Discover. Oncology最新文献

{"title":"Exploration of the shared pathways and common biomarkers in cervical and ovarian cancer using integrated bioinformatics analysis.","authors":"Fang Liu, Min Wang, Tian Zhu, Cong Xu, Guangming Wang","doi":"10.1007/s12672-024-01725-3","DOIUrl":"https://doi.org/10.1007/s12672-024-01725-3","url":null,"abstract":"<p><strong>Objective: </strong>Searching for potential biomarkers and therapeutic targets for early diagnosis of gynecological tumors to improve patient survival.</p><p><strong>Methods: </strong>Microarray datasets of cervical cancer (CC) and ovarian cancer (OC) were downloaded from the Gene Expression Omnibus (GEO) database, then, differential gene expression between cancerous and normal tissues in the datasets was analyzed. Weighted gene co-expression network analysis (WGCNA) was performed to screen for co-expression modules associated with CC and OC. The screened shared genes were then further analyzed for functional pathway enrichment. Next, the least absolute shrinkage and selection operator (LASSO) with tenfold cross validation is used to further screened for common diagnostic biomarkers for the two diseases, and further validation is performed using two independent GEO datasets. Finally, the CIBERSORT algorithm was used to estimate the immune infiltration levels of CC and OC, and the correlation between immune cell infiltration and common biomarkers was explored.</p><p><strong>Results: </strong>After crossing the common DEGs detected by \"Limma\" R package with the common module genes identified by WGCNA, 44 shared genes were obtained. Functional enrichment indicates that these shared genes are mainly related to DNA synthesis pathways. Lasso regression analysis revealed that EFNA1, TYMS, and WISP2 were co-diagnostic markers for CC and OC, and then based on their expression levels and diagnostic efficacy, EFNA1 was selected as the best co-marker for CC and OC. Immune infiltration analysis shows that the immune environment has a significant impact on the occurrence and development of CC and OC, and the expression of EFNA1 is related to changes in immune cells. Gene-drug interaction analyses identified 27 common drug compounds that interact with candidate genes.</p><p><strong>Conclusion: </strong>This study adopted bioinformatics methods to investigate the common pathways and identify diagnostic markers between CC and OC, suggesting that DNA synthesis and immune environment are closely related to the occurrence and development of CC and OC. EFNA1 may be a potential diagnostic indicator and therapeutic target for patients with CC and OC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"826"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning-based identification of histone deacetylase-associated prognostic factors and prognostic modeling for low-grade glioma.","authors":"Keshan Wen, Weijie Zhu, Ziyi Luo, Wei Wang","doi":"10.1007/s12672-024-01713-7","DOIUrl":"https://doi.org/10.1007/s12672-024-01713-7","url":null,"abstract":"<p><strong>Background: </strong>Low-grade glioma (LGG) is a slow-growing but invasive tumor that affects brain function. Histone deacetylases (HDACs) play a critical role in gene regulation and tumor progression. This study aims to develop a prognostic model based on HDAC-related genes to aid in risk stratification and predict therapeutic responses.</p><p><strong>Methods: </strong>Expression data from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) were analyzed to identify an optimal HDAC-related risk signature from 73 genes using 10 machine learning algorithms. Patients were stratified into high- and low-risk groups based on the median risk score. Prognostic accuracy was evaluated using Kaplan-Meier survival analysis and receiver operating characteristic (ROC) curves. Functional enrichment analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA), were performed to explore pathways linked to the gene signature. Immune infiltration and tumor microenvironment characteristics were assessed using Single Sample Gene Set Enrichment Analysis (ssGSEA) and ESTIMATE algorithm. SubMap was applied to predict responsiveness to immune checkpoint inhibitors, and chemotherapeutic sensitivity was analyzed via the Genomics of Drug Sensitivity in Cancer (GDSC) database.</p><p><strong>Results: </strong>A prognostic model consisting of four HDAC-related genes-SP140, BAZ1B, SP100, and SIRT1-was identified. This signature displayed strong prognostic accuracy, achieving a C-index of 0.945. Individuals with LGG were systematically divided into high-risk and low-risk cohorts based on the median risk value, enabling more precise risk stratification. The survival prognosis was significantly worse in the high-risk cohort compared to the low-risk group, highlighting distinct survival trajectories. Notably, the two cohorts exhibited marked shifts in immune checkpoint gene transcriptional profiles and immune cell infiltration maps, underscoring fundamental biological differences that contribute to these differing prognoses.</p><p><strong>Conclusion: </strong>We developed an HDAC-related four-gene prognostic model that correlates with survival, immune landscape, and therapeutic response in LGG patients. This model may guide personalized treatment strategies and improve prognostic accuracy, warranting further validation in clinical settings.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"824"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Programmed cell death pathways in lung adenocarcinoma: illuminating tumor drug resistance and therapeutic opportunities through single-cell analysis.","authors":"Long Li, Shancheng He","doi":"10.1007/s12672-024-01736-0","DOIUrl":"https://doi.org/10.1007/s12672-024-01736-0","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) is a major contributor to cancer-related deaths, distinguished by its pronounced tumor heterogeneity and persistent challenges in overcoming drug resistance. In this study, we utilized single-cell RNA sequencing (scRNA-seq) to dissect the roles of programmed cell death (PCD) pathways, including apoptosis, necroptosis, pyroptosis, and ferroptosis, in shaping LUAD heterogeneity, immune infiltration, and prognosis. Among these, ferroptosis and pyroptosis were most significantly associated with favorable survival outcomes, highlighting their potential roles in enhancing anti-tumor immunity. Distinct PCD-related LUAD subtypes were identified, characterized by differential pathway activation and immune cell composition. Subtypes enriched with cytotoxic lymphocytes and dendritic cells demonstrated improved survival outcomes and increased potential responsiveness to immunotherapy. Drug sensitivity analysis revealed that these subtypes exhibited heightened sensitivity to targeted therapies and immune checkpoint inhibitors, suggesting opportunities for personalized treatment strategies. Our findings emphasize the interplay between PCD pathways and the tumor microenvironment, providing insights into the mechanisms underlying tumor drug resistance and immune evasion. By linking molecular and immune features to clinical outcomes, this study highlights the potential of targeting PCD pathways to enhance therapeutic efficacy and overcome resistance in LUAD. These results contribute to a growing framework for developing precise and adaptable cancer therapies tailored to specific tumor characteristics.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"828"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the role of Disulfidptosis in glioma progression: insights into tumor heterogeneity and therapeutic potential through single-cell RNA sequencing.","authors":"Xiaorong Fan, Maojun Chen","doi":"10.1007/s12672-024-01685-8","DOIUrl":"https://doi.org/10.1007/s12672-024-01685-8","url":null,"abstract":"<p><strong>Background: </strong>Gliomas, particularly glioblastoma (GBM), are the most common and aggressive primary brain tumors in adults, characterized by high malignancy and frequent recurrence. Despite standard treatments, including surgery, radiotherapy, and chemotherapy, the prognosis for GBM remains poor, with a median survival of less than 15 months and a five-year survival rate below 10%. Tumor heterogeneity and resistance to treatment create significant challenges in controlling glioma progression. Therefore, there is an urgent need for new therapeutic targets and strategies.</p><p><strong>Objective: </strong>This study investigates the role of Disulfidptosis, a recently discovered form of programmed cell death, in gliomas. Unlike apoptosis and necrosis, Disulfidptosis is driven by the abnormal accumulation of intracellular disulfide bonds, leading to protein misfolding and cytoskeletal collapse, particularly in cancer cells with metabolic dysregulation. We aim to explore how glioma cells respond to Disulfidptosis and identify potential therapeutic targets by analyzing the heterogeneity of gliomas at the single-cell level using single-cell RNA sequencing (scRNA-seq).</p><p><strong>Methods: </strong>scRNA-seq data from glioma patients were analyzed to uncover differences in ferroptosis-related pathways, including iron metabolism and lipid peroxidation. Cellular subpopulations within gliomas were profiled to assess their sensitivity to Disulfidptosis and the underlying mechanisms. Survival analysis was conducted to evaluate the clinical relevance of Disulfidptosis-related gene expression.</p><p><strong>Results: </strong>Multiple cell subpopulations within gliomas exhibit varying sensitivities to Disulfidptosis, influenced by their metabolic properties. Dysregulated iron metabolism and antioxidant mechanisms were identified as key factors impacting Disulfidptosis sensitivity. Glioma microenvironment signaling pathways also play a role in regulating Disulfidptosis. These findings suggest that activating Disulfidptosis pathways may provide novel therapeutic strategies to overcome treatment resistance in gliomas.</p><p><strong>Conclusion: </strong>This study offers new insights into the role of Disulfidptosis in glioma progression and highlights its potential as a therapeutic target. By leveraging single-cell sequencing data, the research uncovers tumor heterogeneity and identifies specific cell populations resistant to Disulfidptosis. These findings may pave the way for personalized treatment strategies to improve survival outcomes in glioma patients.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"829"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic pan-cancer analysis identifies ZBTB11 as a potential pan-cancer biomarker and immunotherapy target in multiple tumor types.","authors":"Peiyi Xu, Qiuyan Zhang, Jing Zhai, Pu Chen, Xueting Deng, Lin Miao, Xiuhua Zhang","doi":"10.1007/s12672-024-01697-4","DOIUrl":"https://doi.org/10.1007/s12672-024-01697-4","url":null,"abstract":"<p><strong>Background: </strong>ZBTB11 is a putative transcription factor with an N-terminal BTB domain and tandem C-terminal zinc finger motifs. Recent studies have suggested a potential role for ZBTB11 in tumorigenesis. However, the biological significance of ZBTB11 in different cancer types remains uncertain.</p><p><strong>Methods: </strong>The expression levels, prognostic values, genetic mutations, and DNA promoter methylation of ZBTB11 across tumor types were explored via various online websites and databases, including TIMER2.0, GEPIA2, cBioPortal, UALCAN, GSCA, CancerSEA, and others. Additionally, a competing lncRNA-miRNA network of ZBTB11 was constructed, and its interaction with chemicals and genes was investigated.</p><p><strong>Results: </strong>Our findings revealed that ZBTB11 was aberrantly expressed in a multitude of tumor types and exhibited variability across various tumor stages. A survival analysis revealed that ZBTB11 predicted a poor prognosis in BRCA, KIRP, LIHC, PCPG, PRAD, SARC, UCEC, and a good prognosis in CHOL, ESCA, GBM, KIRC, and READ. We also found that the most frequent genetic alterations type of ZBTB11 was mutation, and the DNA methylation level of ZBTB11 decreased in various cancers. Furthermore, ZBTB11 expression correlated with immune cells infiltration and genetic markers of immunodulators in cancers. Moreover, the results of single-cell sequencing demonstrated that ZBTB11 could regulate several tumor biological behaviors, including apoptosis, DNA damage, and angiogenesis. A lncRNA-miRNA network regulating ZBTB11 expression in tumor development and progression was constructed. It is of particular significance that ZBTB11 demonstrated a correlation with the CTRP and GDSC drug sensitivity, and that it served as a mediator between chemicals and cancers.</p><p><strong>Conclusion: </strong>These findings demonstrate that ZBTB11 is associated with multiple tumor types and disease prognosis. ZBTB11 may represent a potential key biomarker and therapeutic target in cancers.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"830"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of arbutin in the inhibition of FBXO5 in hepatocellular carcinoma.","authors":"Shuo Zhang, Kai Yao, Yangjing Pi, Sen Yang, Zheng Huang, Xueshan Pan, Tonggang Li","doi":"10.1007/s12672-024-01729-z","DOIUrl":"https://doi.org/10.1007/s12672-024-01729-z","url":null,"abstract":"<p><strong>Purpose: </strong>This work investigated the effect of FBXO5 in hepatocellular carcinoma (HCC) and the mechanism of action of arbutin in its inhibition.</p><p><strong>Methods: </strong>FBXO5 mRNA and protein expressions in the tumor were assessed using TCGA, ICGC and HPA databases. Cox regression analysis and Kaplan-Meier survival curves were employed to assess the impact of FBXO5 on the survival outcomes of patients with HCC. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA), and Gene Set Variation Analysis (GSVA) were used to investigate the biological function associated with FBXO5-related genes. The role of FBXO5 as oncogene and the inhibitory mechanism of arbutin were confirmed through western blotting (WB), reverse transcription quantitative polymerase chain reaction (RT-qPCR), and in vitro experiments such as scratch wound-healing migration assay, plate clone formation assay, and transwell migration assay.</p><p><strong>Results: </strong>Patients with high FBXO5 expression showed shorted overall survival (OS), progression-free survival (PFS), disease-specific survival (DSS), and disease-free survival (DFS). FBXO5 was identified as an independent prognostic risk factor associated with the cell cycle. In vitro investigations indicated that FBXO5 facilitated HCC progression by modulating the cell cycle, while arbutin suppressed FBXO5 expression and regulated cell cycle dynamics.</p><p><strong>Conclusion: </strong>FBXO5 is a potential diagnostic and prognostic biomarker for HCC, and arbutin may exert anticancer effects through the suppression of FBXO5 expression.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"827"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationships between blood cadmium concentration and risk of nine cancers: evidence from the NHANES 1999-2018 and Mendelian randomization analyses.","authors":"Jiang Wang, Sijia Deng, Guangyi Cheng, Yuyan Wang, Yu Shen, Jiayi Chen, Ke Xu, Bo Wang, Shuguang Han, Liantao Li","doi":"10.1007/s12672-024-01692-9","DOIUrl":"https://doi.org/10.1007/s12672-024-01692-9","url":null,"abstract":"<p><strong>Background: </strong>Previous observational studies examining the relationship between cadmium exposure and various cancers have yielded conflicting results. This study aims to comprehensively clarify the relationship between blood cadmium concentration (BCC) and nine specific cancers.</p><p><strong>Methods: </strong>A retrospective analysis of National Health and Nutrition Examination Survey (NHANES) 1999-2018 identified 36,991 participants. Multivariable logistic regression was used to assess the association between BCC and the risk of nine specific cancers. Additionally, Mendelian randomization (MR) analyses were conducted to investigate potential causal relationships.</p><p><strong>Results: </strong>Multivariable logistic regression analysis of the NHANES data indicated a positive association between BCC and the risk of bladder and lung cancers (P < 0.05) and a negative association with the risk of kidney and prostate cancers (P < 0.05). The MR analyses demonstrated a causal relationship between BCC and kidney cancer (P < 0.05). Additionally, it uncovered causal associations with breast, cervical, and colon cancers (P < 0.05).</p><p><strong>Conclusion: </strong>Elevated BCC was associated with an increased risk of bladder and lung cancers while demonstrating an inverse relationship with kidney and prostate cancers. MR analysis revealed that cadmium exposure may act as a protective factor against breast, cervical, colon, and kidney cancers, that must be confirmed with new studies.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"823"},"PeriodicalIF":2.8,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune checkpoint B7-H3 is a potential therapeutic target in prostate cancer.","authors":"Qi Shen, Kaichen Zhou, Haosen Lu, Jielin Zhang, Qiqing Xu, Chengsi Zhang, Chunhua Yang, Lijun Mao","doi":"10.1007/s12672-024-01674-x","DOIUrl":"https://doi.org/10.1007/s12672-024-01674-x","url":null,"abstract":"<p><p>High expression of immune checkpoint molecule B7-H3 (CD276) in many cancer types makes it a promising immunotherapeutic target. Both coinhibitory and costimulatory effects of B7-H3 in tumors have been demonstrated, but the mechanism of B7-H3 immune response under dual effects is open to question. B7-H3 is crucially involved in the migration and invasion, angiogenesis, metabolism and chemotherapy resistance of prostate cancer. In addition to the potential immune effects on tumor environment, B7-H3 plays a non-immune-mediated role in tumor progression. In this review, we summarize current understanding of molecular mechanism of B7-H3 in prostate cancer and discuss the potential of B7-H3 as a novel therapeutic target for prostate cancer.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"822"},"PeriodicalIF":2.8,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the causality between pulmonary arterial hypertension and cancer: insights from Mendelian randomization.","authors":"Yang Fu, Xinwang Duan, Wei Zhou","doi":"10.1007/s12672-024-01727-1","DOIUrl":"https://doi.org/10.1007/s12672-024-01727-1","url":null,"abstract":"<p><strong>Background: </strong>Previous clinical studies have suggested an increased risk of tumor development in patients with pulmonary arterial hypertension (PAH). However, it remains unclear whether there is a causal relationship between PAH and tumor occurrence. This study investigates the causal link between PAH and cancer from a genetic perspective using Mendelian randomization (MR).</p><p><strong>Method: </strong>Genome-wide association study (GWAS) summary data for PAH and various common cancer types were obtained from the GWAS Catalog. Single nucleotide polymorphisms (SNPs) significantly associated with PAH at the genome-wide significance threshold (P < 1 × 10^-6) were selected as instrumental variables (IVs). Inverse-variance weighted (IVW) was used as the primary method for MR analysis, with sensitivity analyses including tests for heterogeneity and horizontal pleiotropy.</p><p><strong>Results: </strong>The results from the IVW analysis indicate that genetically proxied PAH is associated with an increased risk of liver cancer [odd ratio (OR) 1.11, 95% confidence interval (CI) 1.01-1.22, P = 0.025), while showing no significant causal relationship with other common types of tumors (thyroid cancer: OR 0.95, 95% CI 0.86-1.06, P = 0.360; lung cancer: OR 0.95, 95% CI 0.90-1.01, P = 0.129; gastric cancer: OR 0.97, 95% CI 0.93-1.02, P = 0.243; colorectal cancer: OR 1.01, 95% CI 0.98-1.05, P = 0.412). Except for the MR analysis examining the causal effect of PAH on lung cancer (P = 0.049), the remaining MR analyses displayed no significant heterogeneity (P > 0.05). Additionally, the MR-Egger intercept test did not find evidence of horizontal pleiotropy (P > 0.05).</p><p><strong>Conclusion: </strong>This study highlights that PAH may serve as a potential risk factor for this liver cancer. Future research should aim to elucidate the biological mechanisms at play and explore the potential for early interventions that could mitigate cancer risk in this vulnerable population.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"821"},"PeriodicalIF":2.8,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of gout on colorectal cancer and its survival: a two-sample Mendelian randomization study.","authors":"Li-Qiang Wei, Yi-Bei Song, Dong Lan, Xue-Jing Miao, Chun-Yu Lin, Shu-Ting Yang, Deng-He Liu, Xiao-Jv Chi","doi":"10.1007/s12672-024-01714-6","DOIUrl":"https://doi.org/10.1007/s12672-024-01714-6","url":null,"abstract":"<p><strong>Background: </strong>The relationship between gout and colorectal cancer (CRC) remains unclear, emphasizing the need for additional research to clarify the potential cumulative effect of gout on CRC development.</p><p><strong>Methods: </strong>Leveraging a single nucleotide polymorphism-based genome-wide association study, the potential causal correlation between gout and CRC was initially analyzed using Mendelian randomization (MR). Subsequently, our analysis was expanded to include an assessment of patient survival, with the aim of evaluating the potential causal correlation between gout and CRC and the impact of gout on CRC survival outcomes.</p><p><strong>Results: </strong>According to MR findings, a substantial relationship was observed between gout and the incidence of CRC when CRC was used as the outcome (OR = 0.954, 95% CI = 0.915-0.995). These results indicate a negative relationship between gout and the likelihood of developing CRC. In addition, when evaluating the overall survival (OS) or cancer-specific survival (CSS) of patients with CRC as outcomes, gout exhibited a significant relationship with survival. The inverse variance weighting approach demonstrated a progressive enhancement in CRC survival with the cumulative impact of gout (OS: OR = 2.000 × 10^-4, 95% CI = 1.560 × 10^-7-0.292; CSS: OR = 2.200 × 10^-5, 95% CI = 4.660 × 10^-9-0.104).</p><p><strong>Conclusion: </strong>As gout accumulates, it exerts an inhibitory influence on CRC, indicating a potential protective effect. This study provides robust evidence that can guide the development of future clinical treatment approaches and research priorities.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"819"},"PeriodicalIF":2.8,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}