4","pages":"477-493"},"PeriodicalIF":2.3,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13375411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148580702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Experience of Robotic Partial Nephrectomy for Localized Renal Tumors: Functional and Oncologic Outcomes.","authors":"Tuan Thanh Nguyen, Khac Chuan Hoang, Trong Tri Tran, Le Quy Van Dinh, Xuan Thai Ngo","doi":"10.14740/wjon2791","DOIUrl":"10.14740/wjon2791","url":null,"abstract":"<p><strong>Background: </strong>Evidence comparing outcomes of robot-assisted partial nephrectomy (RAPN) between small and larger malignant renal tumors remains limited, particularly in real-world single-center practice. We aimed to compare perioperative, renal functional, and oncologic outcomes of RAPN according to tumor size and to evaluate predictors of trifecta achievement.</p><p><strong>Methods: </strong>We conducted a retrospective single-center cohort study of 74 patients undergoing transperitoneal RAPN for malignant renal tumors, including 42 patients with T1a tumors (≤ 4 cm) and 32 with tumors > 4 cm. Baseline characteristics, perioperative outcomes, renal functional outcomes, and oncologic outcomes were compared between groups. Trifecta was assessed using an exploratory parsimonious multivariable logistic regression model including tumor size group, RENAL complexity, hilar anatomy complexity, and age, given the limited sample size and event counts.</p><p><strong>Results: </strong>Compared with the T1a group, patients with tumors > 4 cm had significantly higher RENAL scores and a greater proportion of highly complex tumors. Operative time was longer (252.1 vs. 226.3 min, P = 0.030), and hospital stay was longer (median 6 vs. 5 days, P = 0.040). No statistically significant differences were observed in warm ischemia time, estimated blood loss, complication rates, positive surgical margin rates, or trifecta achievement (43.8% vs. 50.0%, P = 0.765), although the study may have been underpowered to detect clinically meaningful differences. Absolute estimated glomerular filtration rate (eGFR) was lower in the > 4 cm group at 3, 6, and 12 months, but eGFR preservation percentages and chronic kidney disease (CKD) upstaging rates did not differ significantly. On exploratory multivariable analysis, tumor size > 4 cm was not independently associated with trifecta achievement (odds ratio (OR) 0.80, 95% confidence interval (CI) 0.28-2.26, P = 0.673), and no statistically significant independent predictor was identified.</p><p><strong>Conclusions: </strong>RAPN for tumors > 4 cm was associated with greater anatomical complexity and modestly increased operative burden. No statistically significant differences were observed in ischemic, complication, oncologic, or relative renal functional outcomes, although these comparisons should be interpreted cautiously because the study may have been underpowered for uncommon events. These findings support the feasibility of RAPN for selected larger malignant renal tumors in a real-world single-center setting.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 4","pages":"588-597"},"PeriodicalIF":2.3,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13375410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148580552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurogenic Small Molecules Reverse miR-342-3p-Mediated Tumorigenesis in Renal Cell Carcinoma.","authors":"Yi Zhou Ye, Zhang Ming Du, Hong Wei Chen, Qian Xu","doi":"10.14740/wjon2753","DOIUrl":"10.14740/wjon2753","url":null,"abstract":"<p><strong>Background: </strong>Cigarette smoking is a major established risk factor for clear cell renal cell carcinoma (ccRCC), yet the molecular mediators linking smoking exposure to tumor biology remain incompletely understood. Here, we investigated whether smoking status influences circulating and tissue miR-342-3p and miR-342-5p expression.</p><p><strong>Methods: </strong>We determined miR-342-3p and miR-342-5p expression levels in tissues and plasmas from ccRCC patients and healthy controls using quantitative reverse transcription polymerase chain reaction. To elucidate the functional relevance of miR-342-3p dysregulation in ccRCC, we integrated miRTARGET and DAVID Gene Ontology analyses to identify ccRCC-related and experimentally validated targets. Cell counting kit-8 assay measured the impact of miR-342-3p mimic and neurogenic small molecules on 293T and 786-O cells.</p><p><strong>Results: </strong>We found that both miR-342-3p and miR-342-5p were significantly upregulated in ccRCC, with miR-342-3p expression showing a strong positive association with smoking status and highest levels observed in current smokers. Receiver operating characteristic analysis demonstrated that combined plasma miR-342-3p and miR-342-5p expression achieved an area under the curve (AUC) of 0.767, with a sensitivity of 81.6% and a specificity of 69.4%. A total of 178 miR-342-3p ccRCC targets were mainly enriched in lipid metabolic and neurogenesis processes. miR-342-3p overexpression significantly enhanced 293T cell proliferation. However, treatment with a neurogenic small-molecule cocktail (SB431542, LDN193189, CHIR99021, and DAPT) markedly attenuated this proliferative effect. In RCC 786-O cells, the same small molecules significantly inhibited cell proliferation, whereas miR-342-3p overexpression reversed their inhibitory effect.</p><p><strong>Conclusion: </strong>Cigarette smoking upregulates miR-342-3p and miR-342-5p expression in ccRCC. Mechanistically, miR-342-3p appears to promote RCC tumorigenesis through repression of neurogenic genes. Neurogenic small molecules may confer therapeutic benefit by antagonizing this effect and thereby suppressing RCC progression.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 4","pages":"442-453"},"PeriodicalIF":2.3,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13375416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148580740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated E2F6 Expression in Colorectal Cancer Tissues and Its Association With Clinicopathological Features.","authors":"Da Tong Zeng, Ke Jun Wu, Jian Di Li, Guo Qiang Chen, Wei Zhang, Zong Yu Li, Jing Wen Ling, Wei Jian Huang, Gang Chen, Hui Li","doi":"10.14740/wjon2707","DOIUrl":"10.14740/wjon2707","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is the third most common malignancy worldwide, and the role of E2F transcription factor 6 (E2F6) in CRC remains controversial.</p><p><strong>Methods: </strong>We analyzed E2F6 mRNA expression across 19 platforms (2,449 CRC patients and 1,328 controls), evaluated expression patterns using single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics, assessed E2F6 dependency using clustered regularly interspaced short palindromic repeats (CRISPR) knockout data from 52 CRC cell lines, and validated protein expression by immunohistochemistry (IHC) in 200 paired CRC and adjacent tissues. Associations between E2F6 and clinicopathological features were analyzed.</p><p><strong>Results: </strong>E2F6 was significantly upregulated in CRC versus controls (summary receiver operating characteristic (sROC) area under the curve (AUC) = 0.93), supported by scRNA-seq and spatial transcriptomics. E2F6 knockout suppressed proliferation across CRC cell lines, and IHC confirmed higher E2F6 protein expression (AUC = 0.91). Elevated E2F6 correlated with adverse clinicopathological features including female sex, age ≥ 60 years, advanced T stage, high-grade tumor budding, and higher histological grade.</p><p><strong>Conclusions: </strong>E2F6 is highly expressed in CRC and is associated with unfavorable clinicopathological features, supporting its potential utility as a diagnostic biomarker and a candidate target for CRC stratification and therapy development.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"322-336"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171258/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring Two Decades of Cancer Trends in Adolescents and Young Adults: Insights From a Resource-Restricted Country.","authors":"Maha Barbar, Asem Mansour, Rawad Rihani, Iyad Sultan, Sarah Abdel-Razeq, Ronny Baqain, Ayat Taqash, Hira Bani Hani, Hikmat Abdel-Razeq","doi":"10.14740/wjon2731","DOIUrl":"10.14740/wjon2731","url":null,"abstract":"<p><strong>Background: </strong>Over 40% of Jordan's population falls within the adolescent and young adult (AYA) age group (15-39 years). Cancer diagnosed in this population has unique biological, clinical, and psychosocial characteristics. This study describes national incidence trends and treatment outcomes among AYA patients in Jordan.</p><p><strong>Methods: </strong>This retrospective observational study utilized data from Jordan Cancer Registry (JCR) reports (2000-2022), King Hussein Cancer Center (KHCC) registry outcomes, and the latest GLOBOCAN report. Descriptive statistics, Kaplan-Meier survival analysis, and log-rank testing were used to evaluate cancer incidence and overall survival.</p><p><strong>Results: </strong>The median age at cancer diagnosis in Jordan is 57 years, significantly younger than in Western countries. Over the past 23 years, the total number of cancer cases among AYA increased from 654 in 2000 to 1,167 in 2022, representing 13.3% of all cancer diagnoses in that year. Most cases (36.8%) occurred in the older AYA subgroup (35-39 years). Age-standardized incidence rates (ASIRs) were consistently higher in females than males across all AYA age groups, largely driven by breast and thyroid cancers. ASIR increased from 17.3 per 100,000 in the youngest group (15-19 years) to 84.4 per 100,000 in the oldest group (35-39 years). The 5-year overall survival (OS) among AYA patients was 73.0% (95% confidence interval (CI), 71.8-74.1), significantly better than older adults at 57.1% (95% CI, 56.4-57.8).</p><p><strong>Conclusion: </strong>Jordan's population is predominantly young, with over 40% classified as AYA. Although cancer incidence is lower in this age group compared with older adults, outcomes are generally more favorable. A comprehensive AYA oncology strategy incorporating specialized psychosocial, fertility, and survivorship services should be prioritized, particularly in resource-restricted settings.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"357-365"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147964531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Arylacetamide Deacetylase-Mediated Extracellular Matrix Remodeling With Immune Exclusion in Pancreatic Cancer.","authors":"Chao Wu, Jun Yang","doi":"10.14740/wjon2727","DOIUrl":"10.14740/wjon2727","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with poor prognosis, characterized by a desmoplastic tumor microenvironment (TME) that limits immune cell infiltration and diminishes response to immunotherapy. Arylacetamide deacetylase (AADAC) is a lipid-processing enzyme, but its role in tumor progression, stromal organization, and immune modulation remains unclear.</p><p><strong>Methods: </strong>We integrated single-cell RNA sequencing (GSE212966) and spatial transcriptomics (GSE235315) to evaluate the association of AADAC with extracellular matrix (ECM)-rich and immune-restrictive niches in PDAC. We performed spatial co-expression analysis, gene set variation analysis (GSVA) using a core COL6A1-ITGA2-ITGB1 signature, CellChat analysis of ligand-receptor interactions, and functional assays after AADAC knockdown in PANC-1 cells.</p><p><strong>Results: </strong>AADAC expression was significantly upregulated in PDAC epithelium and co-localized with ECM markers (COL6A1, ITGA2, ITGB1), cancer-associated fibroblast (CAF)-associated markers (podoplanin (PDPN), fibroblast activation protein (FAP)), and immunosuppressive genes (<i>TGFB1</i>, <i>ARG1</i>, <i>CD163</i>). Spatial analyses further showed that CD8A distribution was constrained within stromalized, suppressive niches, while AADAC knockdown in PANC-1 cells increased apoptosis and reduced proliferation, migration, and invasion.</p><p><strong>Conclusions: </strong>AADAC expression is associated with ECM-rich and immune-restrictive tumor regions in PDAC. These findings support AADAC as a candidate biomarker of epithelial-stromal-immune interactions and justify further mechanistic studies.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"347-356"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147965170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM33 Reverses Cisplatin Resistance in Non-Small Cell Lung Cancer by Regulating the PI3K/AKT Pathway via Ubiquitination-Mediated Degradation of LPCAT1.","authors":"Jie Huang, Bao Qing Wang, Qin Wu, Li Ming Wang, Chao Guan","doi":"10.14740/wjon2729","DOIUrl":"10.14740/wjon2729","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer is the leading cause of cancer-related deaths worldwide, with non-small cell lung cancer (NSCLC) accounting for 80-85% of cases. Cisplatin (DDP) is a first-line chemotherapy drug for NSCLC, but acquired DDP resistance severely limits therapeutic efficacy. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) is involved in tumor progression, but its role in DDP resistance of NSCLC remains unclear. This study aimed to investigate the regulatory mechanism of LPCAT1 in DDP-resistant NSCLC and explore the potential role of tripartite motif-containing 33 (TRIM33) in modulating LPCAT1.</p><p><strong>Methods: </strong>DDP-resistant NSCLC cell lines (A549/DDP, PC-9/DDP) were established by gradual concentration gradient induction. Cell viability was detected by cell counting kit-8 (CCK-8) assay to determine half-maximal inhibitory concentration (IC₅₀) and resistance index (RI). Glucose uptake, intracellular ATP, and lactate levels were measured to evaluate glycolytic activity. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to detect mRNA and protein expression of LPCAT1, TRIM33, and PI3K/AKT pathway-related molecules. Flow cytometry was employed to analyze cell apoptosis. Immunoprecipitation and ubiquitination assays verified the interaction between TRIM33 and LPCAT1. <i>In vivo</i> xenograft models were established to confirm the regulatory role of LPCAT1 and TRIM33 in DDP resistance. Statistical analyses included Student's <i>t</i>-test, one-way analysis of variance (ANOVA), and Student-Newman-Keuls test, with P < 0.05 considered statistically significant.</p><p><strong>Results: </strong>LPCAT1 protein expression was significantly upregulated in DDP-resistant NSCLC cells, while mRNA expression showed no significant difference. LPCAT1 overexpression enhanced DDP resistance, activated the PI3K/AKT signaling pathway, and promoted glycolysis in NSCLC cells, whereas LPCAT1 knockdown reversed these effects. TRIM33 expression was negatively correlated with DDP resistance, and TRIM33 directly interacted with LPCAT1 to promote its ubiquitination and degradation via the proteasomal pathway. Overexpression of TRIM33 inhibited the PI3K/AKT pathway and glycolysis, thereby sensitizing DDP-resistant cells to DDP. <i>In vivo</i> experiments confirmed that LPCAT1 promoted DDP resistance and tumor growth, while TRIM33 overexpression reversed this phenotype.</p><p><strong>Conclusion: </strong>TRIM33 regulates LPCAT1 stability through ubiquitination-mediated degradation, thereby suppressing PI3K/AKT signaling and glycolysis and attenuating DDP resistance in NSCLC. These findings suggest that the TRIM33-LPCAT1 axis may represent a potential therapeutic candidate for DDP-resistant NSCLC and provide a basis for further investigation of strategies to improve DDP sensitivity.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"366-379"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147964946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-World Data on the Use of Cyclin-Dependent Kinase 4/6 Inhibitors in Hormone Receptor-Positive/Human Epidermal Growth Factor Receptor 2-Negative Advanced/Metastatic Breast Cancer.","authors":"Αntria Savvidou, Anastasia Constantinidou, Lefteris Zacharia, Kyriaki Michailidou, Μaria Zanti, Stavroula Kitiri, Yiola Marcou, Ifigenia Konstantinou, Eleni Kakouri, Myria Galazi, Christos Petrou","doi":"10.14740/wjon2750","DOIUrl":"10.14740/wjon2750","url":null,"abstract":"<p><strong>Background: </strong>Cyclin-dependent kinase (CDK)4/6 inhibitors (CDK4/6i) have been shown to improve the outcome of patients with hormone receptor-positive (HR+) human epidermal growth factor receptor 2-negative (HER2-) advanced/metastatic breast cancer (a/mBC). This study aimed to demonstrate the safety and effectiveness of CDK4/6i in HR+/HER2- a/mBC patients, in a single-center study in Cyprus and to confirm whether these are in line with data derived from randomized clinical trials and other real-world data studies.</p><p><strong>Methods: </strong>This retrospective study included 269 patients treated with endocrine therapy (ΕΤ) combined with palbociclib or ribociclib or abemaciclib as first-, second- or third-line treatment at the Bank of Cyprus Oncology Center (2018-2021). Seventy patients from the retrospective study who continued to receive treatment with CDK4/6i-containing regimens, were enrolled in the prospective study (follow-up period: 2021-2024) whereby patients were monitored in real time. Statistical evaluation was performed for differences in progression-free survival (PFS), overall survival (OS), adverse events (AEs)/toxicity, and prognostic factors for effectiveness.</p><p><strong>Results: </strong>The majority of patients received CDK4/6i in the first-line setting (68%, n = 182/269), whilst 25% and 7.8% of patients received CDK4/6i as second and third line of treatment, respectively. The median progression-free survival (mPFS) was 31, 25 and 19 months, with median overall survival (mOS) of 60, 54 and 44 months for palbociclib, ribociclib and abemaciclib, respectively. Neutropenia was the most commonly reported AE, followed by diarrhea, alanine aminotransferase (ALT)/aspartate aminotransferase (AST) increase, pneumonia, thrombocytopenia, erythematous rash and prolonged QT interval. Following subgroup analyses, age > 65 years, higher BC grade, <i>de novo</i> metastatic cancer at initial diagnosis, presence of lymph node/liver or brain metastasis and the larger number of metastatic sites at time of CDK4/6i treatment and the later-line use of CDK4/6i, were associated with a significantly shorter mPFS/mOS.</p><p><strong>Conclusions: </strong>The combination of CDK4/6i with ET is the gold standard treatment in HR+/HER2- a/mBC. Our study results confirm the effectiveness and tolerability of CDK4/6i in clinical routine practice with prognostic factors aligning with those identified in previous studies. This is the first real-world data (RWD) describing the effectiveness and toxicity of three CDK4/6i in the Cypriot patients.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"380-393"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147964592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pan-Cancer Analysis of NOP2 Reveals Its Prognostic Relevance and Association With the Tumor Immune Microenvironment.","authors":"Chuan Kun Yang, Wei Li, Shuang Liu, Yue Qi Wang, Su Su Luo, Wei Xiang Wang","doi":"10.14740/wjon2739","DOIUrl":"10.14740/wjon2739","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;RNA 5-methylcytosine (m&lt;sup&gt;5&lt;/sup&gt;C) modification has emerged as an important layer of epigenetic regulation in cancer biology. NOP2 (also known as NSUN1), a nucleolar RNA methyltransferase involved in ribosomal RNA methylation and ribosome biogenesis, has been reported to promote tumor progression in several individual malignancies. However, the expression pattern, prognostic relevance, and immune-related features across multiple cancer types remain incompletely understood.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We conducted an integrative pan-cancer analysis of NOP2 across 33 tumor types using publicly available datasets and web tools, including The Cancer Genome Atlas (TCGA), the Human Protein Atlas (HPA), Gene Expression Profiling Interactive Analysis 2 (GEPIA2), cBioPortal for Cancer Genomics (cBioPortal), the University of Alabama at Birmingham Cancer data analysis portal (UALCAN), Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), and SangerBox. NOP2 expression differences between tumor and normal tissues were evaluated at both mRNA and protein levels. Survival analyses were conducted using GEPIA2, and genetic alterations were characterized via cBioPortal. The relationships between NOP2 expression and the tumor immune microenvironment were assessed by estimating tumor-infiltrating immune cell proportions with Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts (CIBERSORT), followed by correlation analyses with immune cell infiltration levels, immune checkpoint-related genes, tumor mutational burden (TMB), and microsatellite instability (MSI). Finally, protein-protein interaction and co-expression analyses were conducted to identify NOP2-interacting and NOP2-correlated genes, which were subjected to functional enrichment analyses to infer potential biological pathways associated with NOP2.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;NOP2 mRNA was significantly upregulated in 20 of 33 tumor types compared with normal tissues (|log&lt;sub&gt;2&lt;/sub&gt;FC| ≥ 1, q &lt; 0.01), with protein-level overexpression confirmed in most cancers examined (P &lt; 0.001). High NOP2 expression was associated with shorter overall survival (OS) in 11 cancer types and poorer disease-free survival (DFS) in 13 cancer types (P &lt; 0.05), including renal cell carcinomas, hepatocellular carcinoma, lower-grade glioma, and lung adenocarcinoma. Genetic alterations of NOP2 were most frequent in ovarian cancer (6.1%) and patients with NOP2 genetic alterations were associated with poorer OS, DSS, and PFS in the cBioPortal cohort analysis. NOP2 expression correlated significantly with mast cell infiltration in 24 cancer types and CD8&lt;sup&gt;+&lt;/sup&gt; T-cell infiltration in 19 cancer types (P &lt; 0.05). Positive correlations between NOP2 expression and TMB were observed in 14 of 15 cancer types showing significant associations. Functional enrichment analysis confirmed associations with ribosome biogenesis and RNA processing pathways.&lt;/p&gt;&lt;p&gt;&lt;s","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"394-411"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Could Pretreatment Computed Tomography Imaging Accurately Predict the Pathological Diagnosis of Lymph Node Involvement in Thymic Epithelial Tumors?","authors":"Hao-Yun Liu, Mei-Ci Chen, Jo-Yu Chen, Wen-Jeng Lee, Jang-Ming Lee","doi":"10.14740/wjon2746","DOIUrl":"10.14740/wjon2746","url":null,"abstract":"<p><strong>Background: </strong>Thymic epithelial tumors (TETs) are the most common primary malignancies of the anterior mediastinum. Initial treatment planning for TETs is based on staging determined through computed tomography (CT) imaging. This study aimed to demonstrate that pretreatment CT imaging can provide critical insights into lymph node (LN) metastasis in TETs, potentially guiding surgical decisions.</p><p><strong>Methods: </strong>Thirty patients with TETs treated at National Taiwan University Hospital from 2008 to 2023 were included. Three radiologists independently evaluated the pretreatment CT scans for LN metastasis, with findings validated against postoperative pathology reports. The study assessed the correlation between radiological and pathological LN findings, including criteria such as LN size, density, and morphology.</p><p><strong>Results: </strong>In a cohort of 30 TET patients, 43% were male, with an average age of just over 57 years. All patients underwent N1 LN dissection, and three also received N2 dissections. Pathological results confirmed LN metastasis in four cases (two thymoma B3, two thymic carcinoma), and 40% of patients were Masaoka-Koga stages III-IVb. Three experienced radiologists independently reviewed pretreatment CT scans and identified all four pathology-confirmed metastatic cases, yielding 100% sensitivity and negative predictive value (NPV) in this cohort. However, these findings should be interpreted cautiously because only four patients had pathologically confirmed LN metastasis.</p><p><strong>Conclusions: </strong>Pretreatment CT assessment may provide useful information for the evaluation of suspicious LN involvement in TETs and may assist preoperative planning. However, given the small number of metastatic cases, these findings should be considered preliminary, and further validation in larger, multicenter studies are required.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"412-418"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}