International Journal of Medical Sciences最新文献

{"title":"Expanding Outcomes Beyond Chronic Kidney Disease-Mineral and Bone Disorder: A Propensity Score-Matched Analysis of Parathyroidectomy versus Calcimimetics in Dialysis Patients with Secondary Hyperparathyroidism.","authors":"Yi-Chou Hou, Cai-Mei Zheng, Ko-Lin Kuo, Kuo-Wang Tsai, Joshua Wang, Cheng-Yi Wang, Ruei-Ming Chen, Kuo-Cheng Lu","doi":"10.7150/ijms.131653","DOIUrl":"10.7150/ijms.131653","url":null,"abstract":"<p><strong>Background: </strong>Secondary hyperparathyroidism (SHPT) is a common complication in patients with end-stage renal disease (ESRD) receiving dialysis. Although calcimimetics (CAMs) and parathyroidectomy (PTx) are widely used for severe SHPT, their comparative effects on long-term clinical outcomes beyond mineral and bone disorder remain uncertain.</p><p><strong>Methods: </strong>We conducted a retrospective multicenter cohort study using the TriNetX research network (2010-2024). Adult dialysis patients with ESRD and severe SHPT, defined by at least one historical intact parathyroid hormone level >600 pg/mL prior to treatment initiation, were included. Patients receiving both therapies were excluded. After 1:1 propensity score matching for demographics, comorbidities, medications, and laboratory variables, outcomes including all-cause mortality, major adverse cardiovascular events (MACE), fracture, cognitive impairment, mild cognitive impairment (MCI), and sepsis were compared using Cox proportional hazards models.</p><p><strong>Results: </strong>After propensity score matching, 22,580 patients were included (11,290 in each group), with follow-up extending to 7 years. Compared with CAM therapy, PTx was associated with significantly lower risks of all-cause mortality (hazard ratio [HR] 0.914, 95% confidence interval [CI] 0.860-0.972), mild cognitive impairment (HR 0.646, 95% CI 0.436-0.955), and sepsis (HR 0.844, 95% CI 0.765-0.930). No significant differences were observed for MACE, fracture, hungry bone disease, overall cognitive impairment, or malignancy.</p><p><strong>Conclusion: </strong>In patients with ESRD and severe SHPT, parathyroidectomy was associated with lower risks of mortality, mild cognitive impairment, and sepsis compared with calcimimetic therapy, while cardiovascular and fracture outcomes were comparable. These findings suggest that PTx may confer broader systemic benefits beyond mineral and bone disorder control in selected dialysis patients.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 7","pages":"2277-2289"},"PeriodicalIF":3.7,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148294889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Hypoxia and Immune Escape-Related Gene Signature for the Diagnosis of Prostate Cancer: An Integrated Bioinformatics Study.","authors":"Hexia Gan, Jiana Jiang, Jiebin Yang, Feng Shen, Weihong Lu, Peng Lai, Lingyu Chen, Zhibing Xu, Jianping Zhang, Jianming Guo, Fan Chao","doi":"10.7150/ijms.133397","DOIUrl":"10.7150/ijms.133397","url":null,"abstract":"<p><p>Prostate cancer remains a major global health concern for men, with hypoxia and immune escape being key drivers of tumor progression; however, no reliable diagnostic signature integrating both processes has been established for clinical use. In this study, we integrated RNA sequencing and microarray data from The Cancer Genome Atlas (TCGA)-PRAD, Genotype-Tissue Expression (GTEx), and Gene Expression Omnibus (GEO) datasets to identify hypoxia and immune escape-related genes (HIERGs). Through differential expression analysis, functional enrichment, and machine learning algorithms including Random Forest, SVM-RFE, and LASSO regression, we constructed a robust six-gene diagnostic signature comprising <i>RBMS3</i>, <i>ALDH2</i>, <i>SLC7A11</i>, <i>FGFR2</i>, <i>GDF15</i>, and <i>NCAM1</i>. The model demonstrated high diagnostic accuracy, with area under the curve (AUC) values exceeding 0.9 across all validation cohorts, as confirmed by calibration curves, decision curve analysis, and receiver operating characteristic curves. Functional analysis revealed significant enrichment in translation-related pathways and smooth muscle contraction, and the RiskScore was significantly associated with altered immune cell infiltration in the tumor microenvironment. Regulatory network analysis further uncovered potential upstream regulators and therapeutic agents targeting the key genes. In conclusion, we developed and validated a hypoxia and immune escape-related gene signature with robust diagnostic performance for prostate cancer. Exploratory grouping by the model-derived RiskScore revealed differences in pathway and immune infiltration patterns, suggesting an association between the signature and intratumoral molecular heterogeneity. These exploratory findings primarily serve to characterize the biological features related to the model and provide supplementary clues for understanding molecular alterations in prostate cancer; they should be interpreted with caution.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 7","pages":"2225-2251"},"PeriodicalIF":3.7,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148294871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Insight into the Therapeutic Targets for Spinal Degenerative Diseases Gained by a Post-Genome-Wide Association Study.","authors":"Xuan Zhao, Qijun Wang, Chunjie Wang, Haixia Huang, Peng Wang, Wei Wang, Jie Lu, Shibao Lu","doi":"10.7150/ijms.127489","DOIUrl":"10.7150/ijms.127489","url":null,"abstract":"<p><p>Degenerative spinal diseases are a group of conditions that affect the structure and function of the spine, which can severely impact patient prognosis. Elucidating the druggable genes governing degenerative spinal diseases plays a pivotal role. GWAS data on degenerative spinal diseases, druggable genes, and eQTL data were acquired and Mendelian Randomization (MR) analysis was conducted. Colocalization analysis was performed and the side effects or additional indications of the identified drug targets was assessed using a phenome-wide association study. Finally, the differential expression of druggable genes in different cell subtypes of osteoporosis and intervertebral disc degeneration was analyzed, and molecular docking of actionable drugs for target genes was performed. In total, 31 druggable genes associated with osteoporosis and 22 druggable genes associated with spinal stenosis were identified. Four genes reached significant colocalization in blood for osteoporosis and eleven genes showed colocalization in spinal stenosis blood. Besides GPX1, KLRC2, and TCF19, the other 13 potential therapeutic targets for spinal degenerative diseases had no significant adverse effects. Furthermore, it was found that PAK4 and ESR1 were highly expressed in mesenchymal stem cells (MSCs) derived from bone marrow (BM-MSCs) in osteoporosis samples. SORCS2 expression was higher in nucleus pulposus cells (NPCs) in samples with severe than in samples with mild intervertebral disc degeneration. Lastly, drug analysis supported Fostamatinib might be potential therapeutics for osteoporosis and spinal stenosis by inhibiting PAK4 and PI4KB, respectively. In conclusion, our research suggested that PAK4, ESR1, and PI4KB might be promising targets for spinal degenerative diseases, and the effectiveness of Fostamatinib in these diseases warrants further investigation.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 7","pages":"2209-2224"},"PeriodicalIF":3.7,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148294874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Origin and Application of Cardiomyocyte-Derived Small Extracellular Vesicles: A Systematic Review.","authors":"Shaojiao Liu, Yu Teng, Sha Su, Meng Wang, Lei Wang, Mingjing Zhao","doi":"10.7150/ijms.133199","DOIUrl":"10.7150/ijms.133199","url":null,"abstract":"<p><p><b>Background/Aims</b>: Cardiomyocyte-derived small extracellular vesicles (CM-sEVs) have emerged as important mediators of intercellular communication in cardiovascular diseases (CVDs). However, their origin-tracing markers, molecular signatures, and clinical applications remain incompletely characterized and lack systematic synthesis. This systematic review aimed to comprehensively evaluate CM-sEVs-specific markers, disease-associated cargos alterations, and their roles in intercellular communication.</p><p><strong>Methods: </strong>A PRISMA-guided systematic search was conducted across major databases, including Web of Science, PubMed, Embase, and the Cochrane Library. Study screening, data extraction, and quality assessment were independently performed by two investigators according to predefined eligibility criteria.</p><p><strong>Results: </strong>Thirty-four studies were included and three sets of information were systematically analyzed. Ldb3, Ambra1, and CD172a were verified as potential origin-tracing markers of CM-sEVs, and miR-208a, cTnT/Tnnt2, and α-MHC/Myh6 served as auxiliary markers. Several CM-sEVs-associated molecules, including CD172a, Ambra1, miR-9-5p, and lncRNA HCG15, demonstrated diagnostic or prognostic potential in CVDs populations. Functionally, CM-sEVs regulate fibrosis, angiogenesis, autophagy, and immune responses through cardiomyocyte-noncardiomyocyte communication networks.</p><p><strong>Conclusion: </strong>This review systematically summarizes current evidence on potential origin-tracing markers, cargos characteristics, and intercellular communication roles of CM-sEVs, providing a theoretical basis for their identification and translational application in cardiovascular diseases.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 7","pages":"2252-2276"},"PeriodicalIF":3.7,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyinosinic:polycytidylic acid causes epithelial-mesenchymal transition via BAFF expression in Beas-2B human bronchial epithelial cells.","authors":"Yatham Naga Satya Mani, Dae Heum Yun, Eun-Yi Moon","doi":"10.7150/ijms.129414","DOIUrl":"10.7150/ijms.129414","url":null,"abstract":"<p><p>The bronchial epithelium acts not only as the primary physical barrier but also as an active sensor that responds to exogenous materials such as bacteria and viruses, by producing various cytokines including B-cell activating factor (BAFF). Although BAFF is a well-known protein in B-cell functions, its role in bronchial cell function remains undefined. Polyinosinic-polycytidylic acid (Poly (I:C)), a synthetic double-stranded RNA, serves as a model for viral infection that binds to toll-like receptor (TLR) 3 to trigger intracellular signal pathways. In this study, we investigated the effect of Poly (I:C)-induced BAFF expression on airway cell migration using Beas-2B human bronchial epithelial cells. Poly (I:C) increased BAFF expression and cell migration, along with the increased expression of N-cadherin, Vimentin and Slug (SNAI2), which are three primary markers for epithelial-mesenchymal transition (EMT). Cell migration was attenuated by small interfering RNA (siRNA) against BAFF, which also inhibited the expression of these EMT markers. Phosphorylation of c-Jun N-terminal kinase (JNK) was enhanced by Poly (I:C) and inhibited by SP600125, JNK inhibitor, leading to a decreased expression of BAFF and aforementioned EMT markers. Poly (I:C) increased reactive oxygen species (ROS), resulting in a ROS-dependent up-regulation of antioxidants (Catalase, superoxide dismutase (SOD)1 and heme oxygenase (HMOX)1) and Nrf2. Pre-treatment with N-acetylcysteine (NAC), ROS scavenger, inhibited Nrf2 activation and JNK phosphorylation. The increase in Nrf2 levels induced by Poly (I:C) was also attenuated by SP600125. Additionally, while NAC treatment inhibited BAFF expression, it caused little change in the expression of the three EMT markers. Increased BAFF expression was confirmed by Nrf2 binding to the BAFF promoter or an increase in the luciferase activity of BAFF promoter co-transfected with Nrf2 plasmids. Treatment with recombinant BAFF protein also increased cell migration and EMT marker expression. Taken together, our results demonstrate that Poly (I:C) promotes a regenerative migration of bronchial epithelial cells by inducing BAFF expression through the ROS-dependent JNK-Nrf2 signaling axis.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 7","pages":"2181-2196"},"PeriodicalIF":3.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148294907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Adjunctive Role of Hyperbaric Oxygen Therapy in Microbial Infection-Related Conditions.","authors":"Wentian Zhang, Xinxin Li, Hongwei Ma, Ya Li, Yuanhang Xi, Wenlan Wang, Yong Liu, Peijun Han","doi":"10.7150/ijms.127803","DOIUrl":"10.7150/ijms.127803","url":null,"abstract":"<p><p>Hyperbaric oxygen therapy (HBOT) demonstrates expanding applications in infectious diseases through its multimodal mechanisms. As an adjunctive treatment, HBOT directly exerts antimicrobial effects through oxygen toxicity and reactive oxygen species generation, while indirectly enhances host immunity by improving neutrophil function and promoting tissue repair. Clinical evidence supports its adjunctive use in complex infections including diabetic foot wounds, necrotizing soft tissue infections, COVID-19, and mucormycosis, particularly in hypoxic wounds where conventional therapies show limited efficacy. While current studies are promising, further randomized trials are needed to standardize protocols and confirm efficacy.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 6","pages":"2154-2165"},"PeriodicalIF":3.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13181385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CXCL14 promotes osteosarcoma cell migration and invasion by inducing epithelial-to-mesenchymal transition.","authors":"Chun-Han Hou, Ming-Lung Hsu, Chen-Hsuan Wang, Ju-Fang Liu, Po-Chun Chen","doi":"10.7150/ijms.127140","DOIUrl":"10.7150/ijms.127140","url":null,"abstract":"<p><p>Osteosarcoma, an aggressive malignancy of long bones in children and young adults, responds poorly to conventional chemotherapy, and distant metastasis remains the principal cause of death. Here we identify chemokine CXCL14 as a driver of epithelial-to-mesenchymal transition (EMT) and metastatic behavior. CXCL14 expression was markedly higher in osteosarcoma cells than in normal osteoblasts. Knockdown of CXCL14 significantly reduced cell migration and wound closure, accompanied by a shift from spindle-like to cobblestone morphology and restoration of epithelial markers. Recombinant CXCL14 promoted EMT with dose-dependent effects. Western blotting showed CXCL14 suppressed E-cadherin while elevating N-cadherin and vimentin, consistent with EMT induction. Pharmacologic and genetic inhibition revealed that PI3K/AKT, MAPK, and NF-κB signaling cascades mediate CXCL14-driven EMT. In an orthotopic mouse model, silencing CXCL14 retarded tumor growth and reduced mesenchymal marker expression <i>in vivo</i>. Collectively, our results demonstrate that CXCL14 activates PI3K/AKT/MAPK/NF-κB pathways to promote EMT and osteosarcoma progression. Therapeutic targeting of CXCL14 or its downstream signaling may suppress metastasis and improve outcomes for patients with osteosarcoma. These data position CXCL14 as both a biomarker of aggressive phenotypes and an actionable molecular target in pediatric bone cancer patients, warranting preclinical and clinical validation.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 7","pages":"2166-2180"},"PeriodicalIF":3.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148294914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Evidence for the Benefits and Risks of Glucose-Lowering Drugs on Cardiovascular-Kidney-Metabolic Syndrome: A Drug-Target Mendelian Randomization Study.","authors":"Jian Lu, Shuaigang Sun, Xinru Shang, Shimin Jiang, Zekai Deng, Shunwei Wang, Chenping Wei, Jiaqi Hu, Wenge Li","doi":"10.7150/ijms.133077","DOIUrl":"10.7150/ijms.133077","url":null,"abstract":"<p><strong>Background: </strong>To explore the potential benefits and risks of glucose-lowering drugs on cardiovascular-kidney-metabolic (CKM) syndrome outcomes using drug-target Mendelian randomization (MR).</p><p><strong>Methods: </strong>Genetic instruments for eight glucose-lowering drugs were identified from variants associated with glycated hemoglobin (HbA1c) and drug target gene expression. We employed two-sample MR and meta-analysis to estimate associations with nine CKM syndrome-related diseases, including coronary artery disease (CAD), myocardial infarction (MI), stroke, heart failure (HF), atrial fibrillation (AF), venous thromboembolism (VTE), peripheral artery disease (PAD), chronic kidney disease (CKD), and metabolic syndrome (MetS), using data from UK Biobank, FinnGen, and other large GWAS consortia. Supplementary analyses included summary-data-based MR (SMR) and colocalization.</p><p><strong>Results: </strong>Genetic proxies for sodium-glucose cotransporter 2 inhibitors (SGLT2i) were associated with reduced risks of CAD (OR 0.85, 95% CI 0.73-0.98), HF (OR 0.66, 95% CI 0.44-0.98), and MetS (OR 0.64, 95% CI 0.50-0.82). GLP-1 receptor agonists (GLP-1RA) were linked to lower risks of CAD (OR 0.90, 95% CI 0.84-0.96), HF (OR 0.92, 95% CI 0.86-0.99), and CKD (OR 0.87, 95% CI 0.79-0.95). Metformin showed protective association with CAD (OR 0.51, 95% CI 0.40-0.66) and PAD (OR 0.99, 95% CI 0.99-1.00). Sulfonylureas showed a modest association with reduced CAD (OR 0.98, 95% CI 0.96-1.00). Conversely, insulin was associated with a higher risk of MetS (OR 1.07, 95% CI 1.02-1.13), and thiazolidinediones (TZDs) with an increased risk of HF (OR 1.12, 95% CI 1.05-1.20). SMR provided additional evidence for protective roles of <i>GLP1R</i> and <i>VEGFA</i> for CAD, <i>KCNJ11</i> for HF<i>, ABCC8</i> for HF and AF, and <i>PRKAB1</i> for multiple cardiovascular outcomes. The detrimental effects of <i>INSR</i> on MetS and <i>SERPINE1</i> on CKD and MetS were also verified.</p><p><strong>Conclusions: </strong>This study provides genetic evidence revealing the potential benefits and risks of certain glucose-lowering drugs in the management of CKM syndrome. These findings may inform target validation, drug repurposing, and personalized therapies for CKM syndrome.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 7","pages":"2197-2208"},"PeriodicalIF":3.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148294945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 Macrophages in Acute Pancreatitis: From Inflammatory Drivers to Therapeutic Targets.","authors":"Zhihong Xu, Yi-Chen Sui, Li-Ping Sheng","doi":"10.7150/ijms.111818","DOIUrl":"10.7150/ijms.111818","url":null,"abstract":"<p><p>Acute pancreatitis (AP) involves activation of the innate immune system and an imbalanced inflammatory response. Both pancreatic and systemic inflammation associated with AP are mediated by macrophages. This review summarizes research on macrophage functions in AP pathogenesis and treatment. Relevant studies investigating macrophage activation, phenotypes, autophagy, and their roles in local and systemic inflammation were analyzed. During AP, macrophages initially adopt a pro-inflammatory phenotype to amplify inflammation. Macrophages located in tissues including the pancreas, adipose tissue, liver, lung, and spleen play a role in this process. As the disease progresses, they transition to an M2 phenotype to promote resolution. Macrophage-centered modulation of the innate immune response represents a promising therapeutic strategy. However, further exploration of macrophage interactions with other immune cells and pancreatic acinar cells is still needed. Targeting specific macrophage functions may improve AP management, which is the focus of this review.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 6","pages":"2081-2087"},"PeriodicalIF":3.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13181366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of <i>IGF2BP2</i> genetic variants and expression levels with the progression of endometrial cancer.","authors":"Chieh-Yi Kan, Yi-Hung Sun, Chung-Yuan Lee, Shih-Chi Su, Cheng-Chang Chang, Chih-Hsin Tang, Hsiao-Ju Chu, Po-Hui Wang, Shun-Fa Yang","doi":"10.7150/ijms.132120","DOIUrl":"10.7150/ijms.132120","url":null,"abstract":"<p><p>Endometrial cancer (EC) is the most common gynecological cancer among women in high-income countries, and its intricate etiology involves a composite of genetic factors. Insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) targets distinct types of RNA species to orchestrate tumor cell metabolism, invasion, and metastasis. Nevertheless, the impact of <i>IGF2BP2</i> gene polymorphisms on the development of EC remains poorly understood. Here, to clarify the genetic association between <i>IGF2BP2</i> and EC development, genotyping of three single-nucleotide polymorphisms (SNPs) of <i>IGF2BP2</i> gene, including rs11705701, rs4402960, and rs1470579, were conducted in 190 patients and 295 cancer-free women. We found that none of these three loci was in association with the risk of developing EC. Further evaluation on their correlation with key clinicopathological features revealed that EC patients carrying at least one minor allele of rs1470579 (C) or rs4402960 (T) tend to develop cervical invasion more frequently than do those homozygous for the major allele. Analysis of omics data available in the Genotype-Tissue Expression (GTEx) Portal and The Cancer Genome Atlas (TCGA) indicated that genotypes of rs1470579 and rs4402960 are associated with elevated IGF2BP2 expression, and IGF2BP2 induction in tumors was linked to progression to advanced disease and poor survival in patients with uterine corpus endometrial carcinoma. These results suggest that alterations in IGF2BP2 levels attributed by genetic variants may influence EC aggressiveness.</p>","PeriodicalId":14031,"journal":{"name":"International Journal of Medical Sciences","volume":"23 6","pages":"2088-2095"},"PeriodicalIF":3.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13181388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}