World Journal of Oncology最新文献

{"title":"TP53 Loss Fuels mTORC1 Activation and Autophagy Suppression to Drive Immune-Cold Colorectal Cancer.","authors":"Eunseuk Lee, Dana Al-Assi, Randy Rivera-Rueda, Sharon Susan Paul, Aksa Joy","doi":"10.14740/wjon2695","DOIUrl":"10.14740/wjon2695","url":null,"abstract":"<p><strong>Background: </strong>Microsatellite-stable colorectal cancer (MSS CRC) is typically resistant to immune checkpoint blockade and remains an \"immune-cold\" disease. Wild-type p53 is known to restrain mTOR signaling and support autophagy, yet how TP53 loss integrates metabolic rewiring with immune suppression in MSS CRC-especially with protein- and phosphosite-level validation-remains incompletely defined. We tested whether p53 deficiency is associated with coordinated mTORC1 activation, autophagy attenuation, and immune-cold remodeling across multi-omics datasets.</p><p><strong>Methods: </strong>We analyzed GSE146009 (paired tumor-normal RNA-seq pairs), TCGA-COAD/READ (n = 647, mutation annotated), GSE108989 (11,138 tumor-infiltrating T cells), and CPTAC colon proteome/phosphoproteome cohorts. Pathway activities were quantified by single-sample gene set enrichment analysis (ssGSEA) and Seurat module scoring. Group differences were tested by Kruskal-Wallis and Wilcoxon analyses with false-discovery-rate correction. CPTAC phosphosite-to-protein ratios were compared between TP53-mutant or p53-low versus wild-type or p53-high tumors.</p><p><strong>Results: </strong>Across bulk transcriptomes, TP53-mutant tumors showed higher mTORC1 signaling, lower autophagy scores, higher FOXP3, and reduced CD8A/FOXP3 ratios consistent with a regulatory T-cell-skewed immune-cold state. Single-cell analysis confirmed subset-specific immunometabolic programs, highlighting metabolically active regulatory/exhausted states with relatively blunted inflammatory output. Proteomic/phosphoproteomic data supported post-translational mTOR pathway activation in p53-deficient tumors, including increased phosphorylation of canonical mTOR substrates (EIF4EBP2 S65; RPS6KB1 T421/S424) and reduced phosphorylation at inhibitory RPTOR sites (S705/T725/S726), consistent with sustained mTORC1 activity.</p><p><strong>Conclusions: </strong>In MSS CRC, p53 deficiency is consistently associated with immunometabolic remodeling marked by persistent mTOR pathway activation, relative autophagy attenuation, and FOXP3-dominant immune-cold features across transcriptomic, single-cell, and proteomic layers. These findings add protein- and phosphosite-level evidence linking TP53 loss to an immune-suppressive metabolic state and support biomarker-guided evaluation of mTOR kinase (TORC1/2) inhibition, which more fully suppresses 4E-BP/S6K phosphorylation, combined with PD-1/PD-L1 (± CTLA-4) blockade in TP53-deficient MSS CRC.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"143-156"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147445263","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":"Multi-Omics and Single-Cell Mendelian Randomization Reveal a Potential Role of <i>VNN2</i> in Lung Adenocarcinoma in Resting Natural Killer Cells.","authors":"Zhi Chun Xue, Jing Lin, Jian Hui Wu, Zhi Wen Peng, Mei Yan Tang, Peng Liang, Hui Ling Chen, Gui Ju Fang, Qing Xue","doi":"10.14740/wjon2689","DOIUrl":"10.14740/wjon2689","url":null,"abstract":"<p><strong>Background: </strong>We aimed to evaluate the potential association between genetically predicted vanin-2 (<i>VNN2</i>) expression and lung adenocarcinoma (LUAD) risk, and to explore the immune cell subtype that may underlie this relationship.</p><p><strong>Methods: </strong>We integrated whole-blood expression quantitative trait loci (eQTL) data from eQTLGen, plasma protein quantitative trait loci (pQTL) data from deCODE, and LUAD genome-wide association study (GWAS) data from European-ancestry cohorts, together with differential expression analysis using GEPIA2, to identify candidate genes for subsequent single-cell eQTL (sc-eQTL) Mendelian randomization (MR) analysis. For the sc-eQTL analysis, <i>VNN2</i>-associated eQTLs from 14 immune cell types profiled in the OneK1K single-cell eQTL resource were tested for associations with LUAD risk.</p><p><strong>Results: </strong>Bulk-level MR analysis showed that genetically predicted increases in <i>VNN2</i> expression and protein levels were significantly associated with a reduced risk of LUAD (eQTL-MR: odds ratio (OR) = 0.964, 95% confidence interval (95% CI), 0.934-0.995; P = 0.024; pQTL-MR: OR = 0.946, 95% CI, 0.921-0.970; P = 2.87 × 10^-5). Transcriptomic analyses confirmed significant downregulation of VNN2 in LUAD tumors compared with normal lung tissues. sc-eQTL MR identified the strongest association in resting natural killer (rNK) cells (OR = 0.896, 95% CI, 0.829-0.967; P = 0.005).</p><p><strong>Conclusions: </strong>Multi-omics and sc-eQTL MR analyses indicated that genetically predicted increases in <i>VNN2</i> expression were associated with a reduced risk of LUAD, with the most pronounced effect observed in rNK cells. These findings suggest a potential cell type-specific role of <i>VNN2</i> in LUAD susceptibility and warrant further studies to validate its biological relevance and clinical implications.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"247-255"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444750","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":"Expression of Bruton's Tyrosine Kinase Reflects Immune Cells Infiltration and Cell Proliferation in Breast Cancer.","authors":"Tamrah AlRammah, Rongrong Wu, Kohei Chida, Kei Kawashima, Kenichi Hakamada, Takashi Ishikawa, John M L Ebos, Kazuaki Takabe","doi":"10.14740/wjon2708","DOIUrl":"10.14740/wjon2708","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Bruton's tyrosine kinase (BTK) is a downstream mediator in B-cell receptor (BCR) signaling and is essential for B-cell differentiation and proliferation. BTK inhibitors are approved and in clinical use for hematological cancers such as lymphoma and leukemia, with testing underway in solid tumors. Because BTK is expressed in myeloid-derived suppressor cells (MDSCs) known to worsen breast cancer (BC) outcomes, we investigated the clinical relevance of BTK expression in multiple BC subtypes as a predictor of progression and/or response to treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We performed an integrative transcriptomic analysis of tumor BTK expression across three large BC cohorts (The Cancer Genome Atlas (TCGA), Molecular Taxonomy of Breast Cancer International Consortium (METABRIC), and Sweden Cancerome Analysis Network-Breast (SCAN-B); total n = 5,240), 10 neoadjuvant chemotherapy (NAC) datasets, and the I-SPY2 neoadjuvant immunotherapy trial cohort. Gene set enrichment analysis (GSEA) and xCell deconvolution were used to evaluate associations with cell proliferation, immune infiltration, and tumor microenvironment (TME) composition while single-cell sequencing datasets (SCP1039, SCP1106) were used to identify BTK-expressing cell populations. Survival analyses were performed using Kaplan-Meier and log-rank tests.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;BTK levels were the highest in triple-negative BC (TNBC) among the subtypes and unexpectedly drove stronger proliferation gene set enrichment in estrogen receptor-positive (ER&lt;sup&gt;+&lt;/sup&gt;)/human epidermal growth factor receptor 2-negative (HER2&lt;sup&gt;-&lt;/sup&gt;) tumors (e.g., MITOTIC_SPINDLE, G2M_CHECKPOINT). However, BTK expression did not correlate with American Joint Committee on Cancer (AJCC) stage or overall, disease-free, or disease-specific survival across cohorts or molecular subtypes. Notably, BTK-high tumors showed robust enrichment of immune pathways (interferon gamma (IFN-γ) response, interleukin-6 (IL-6)/Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3), tumor necrosis factor-α (TNF-α) signaling) and exhibited elevated tumor-infiltrating leukocyte and lymphocyte fractions, increased cytolytic activity, and greater abundance of myeloid and lymphoid cell populations. BTK expression was not consistently associated with NAC response as only one of 10 datasets (GSE25066) showed a weak association within ER&lt;sup&gt;+&lt;/sup&gt; and HER2-positive subtypes. Similarly, BTK levels did not predict response in I-SPY2 patients receiving durvalumab plus olaparib, despite strong correlations with programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) expression. Single-cell analysis localized BTK transcripts primarily to myeloid and B cells.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;BTK expression in BC reflects a proliferative and immune-active TME, particularly in TNBC and HER2-positive subtypes, but lacks prognostic or predictive value for NA","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"209-222"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444226","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":"Functional and Survival Outcomes of Partial Versus Radical Nephrectomy in Renal Cell Carcinoma Patients With Pre-Existing Chronic Kidney Disease: A Real-World Study.","authors":"Luan Kinh Thai, Viet Quang Luu, Sam Minh Thai","doi":"10.14740/wjon2728","DOIUrl":"10.14740/wjon2728","url":null,"abstract":"<p><strong>Background: </strong>Managing renal cell carcinoma (RCC) in patients with pre-existing chronic kidney disease (CKD) or a solitary kidney requires balancing oncologic control with maximal renal functional preservation. This study analyzes long-term renal function, survival, and complications between partial nephrectomy (PN) and radical nephrectomy (RN) in this high-risk Vietnamese cohort.</p><p><strong>Methods: </strong>We retrospectively reviewed 90 patients with RCC and reduced pre-operative estimated glomerular filtration rate (eGFR, < 60 mL/min/1.73 m²) or a solitary kidney who underwent surgery at Cho Ray Hospital between 2019 and 2024. Outcomes included changes in eGFR, CKD stage progression, overall survival (OS), cancer-free survival (CFS), and dialysis-free survival (DFS).</p><p><strong>Results: </strong>Forty-one patients underwent RN and 49 PN. RN cases had significantly larger tumors and higher RENAL complexity scores (P < 0.001). At a mean follow-up of 45.7 months, PN demonstrated a smaller eGFR decline (-13.2 ± 3.5 mL/min/1.73 m²) compared with RN (-23.3 ± 6.0 mL/min/1.73 m²) (P < 0.001), including in the subgroup with eGFR ≤ 45 mL/min/1.73 m² (P = 0.002). CKD stage progression occurred in 100% of RN versus 62.2% of PN patients. Long-term OS, CFS, and DFS were comparable between groups (all P > 0.05). Age (hazard ratio (HR) 1.1) and positive proteinuria (HR 5.4) were independent predictors of overall mortality.</p><p><strong>Conclusions: </strong>PN is the preferred strategy for RCC patients with compromised renal function, when technically feasible, due to its superior functional outcomes. We propose a proteinuria-driven risk stratification approach; the presence of pre-operative proteinuria should strongly favor nephron-sparing surgery and necessitate rigorous long-term nephrological co-management to optimize survival.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"237-246"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444662","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":"Strong Signals of Adverse Events in Tyrosine Kinase Inhibitor Therapy for Liver Cancer Treatment.","authors":"Wen Xuan Zhou, Jun Hao Fan, Qian Wen Ni, Ming Kai Liu, Zhen Peng, Yuan Xu, Su Su Luo","doi":"10.14740/wjon2685","DOIUrl":"10.14740/wjon2685","url":null,"abstract":"<p><strong>Background: </strong>This study was to identify strong adverse event (AE) signals associated with four tyrosine kinase inhibitors (TKIs) (sorafenib, regorafenib, lenvatinib, and cabozantinib), and compare these signals with regulatory drug facts from multiple global agencies.</p><p><strong>Methods: </strong>Data from the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS, 2007 - 2024) were analyzed. Each AE was treated as a binary variable, and logistic regression with robust error estimation was used to identify strong signals (odds ratio > 2, lower 95% confidence interval > 1). AE signals were compared with drug facts from the FDA (USA), European Medicines Agency (EMA, European Union), Pharmaceuticals and Medical Devices Agency (PMDA, Japan), and National Medical Products Administration (NMPA, China).</p><p><strong>Results: </strong>Among 33,801 identifiers (137,345 records), 816 strong AE signals were found. Sorafenib had the most (373), followed by regorafenib (207), lenvatinib (126), and cabozantinib (110). Notable AEs included pharyngeal hemorrhage (sorafenib), retinal artery occlusion (regorafenib), intracranial aneurysm (lenvatinib), and mood swings (cabozantinib). Thirty-two signals had a 100% likelihood of critical outcomes, with no overlap across drugs. AEs were more frequent in males and older populations. Significant discrepancies in AE profiles were observed among regulatory agencies, with low overlap between FAERS and agency data.</p><p><strong>Conclusions: </strong>This study provides a comprehensive analysis of AE signals for four TKIs in liver cancer, identifying associations rather than causal relationships. The findings highlight significant variation in AE profiles and discrepancies between clinical trial data and real-world evidence. These results are hypothesis-generating and emphasize the need for personalized treatments, enhanced monitoring and intervention, and improved global AE reporting, while acknowledging the inherent limitations of spontaneous reporting systems.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"223-236"},"PeriodicalIF":2.3,"publicationDate":"2026-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147445079","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":"Identification of Genes and Construction of Prognostic Model of Lung Adenocarcinoma Based on Propionate Metabolism-Related Genes.","authors":"Min Min Li, Wei Jia Fu, Ying Zhou, Huan Huan Zhang, Hai Ning Li, Chu Zhang, Jin Yang","doi":"10.14740/wjon2680","DOIUrl":"10.14740/wjon2680","url":null,"abstract":"<p><strong>Background: </strong>Dysregulation of propionate metabolism can enhance the invasive properties of lung adenocarcinoma (LUAD) cells and increase their metastatic potential. Therefore, we constructed a predictive model based on propionate metabolism-related genes (PMRGs) to evaluate the prognosis of patients with LUAD.</p><p><strong>Methods: </strong>mRNA expression profiles and clinical data of LUAD patients were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The predictive model was constructed using least absolute shrinkage and selection operator (LASSO). The associations between the risk score and tumor prognosis, immune infiltration, drug sensitivity, signaling pathways, and clinical features were evaluated using the CIBERSORT algorithm, the Genomics of Drug Sensitivity in Cancer (GDSC) database, gene set variation analysis (GSVA), gene set enrichment analysis (GSEA), and nomogram analyses. For hub genes, motif enrichment, genome-wide association study (GWAS) analysis and single-cell analysis were performed. Expression differences between LUAD cells and normal lung epithelial cells were validated using quantitative real-time polymerase chain reaction (qRT-PCR).</p><p><strong>Results: </strong>We established a LUAD prognostic model containing 16 hub genes. The area under the receiver operating characteristic curve (AUC) values for the model were 0.722 (1-year overall survival (OS)), 0.696 (3-year OS), and 0.700 (5-year OS). GSVA revealed significant enrichment in the G2/M checkpoint, E2F targets, and glycolysis pathways. GSEA indicated enrichment of the hypoxia-inducible factor-1 (HIF-1), interleukin (IL)-17, and p53 signaling pathways. Transcription factor analysis identified the motif cisbp-M4287 as the most significantly enriched, with a normalized enrichment score (NES) of 5.9. qRT-PCR results showed that the expression of ADIPOQ, CYP27A1, and GCDH was downregulated, while the expression of SERPINE1 was upregulated. No statistically significant differences were observed in the expression of CYP17A1 and EHHADH.</p><p><strong>Conclusions: </strong>A novel prognostic model based on PMRGs was established to predict overall survival in LUAD patients.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"191-208"},"PeriodicalIF":2.3,"publicationDate":"2026-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444729","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":"Neurotoxicity of Immunotherapy: Immune Checkpoint Inhibitor-Related Encephalitis vs. Immune Effector Cell-Associated Neurotoxicity Syndrome.","authors":"Takumi Sato, Kohei Chida, Shipra Gandhi, Kazuaki Takabe","doi":"10.14740/wjon2660","DOIUrl":"10.14740/wjon2660","url":null,"abstract":"<p><p>Immune checkpoint inhibitors and engineered T-cell therapies such as chimeric antigen receptor T-cell (CAR-T) cells and bispecific T-cell engagers (BiTEs) have revolutionized oncology care, and with them came two neurologic syndromes that look deceptively alike at the bedside with confusion, seizures, and encephalopathy: immune checkpoint inhibitor-related encephalitis (irEncephalitis) and immune effector cell-associated neurotoxicity syndrome (ICANS). Several differential observations between the two syndromes motivated this review: 1) although loss of immune tolerance likely drives irEncephalitis, ICANS on the other hand is dominated by cytokine-endothelial-microglial cascades. The biology of both entities remains incompletely resolved and these lines blur in real patients, 2) irEncephalitis is uncommon in ICI recipients (∼ 0.1-1%), whereas ICANS is common after CAR-T (∼ 40% and generally lower with most T-cell engagers), 3) lack of diagnostic and grading systems, especially the absence of a dedicated irEncephalitis grading system, remains the key barrier to consistent outcomes and meaningful comparison across clinical trials, and 4) management philosophies are asymmetric (restoring immune tolerance with selective immunomodulation in irEncephalitis vs. rapidly suppressing cytokine-mediated neuroinflammation with corticosteroids as well as anti-cytokine agents in ICANS). Here we review the existing literature on pathophysiology and current landscape of the diagnostics, management, and clinical trials to gain further structured understanding of these intriguing disorders. In doing so, we conclude that: 1) although the syndromes share similar clinical features, their pathogenesis points to distinct management algorithms based on timing of onset and response profiles, making mechanism-informed intervention central to improving outcomes; 2) early T-cell engager trials hint at molecule-dependent ICANS risk and responsiveness, warranting standardized reporting and accumulation of platform-specific data; and 3) emerging biomarkers and targets that index microglial signaling and blood-brain barrier integrity promise more precise, effective management as the field matures. In this review, we adopt a mechanism-first, side-by-side comparison that links diagnosis, management, and evolution to bedside decisions, with the aim of enabling precise diagnosis and management for oncologists, neurologists, and trialists operating in the rapidly expanding era of T-cell-based immunotherapy.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 1","pages":"1-13"},"PeriodicalIF":2.3,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12758050/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145901306","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":"Reduced Peripheral Blood Natural Killer Cell Proportion Predicts Poor Overall Survival in Advanced Gastric Cancer Patients Treated With Apatinib.","authors":"Niu Zhang, Si Yu Hu, Yu Ting Wang, Hui Shan, Guang Yu Tian, Yan Wang, Ye Qing Zhang, Zhi Yuan Qiu","doi":"10.14740/wjon2655","DOIUrl":"10.14740/wjon2655","url":null,"abstract":"<p><strong>Background: </strong>Angiogenesis inhibition represents a key therapeutic strategy in oncology, with apatinib showing significant efficacy for advanced gastric cancer (AGC) therapy. Currently, no biomarkers can reliably predict which AGC patients will benefit most from apatinib. The purpose of this study was to evaluate apatinib plus tegafur gimeracil oteracil potassium capsule (S-1) as a second-line therapy in AGC and to investigate prognostic biomarkers associated with outcomes.</p><p><strong>Methods: </strong>All 60 patients received apatinib (250 or 500 mg once daily) in combination with S-1 (40 mg/m², administered twice daily from day 1 to day 14). Treatment was administered in 28-day cycles, with each course encompassing two such cycles. Multiparameter flow cytometry was used to analyze the subset distribution and immunophenotypes of T cells and natural killer (NK) cells in peripheral blood mononuclear cell samples from AGC patients.</p><p><strong>Results: </strong>Among all 60 evaluable patients, no complete responses were observed. Partial responses were observed in 33.3% (20/60) of patients (95% confidence interval (CI): 21.1-45.6%), stable disease was observed in 38.3% (23/60) of patients (95% CI: 25.7-51.0%), while progressive disease occurred in 28.3% (95% CI: 16.6-40.1%). Notably, patients with NK cell proportions greater than 17% experienced longer progression-free survival (PFS) and overall survival (OS) than those with lower proportions.</p><p><strong>Conclusions: </strong>Apatinib combined with S-1 exhibited favorable tolerability and promising clinical activity as a second-line option for AGC patients. Importantly, we identified peripheral blood NK cell proportion as a potential predictor of treatment response, where a low NK cell proportion correlated with poorer outcomes.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 6","pages":"546-554"},"PeriodicalIF":2.3,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12591252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145483178","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":"A Comparison of Bidirectional Stratafix Continuous Suture Versus Conventional Interrupted Suture in Breast Mastectomy.","authors":"Masanori Oshi, Akimitsu Yamada, Kei Kawashima, Mahato Sasamoto, Itaru Endo","doi":"10.14740/wjon2642","DOIUrl":"10.14740/wjon2642","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to compare surgical outcomes between Stratafix barbed sutures and conventional sutures in patients undergoing total mastectomy for breast cancer.</p><p><strong>Methods: </strong>This retrospective study analyzed patients who underwent total mastectomy and/or axillary lymph node dissection at our hospital.</p><p><strong>Results: </strong>A total of 29 patients were included. No significant differences were observed in clinicopathological features between the two groups. However, the percentage of suturing time within the total operative time was significantly lower in the Stratafix group compared to conventional group (10% vs. 8%). In addition, the suturing time per centimeter was also significantly shorter with Stratafix group (P < 0.001). No wound-related complications were observed in either group during at least 3 months of follow-up.</p><p><strong>Conclusions: </strong>The use of barbed sutures for wound closure in mastectomy procedures effectively reduces suturing time without increasing the incidence of wound complications. Bidirectional Stratafix barbed sutures offer an improved and efficient alternative to conventional sutures for breast surgeons.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 5","pages":"525-529"},"PeriodicalIF":2.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12479069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201439","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":"Predictors of All-Cause In-Hospital Mortality in Patients With Malignant Well-Differentiated Gastroenteropancreatic Neuroendocrine Tumors.","authors":"Elvis Obomanu, Tarfa Verinumbe, Tinsae Anebo, Colton Jones, Claudia Dourado","doi":"10.14740/wjon2614","DOIUrl":"10.14740/wjon2614","url":null,"abstract":"<p><strong>Background: </strong>Factors influencing in-hospital mortality in patients with well-differentiated gastroenteropancreatic neuroendocrine tumors (GEP-NETs) remain understudied, highlighting gaps in optimizing acute clinical outcomes. This study aimed to identify sociodemographic and clinical predictors of all-cause in-hospital mortality in this population.</p><p><strong>Methods: </strong>Using 2016 - 2020 data from the National Inpatient Sample (NIS), patients with malignant well-differentiated GEP-NETs were identified via the International Classification of Diseases, 10th Revision (ICD-10) codes. The primary outcome was in-hospital mortality. Sociodemographic and clinical variables (heart failure (HF), malnutrition, Charlson Comorbidity Index (CCI), and tumor site) were analyzed using multivariable logistic regression.</p><p><strong>Results: </strong>Among 5,642 patients (mean age 64, standard deviation (SD) 12.9), multivariable analysis identified HF (adjusted odds ratio (aOR) 2.09, 95% confidence interval (CI): 1.10 - 3.95), malnutrition (aOR 1.84, 95% CI: 1.29 - 2.62), pancreatic (aOR 1.52, 95% CI: 1.01 - 2.30) or colon tumors (aOR 2.31, 95% CI: 1.51 - 3.53), CCI ≥ 5 (aOR 1.49, 95% CI: 1.06 - 2.10), hypertension (aOR 0.65, 95% CI: 0.47 - 0.91) and elective admissions (aOR 0.40, 95% CI: 0.25 - 0.63) as clinically relevant factors associated with in-hospital mortality.</p><p><strong>Conclusions: </strong>Advanced age, tumor location, malnutrition, and HF may be critical mortality predictors among patients with GEP-NETs. These findings advocate for integrated care models prioritizing nutritional support, cardiovascular monitoring, and early elective interventions to improve outcomes.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 5","pages":"478-486"},"PeriodicalIF":2.2,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12479075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201481","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}