Flap endonuclease 1 (FEN1) has emerged as an important enzyme in the maintenance of genomic instability and preventing carcinogenesis. The relationship between FEN1 -69G>A (rs174538)+4150G>T (rs4246215) polymorphisms and cancer susceptibility has been reported; however, results were inconclusive. In the present study, a meta-analysis of data from eligible reports was carried out to summarize the possible relationship between FEN1 polymorphisms and cancer risk. A total of 11 articles, including 20 studies with 7366 cases and 9028 controls and 18 studies with 6649 cases and 8325 controls for FEN1 rs174538 and FEN1 rs4246215 polymorphisms, respectively, were recruited for meta-analysis. Overall, meta-analyses showed that FEN1 rs174538 and rs4246215 polymorphisms are significantly associated with the decreased risk of cancer. The stratified analysis proposed that both variants were associated with protection against gastrointestinal cancer, breast cancer, hepatocellular cancer, esophageal cancer, gastric cancer, colorectal cancer, and lung cancer. In conclusion, this meta-analysis revealed an association between FEN1 polymorphisms and cancer risk. Additional studies in a larger study population that include subjects from a variety of ethnicities are warranted to further verify our findings.
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http://dx.doi.org/10.1002/jcb.28633 | DOI Listing |
Cells
December 2024
BIH Center for Regenerative Therapies (BCRT), Therapy-Induced Remodeling in Immuno-Oncology, Berlin Institute of Health at Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany.
Antibody-dependent cell-mediated cytotoxicity (ADCC) by NK cells is a key mechanism in anti-cancer therapies with monoclonal antibodies, including cetuximab (EGFR-targeting) and avelumab (PDL1-targeting). Fc gamma receptor IIIa (FcγRIIIa) polymorphisms impact ADCC, yet their clinical relevance in NK cell functionality remains debated. We developed two complementary flow cytometry assays: one to predict the FcγRIIIa-V158F polymorphism using a machine learning model, and a 15-color flow cytometry panel to assess antibody-induced NK cell functionality and cancer-immune cell interactions.
View Article and Find Full Text PDFCardiovasc Diagn Ther
December 2024
Department of Radiology, University of Cagliari, Cagliari, Italy.
Background And Objective: Interleukin-6 (IL-6) plays multifaceted roles in cancer and atherosclerosis. Initially recognized for its role in immune response and inflammation, IL-6 promotes tumor progression via the JAK-STAT and MAP kinase pathways and is associated with poor cancer prognoses. In atherosclerosis, IL-6 contributes to endothelial dysfunction and plaque formation.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Epidemiology, Geisel School of Medicine at Dartmouth, Hanover, NH, USA.
Genome-wide association studies (GWAS) have detected several susceptibility variants for urinary bladder cancer, but how gene regulation affects disease development remains unclear. To extend GWAS findings, we conducted a transcriptome-wide association study (TWAS) using PrediXcan to predict gene expression levels in whole blood using genome-wide genotype data for 6180 bladder cancer cases and 5699 controls included in the database of Genotypes and Phenotypes (dbGaP). Logistic regression was used to estimate adjusted gene-level odds ratios (OR) per 1-standard deviation higher expression with 95% confidence intervals (CI) for bladder cancer risk.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Laboratory Medicine, Clinical Pathology and Genetics, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Vulvar cancer is a rare gynaecological disease that can be caused by infection with human papillomavirus (HPV). The mutational frequencies and landscape for HPV-associated and HPV-independent vulvar tumor development are supposedly two distinctly different pathways and more detailed knowledge on target biological mechanisms for individualized future treatments is needed. The study included formalin-fixed paraffin-embedded (FFPE) samples from 32 cancer patients (16 HPV-negative and 16 HPV-associated), treated in Örebro, Sweden from 1988 to 2008.
View Article and Find Full Text PDFPLoS One
January 2025
Institute for Health Systems Science, Faculty of Technology, Policy and Management, Delft University of Technology, Delft, The Netherlands.
Mathematical modeling plays an important role in our understanding and targeting therapy resistance mechanisms in cancer. The polymorphic Gompertzian model, analyzed theoretically and numerically by Viossat and Noble to demonstrate the benefits of adaptive therapy in metastatic cancer, describes a heterogeneous cancer population consisting of therapy-sensitive and therapy-resistant cells. In this study, we demonstrate that the polymorphic Gompertzian model successfully captures trends in both in vitro and in vivo data on non-small cell lung cancer (NSCLC) dynamics under treatment.
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