While observational studies have identified associations between gastroesophageal reflux disease (GERD) and laryngeal cancer (LC), the causal direction remains undetermined. This study employed a bidirectional 2-sample Mendelian randomization (MR) approach complemented by meta-analysis to investigate potential causal relationships between GERD and LC. Analysis leveraged publicly accessible genome-wide association study resources. Instrumental variables meeting MR assumptions were rigorously selected. The inverse variance weighted method served as primary analysis, with horizontal pleiotropy assessed through MR-Egger intercept tests. Sensitivity evaluations included Cochran Q test for heterogeneity and leave-one-out analysis. Findings from multiple databases were consolidated via meta-analysis. Inverse variance weighted estimates demonstrated no significant causal effect of GERD on LC risk (odds ratio [OR] = 1.11, 95% confidence interval [CI] = 0.83-1.48). In addition, reverse MR analysis revealed no causal impact of LC genetic liability on GERD development (odds ratio = 1.01, 95% CI = 0.99-1.02). All sensitivity analyses supported consistent results. This bidirectional MR investigation provides no genetic evidence for causal associations between GERD and LC in either direction.

Vulvar squamous cell carcinoma (VSCC) is subdivided into TP53-mutant (TP53mut) and HPV-associated (HPV+). In recent years, a third group unrelated to TP53 mutation or HPV-association (TP53wt/HPV-) has emerged. However, its prognosis is unclear.

To evaluate the risk of cardiovascular adverse events associated with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in patients with EGFR-mutated non-small cell lung cancer (NSCLC).

Cancer development involves complex interactions between immune mechanisms and the tumor microenvironment, with regulatory T cells (Tregs) being implicated in suppressing anti-tumor immunity. The X-linked gene Forkhead Box P3 (FOXP3), which regulates Tregs' function, and its promoter variant rs3761548 C>A have been widely studied for their role in tumorigenesis. This meta-analysis aims to re-evaluate the association between rs3761548 and cancer risk using two statistical approaches to account for sex-based genotypic differences and X-chromosome statistical challenges.

Colorectal cancer (CRC) is a highly aggressive and extensive malignancy. Although long noncoding RNAs (lncRNAs) are often used as diagnostic biomarkers, their diagnostic effectiveness in CRC remains uncertain.

Background & objectives Kinesin superfamily proteins (KIFs), essential motor proteins involved in processes like mitosis and intracellular transport, have emerged as critical players in breast cancer (BC) progression. Recent studies highlight their potential as prognostic biomarkers and therapeutic targets. This research explores the association between the expression of KIFs and survival outcomes, including overall survival (OS), recurrence-free survival (RFS), and distant metastasis-free survival (DMFS). Methods In this study, we carried out a meta-analysis as per the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A thorough literature search was conducted using the PubMed and ScienceDirect databases, covering the period from June 1996 to October 2024. Hazard ratios (HRs) and their corresponding 95 per cent confidence intervals (CIs) were extracted from eligible studies and analysed using the RevMan software. Results Initially, we screened 220 articles for this systematic review, from which 11 studies met the inclusion criteria for the meta-analysis. In our analysis, we have observed that elevated KIFs levels were associated with poor OS (HR=1.77 with 95% CI=1.58-1.98 and P<0.00001), RFS (HR=1.40, 95% CI=1.31-1.49, P<0.00001), and DMFS (HR=1.72, 95% CI=1.49-1.99, P<0.00001). These findings suggest that increased expression of kinesin family members contributes to reduced survival rates and increases the risks of recurrence and metastasis in BC patients. Interpretation & conclusions Our study highlights the potential of kinensin family members as prognostic biomarkers for BC progression, providing insights that may help in clinical decision-making and patient management.

Lung cancer (LC) is the leading cause of cancer-related mortality worldwide, accounting for millions of deaths annually. Its major subtypes-lung squamous carcinoma (LUSC), lung adenocarcinoma, and small-cell LC-exhibit distinct risk factors and genetic susceptibilities, necessitating the use of subtype-specific biomarkers. Two-sample Mendelian randomization (MR) analyses were conducted using protein quantitative trait loci from the UK Biobank Pharma Proteomics Project and deCODE datasets. A robust analytical framework, including reverse MR, meta-analysis, summary-data-based MR tests, and colocalization, cisMR-cML, MR.CUE and phenotype scanning analyses were used to identify proteins associated with LC risk. We conducted a systematic review to contextualize our research findings. Follow-up analyses, including pathway enrichment, protein-protein interaction network analysis, and druggability evaluations, were used to explore the mechanisms and therapeutic potential of the identified proteins. Significant proteins were validated using population-level proteomic data from the UK Biobank (UKB). The results showed that twenty-five proteins were significantly associated with LC or its subtypes, including 15 novel findings. 60S ribosomal protein L14 (RPL14) and advanced glycosylation end-product-specific receptor (AGER) emerged as the strongest discovery, demonstrating consistent and significant associations across both MR and population-level analyses. RPL14 exhibited positive associations with overall LC risk (MR_meta: odds ratio [OR]: 2.012, 95% confidence interval [CI]: 1.297-3.119; UKB: OR: 1.509, 95% CI: 1.015-2.244). Similarly, AGER showed significant protective effects against LUSC risk (MR_meta: OR: 0.572, 95%CI: 0.368-0.889; UKB: OR: 0.366, 95% CI: 0.158-0.850). Pathway analysis revealed the involvement of these proteins in immune regulation and tumorigenesis. Among the 13 identified druggable targets, RPL14 and AGER showed therapeutic potential as approved or investigational drugs targeting these proteins. These findings offer new insights into the pathogenesis of LC and potential therapeutic targets.

Circulating tumor DNA (ctDNA) is evolving into a promising non-invasive approach for the detection of ALK rearrangement. This meta-analysis was designed to determine the diagnostic value of ctDNA for ALK rearrangement in lung cancer patients.

To evaluate the association between GSTP1 rs1695 A>G polymorphism and colorectal cancer (CRC) risk in an Iranian cohort, and to validate findings through a systematic review and meta-analysis.

Small nucleolar RNA host gene 22 (SNHG22) is a novel long non-coding RNA (lncRNA) that functions as an oncogene and promotes the progression of various cancers. This pooled analysis aimed to clarify the prognostic role of SNHG22 in solid tumors and to explore its correlation with disease characteristics.

Colorectal cancer remains a major global health challenge, necessitating the development of accurate non-invasive diagnostic tools. Circulating and excretory microRNAs (miRNAs) are promising biomarkers owing to their stability and regulatory roles in tumorigenic pathways. While single miRNA assays often lack sufficient diagnostic accuracy, panels combining multiple miRNAs have shown enhanced performance. This systematic review and meta-analysis evaluated the diagnostic accuracy of multi-miRNA panels and explored their mechanistic relevance to colorectal cancer pathogenesis.

Patients with brain cancers are diagnosed based on MRI in the clinical setting while molecular signatures offer potential therapeutic targets. The necessity to re-form molecular and imaging information motivated our meta-analysis to decipher the correlation between the MRI-classified tumor locations, gene expression, and protein signatures in GBM.

This study aimed to systematically evaluate the efficacy and safety of combination therapies with immune checkpoint inhibitors (ICIs) in patients with driver gene-negative non-small cell lung cancer (NSCLC) and liver metastases. These patients typically have poor prognosis and limited responses to immunotherapy. This study synthesized existing literature by conducting a network meta-analysis to determine the most effective first-line ICI combination regimen to guide clinical treatment decisions.

We aimed to explore the prognostic role of circulating DNA-related markers to improve clinical decision-making in patients with lung malignancies.

Poly (ADP-ribose) polymerase inhibitors (PARPi) have become a key treatment for ovarian cancer, particularly in patients with BRCA mutations or homologous recombination deficiency (HRD).

Metastatic uveal melanoma (mUM) is a rare disease associated with poor prognosis and limited therapeutic options. Recent studies showed that detecting ctDNA is feasible and can aid treatment decisions for patients with mUM. We systematically searched PubMed, EMBASE, and Cochrane databases for eligible studies published up to May 2025 that included patients with mUM and reported data on the association between ctDNA and survival outcomes (OS and PFS). Statistical analyses were performed using Review Manager 5.4 software. Of the initial 450 records, seven studies met eligibility, including 518 patients with mUM. At baseline, ctDNA positivity was associated with significantly worse PFS (HR 2.34; 95% CI 1.56-3.51; p < 0.01; I2 = 0%) and OS (HR 3.32; 95% CI 2.09-5.29; p < 0.01; I2 = 48%). In patients treated with tebentafusp, ctDNA clearance was associated with superior OS (HR 0.19; 95% CI 0.07-0.49; p < 0.01; I2 = 46%) and any decrease in ctDNA was associated with better OS (HR 0.42; 95% CI 0.22-0.80; p < 0.01; I2 = 0%). This meta-analysis underscores ctDNA as a potential predictor of worse survival in patients with mUM, highlighting its potential to refine risk stratification and guide treatment strategies. Trial Registration: International Prospective Register of Systematic Reviews (PROSPERO): CRD42025638076.

The skin microbiome has been linked to the etiology and progression of skin cancer, but the causal relationship remains unclear. This study employs two-sample Mendelian randomization (TSMR) and meta-analysis techniques to elucidate the putative genetic causal relationships between skin microbiota and skin cancer. Genetic variant data for the skin microbiome and skin cancer, drawn from large-scale genome-wide association studies, were extracted from European populations. TSMR analysis, heterogeneity tests, horizontal pleiotropy assessments, sensitivity analysis, and directional tests were conducted, followed by a meta-analysis to enhance the reliability of the findings. The TSMR and meta-analysis results indicate a significant association between the Proteobacteria phylum, including Gammaproteobacteria, and an increased risk of melanoma. Conversely, the Staphylococcus genus is significantly associated with a reduced risk of melanoma. Additionally, the Bacteroidetes phylum exhibits a statistically significant association with an elevated risk of basal cell carcinoma. This study furnishes genetic evidence substantiating the causal nexus between the skin microbiome and skin cancer. Further research is warranted to elucidate the underlying mechanisms and explore skin microbiome-centric prophylactic and therapeutic strategies for skin cancer.

Type 1 Diabetes Mellitus (T1DM) is related to increased Polycystic Ovary Syndrome (PCOS) prevalence in women. However, the molecular mechanisms have not been fully elucidated.

Most studies suggest that NOTCH1 alterations are associated with prognosis in adenoid cystic carcinoma (ACC), but findings remain fragmented. We conducted an integrative analysis to evaluate the prognostic value of NOTCH1-related biomarkers in ACC.

To synthetically evaluate the diagnostic performance of circulating tumor DNA (ctDNA) methylation for colorectal cancer (CRC).