Ovarian cancer (OV) is the most prevalent and lethal gynecologic malignancy globally. Cisplatin remains the first-line chemotherapeutic regimen for OV; however, chemotherapy resistance poses a persistent clinical challenge in gynecologic oncology. Parthenolide, a naturally derived phytochemical, exhibits broad-spectrum antitumor activity. Recent studies suggest that parthenolide may reverse cisplatin-resistance in OV when used in combination therapy. This study aims to elucidate the molecular targets and mechanisms underlying parthenolide-mediated reversal of cisplatin-resistance by integrating network pharmacology and molecular docking approaches.

In recent years, some circRNAs and RNA methylation enzymes (including RNA methyltransferases and RNA demethylases) have been reported to be associated to the prognosis of bladder cancer, but the findings have been inconsistent. Therefore, the aims of this study is to comprehensively evaluate the prognostic value of circRNAs and RNA methylation enzymes as a whole in bladder cancer by Meta-analysis. A comprehensive literature search was performed in PubMed, Cochrane Library, EMbase, Web of Science, CNKI, WanFang, and VIP databases from the establishment of the database to March 2024. Data were extracted from the included literature and statistically analyzed using Stata 18.0 MP. (1) Overall survival (OS): high expression of circRNAs decreased OS of bladder cancer (HR = 1.74, 95% CI: 1.26-2.41, P = 0.001); and high fat mass and obesity-associated protein (FTO) expression led to poor OS in bladder cancer (HR = 2.38, 95% CI: 1.08-2.25, P = 0.032). (2) Disease-free survival (DFS): low circRNAs expression resulted in poor DFS (HR = 1.74, 95% CI: 1.38-2.18, P < 0.001); (3) Recurrence-free survival (RFS): high expression of circ-CCT3 and circ-RHOT1 decreased bladder cancer patients' RFS (HR = 2.26, 95% CI: 1.63-3.12, P < 0.001); and low expression of circ0004826 and circ0077837 also affected RFS (HR = 0.19, 95% CI: 0.08-0.43, P < 0.001). (4) 5-year survival: high expression of circRNAs decreased 5-year survival of bladder cancer patients (HR = 3.26, 95% CI: 1.90-5.57, P < 0.001). CircRNAs and FTO can be prognostic factors for bladder cancer.

The role of the CYP17A1 gene's rs743572 polymorphism in cancer susceptibility has been a subject of extensive investigation, yet existing evidence remains inconclusive. In this meta-analysis, we systematically reviewed and synthesized data from 29 studies to assess the CYP17A1 rs743572 polymorphism's relationship with cancer susceptibility. We strictly searched on EMBASE, PubMed, and Web of Science databases and explored rs743572 polymorphism's association with cancer risks according to search strategy, enrolling 29 studies (13,767 cases and 17,441 controls). rs743572 was markedly related to enhanced cancer susceptibility risk; FPRP and TSA analyses were employed for confirmation. According to cancer type-based stratified analyses, rs743572 exhibited a notable association with bladder cancer, breast cancer, non-Hodgkin lymphoma, and hepatocellular cancer. In conclusion, systematic meta-analysis suggests a significant role for the rs743572 polymorphism in cancer pathogenesis, with particular prominence observed in bladder cancer, breast cancer, non-Hodgkin lymphoma, and hepatocellular cancer.

Breast cancer (BC) is the most common cancer in women. Taxanes are widely used, but their neurotoxicity affects patients' quality of life. Genetic polymorphisms in CYP450 enzymes influence taxane metabolism, leading to variability in toxicity risk.

This review aimed to evaluate the impact of cyclin-dependent kinases 2 A/2B (CDKN2A/2B) deletion on survival in pediatric acute lymphoblastic leukemia (ALL). We pooled hazard ratios (HRs) and risk ratios (RRs) with 95% CIs, which were calculated using random-effects models. Individual patient data (IPD) were extracted from published survival curves of included studies, and combined HR was estimated. Fourteen studies (n = 2532 subjects) were included. CDKN2A/2B deletion was found to be associated with poor event/disease/relapse-free survivals at both study levels (HR 2.18; 95% CI: 1.46-3.27; I2 51%) and IPD level (HR 3.45; 95% CI 2.76-4.32 and p < 0.001); and poor overall survival at the IPD level (HR 3.22; 95% CI: 1.78-5.84 and p < 0.001). CDKN2A/2B deletion was also associated with a higher risk of poor prednisolone response (RR 1.38; 95% CI: 1.09-1.74; I2 7%) and relapse rates (RR 3.83; 95% CI: 2.76-5.3; I2 -0%). The meta-analysis highlights the negative impact of CDKN2A/2B deletions on disease outcome and treatment response. Hence, incorporating these alterations should improve risk stratification and risk-adapted treatment strategies for childhood ALL.

Approximately 10% of breast and 20% of ovarian cancers are hereditary in nature. The most commonly implicated genes are the BRCA genes, and the current gold standard for testing is by direct DNA sequencing. This process is expensive, time-consuming, and has a turnaround time of several weeks. Radiogenomics involves extracting quantitative data from medical imaging and using mathematical models to predict the underlying genetic makeup of tissues.

Recent research suggests a link between KRAS mutations and the effectiveness of ICIs, as KRAS-driven tumors may possess unique immunogenic features that influence the tumor microenvironment. These mutations can increase tumor mutation burden (TMB) and neoantigen load, potentially leading to improved responses to ICIs. This meta-analysis aims to consolidate existing evidence on the impact of KRAS mutations as a predictive factor for survival and treatment outcomes in patients with advanced NSCLC treated with ICIs. A comprehensive search strategy was designed by a biostatistician and pulmonologist, targeting PubMed, Web of Science, and Scopus databases up to May 2022. The outcomes assessed included overall survival (OS) and progression-free survival (PFS), reported as log hazard ratios (HRs) with corresponding standard errors (SEs). A pooled estimate of the HR effect size was calculated using Review Manager (RevMan, Cochrane Collaboration, London, UK). Heterogeneity among studies was evaluated using the Cochran Q test and the I2 statistic. Ultimately, 10 articles were deemed suitable for inclusion in the systematic review from a total of 8722 screened titles and abstracts. The presence of KRAS+ mutations had a significant prognostic factor for better OS in NSCLC patients treated with checkpoint inhibitors (HR = 0.89, 95% CI: 0.79-0.99) and for better PFS in NSCLC patients treated with checkpoint inhibitors (HR = 0.72, 95% CI: 0.59-0.87). In conclusion, our study indicates that KRAS mutations may serve as a potential positive predictive biomarker in patients with advanced non-small-cell lung cancer treated with immune checkpoint inhibitor monotherapy.

The epidermal growth factor receptor (EGFR) plays a key role in non-small cell lung cancer (NSCLC) and is fundamental in therapeutic decision-making. The Idylla™ EGFR Mutation Test (Idylla™ MT) is an automated platform designed to detect mutations in EGFR. This meta-analysis evaluates its diagnostic test accuracy (DTA) in comparison with reference methods such as next-generation sequencing (NGS) and real-time PCR (qPCR).

The Human Leukocyte Antigen (HLA) genes, located within the Major Histocompatibility Complex on chromosome 6p21, are highly polymorphic and play a vital role in immunity and has strong associations with autoimmune disorders. However, its role in cancers including oral cancers and oral potentially malignant disorders (OPMD) is still being explored and there is no strong evidence available for this association. Hence the present systematic review was performed to synthesize the current available evidence of genetic propensity of HLA alleles in protective or susceptibility role in occurrence of OPMD.

Sentinel lymph node biopsy (SLNB) is an invasive procedure that detects microscopic nodal metastasis, crucial for accurate staging and optimal management. In melanoma, most patients who undergo the procedure have no sentinel lymph node (SLN) metastasis detected. The CP-GEP model (Merlin Assay) was developed to identify patients who do not have SLN metastases and who may therefore safely forgo SLNB, based upon clinicopathologic and gene expression features of the primary tumour. While the Merlin Assay has been validated by independent cohorts with relatively moderate sample sizes, this meta-analysis aims to assess the overall predictive performance of the model and examine potential heterogeneity between the external validation cohorts.

Lynch syndrome (LS) is an inherited disorder associated with an increased risk of colorectal and extracolonic malignancies, including gastric cancer (GC). This study quantifies the association between specific risk factors and GC development in patients with LS.

The functional polymorphisms of VEGF can affect different cellular processes and play a major role in angiogenesis and tumor development. Several case-control studies have explored the association of VEGF +405C/G polymorphism with GIT cancer risk, however, the results were inconsistent. Therefore, the meta-analysis was conducted to clarify the association.

Epidermal growth factor receptor (EGFR) mutations are a common driver of oncogenesis in non-small cell lung cancer (NSCLC). Lazertinib, a third-generation EGFR tyrosine kinase inhibitor (TKI), has shown promise as a first-line treatment for patients with locally advanced or metastatic EGFR-mutated NSCLC. However, the comparative efficacy and safety of lazertinib in this setting have not been thoroughly investigated. This study aims to evaluate the efficacy and safety of lazertinib for EGFR-mutated locally advanced NSCLC.

Immunotherapy combined with chemotherapy has emerged as a potential strategy to overcome tyrosine kinase inhibitors (TKIs)-resistant for advanced non-small-cell lung cancer (NSCLC); however, the efficacy and safety of PD-1/PD-L1 inhibitors plus chemotherapy (PIC) compared to chemotherapy alone require further investigation.

Ponatinib, a third-generation tyrosine kinase inhibitor (TKI), has shown efficacy in Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), including cases with and without BCR-ABL1 kinase domain mutations. This meta-analysis compares ponatinib with other TKIs (imatinib, dasatinib, nilotinib etc.) in terms of complete molecular response (CMR), overall survival (OS), and event-free survival (EFS).

To identify the predictive role of circulating tumor DNA (ctDNA)-based molecular residual disease (MRD) for long-term outcomes in non-small cell lung cancer (NSCLC) patients.

Background and aims: the intricate relationships between socioeconomic factors, modifiable lifestyle choices, and esophageal cancer risk remain uncertain. We aim to investigate the associations of socioeconomic status, modifiable lifestyle factors, and esophageal cancer risk. Methods: we employed multiple Mendelian randomization (MR) analyses, including three different MR approaches. GWAS databases from European and East Asian populations, encompassing variables such as household income, educational attainment, and the Townsend deprivation index (TDI), were analyzed. The risk of esophageal cancer was assessed using data from three distinct cohorts of European and East Asian descent (Database 1: n = 476,306; Database 2: n = 372,756; Database 3: n = 160,589). Nine modifiable lifestyle factors were incorporated in the multivariable and mediation MR analyses. Meta-analysis was employed to synthesize results across the three datasets. Results: higher household income was connected with a reduced esophageal cancer risk (odds ratio (OR) = 0.698, 95 % confidence interval (95 % CI): 0.556-0.876, p = 0.002). Body mass index (BMI) partially mediated the relationship between household income and the risk of esophageal cancer (OR = 0.914, 95 % CI: 0.841-0.992, p = 0.031, mediation ratio: 27.23 %). However, no significant evidence was found to support a direct association between educational attainment, TDI, and esophageal cancer risk. Conclusions: these findings suggest that higher household income is inversely associated with esophageal cancer risk, with BMI acting as a partial mediator of this relationship. Accordingly, targeted early screening and preventive measures for esophageal cancer should be prioritized among low-income populations, particularly those with obesity.

To evaluate the efficacy and safety of early brain radiotherapy combined with EGFR-TKI versus EGFR-TKI alone in EGFR-mutation-positive non-small cell lung cancer (NSCLC) patients with brain metastases (BMS). A systematic literature search was conducted in several databases. The primary outcome measures were overall survival (OS) and intracranial progression-free survival (iPFS), while secondary outcome measures included adverse events (AEs). Meta-analysis was performed using STATA 15.1 software. A total of 18 retrospective trials involving 2,119 patients were included. Meta-analysis showed that early brain radiotherapy combined with EGFR-TKI was superior to monotherapy in improving OS (HR = 0.87, 95% CI, 0.76-0.99) and iPFS (HR = 0.77, 95% CI, 0.61-0.97). Subgroup analysis indicated that among patients treated with Osimertinib, monotherapy showed a trend towards improved OS (HR = 1.44, 95% CI, 0.94-2.22) and iPFS (HR = 1.10, 95% CI, 0.76-1.60), though without statistical significance. In contrast, first- and second-generation EGFR-TKI combined with early brain radiotherapy significantly prolonged OS (HR = 0.83, 95% CI, 0.72-0.95) and iPFS (HR = 0.72, 95% CI, 0.55-0.93). Regarding AEs, the incidence of neurological adverse reactions was significantly higher in the combined treatment group (RR = 15.82, 95% CI, 2.31-108.54). Early brain radiotherapy combined with EGFR-TKI can significantly improve OS and iPFS in EGFR-mutated NSCLC patients with BMS but may increase the risk of neurological adverse reactions. Further research is needed to verify the efficacy differences between monotherapy and combination therapy for patients using Osimertinib.

To evaluate the diagnostic accuracy and detection rate of lymph node metastases (LNM) in Papillary Thyroid Carcinoma (PTC) using the One-Step Nucleic Acid Amplification (OSNA) technique compared to conventional pathological methods.

Uveal melanoma (UM) is a rare but frequently metastasizing cancer. Genome-wide association studies have identified three common genome-wide significant germline risk loci. Here, we perform a genome-wide association study on 401 new cases and conduct a meta-analysis with three independent previously published cohorts for a total sample size of 2,426 cases. We confirm the three previously identified risk loci and identify four additional genome-wide significant loci. We find that eye pigmentation-decreasing variants are systematically associated with increased UM risk and that selection for lighter pigmentation in the past 5,000 years explains about 73% of the difference in UM incidence between Northern and Southern Europe. We find evidence of effect size heterogeneity at significant loci across cohorts, in particular, a weaker association between eye pigmentation and UM in a Finnish cohort. Finally, we confirm differential effect sizes between uveal melanoma cases with and without loss of chromosome 3, the major determinant of metastatic risk. Our study identifies novel germline risk factors for UM and highlights genetic and environmental heterogeneity in its etiology.