Objective and Background This research aims to explore the potential of single-nucleotide polymorphisms (SNPs) in PAX8 rs10175462, PBX2 rs2856437, and TERT rs2853669 genes as biomarkers for cervical cancer by examining their association with the disease. Methodology The study involved 600 participants, comprising 300 healthy controls and 300 patients. DNA was extracted from blood followed by polymerase chain reaction. Results A significant correlation with an approximately two-fold elevated risk of developing cervical cancer is noted in the (TT) homozygous mutant of the rs10175462 SNP of the PAX8 gene (odds ratio (OR) = 2.91; p = 0.0001). A highly significant correlation is observed in the heterozygote genotype (GT) of the same SNP (OR = 0.46; p = 0.0001). Significant correlation with high risk of disease by one-fold is noted in heterozygote genotype (GA) of rs2856437 of gene PBX2 (OR = 1.88; p = 0.0003), while an increase in risk by one-fold is noted in homozygous mutant (AA) (OR = 1.05; p = 0.81). The homozygous mutant genotype (GG) in rs2853669 shows a significant correlation (OR = 0.36; p = 0.0001), whereas in the heterozygote genotype (AG), the risk increases by two-fold and exhibits a significant correlation (OR = 2.57; p = 0.0001).
Objective and Background This research aims to explore the potential of single-nucleotide polymorphisms (SNPs) in PAX8 rs10175462, PBX2 rs2856437, and TERT rs2853669 genes as biomarkers for cervical cancer by examining their association with the disease. Methodology The study involved 600 participants, comprising 300 healthy controls and 300 patients. DNA was extracted from blood followed by polymerase chain reaction. Results A significant correlation with an approximately two-fold elevated risk of developing cervical cancer is noted in the (TT) homozygous mutant of the rs10175462 SNP of the PAX8 gene (odds ratio (OR) = 2.91; p = 0.0001). A highly significant correlation is observed in the heterozygote genotype (GT) of the same SNP (OR = 0.46; p = 0.0001). Significant correlation with high risk of disease by one-fold is noted in heterozygote genotype (GA) of rs2856437 of gene PBX2 (OR = 1.88; p = 0.0003), while an increase in risk by one-fold is noted in homozygous mutant (AA) (OR = 1.05; p = 0.81). The homozygous mutant genotype (GG) in rs2853669 shows a significant correlation (OR = 0.36; p = 0.0001), whereas in the heterozygote genotype (AG), the risk increases by two-fold and exhibits a significant correlation (OR = 2.57; p = 0.0001).
Background The global prevalence of thyroid nodules is rising, prompting heightened clinical concern given their potential for malignant transformation. Although tumor markers are routinely assessed to aid in malignancy evaluation, their potential to predict thyroid nodule development and their value for early risk stratification remain insufficiently established. Methods In this prospective cohort study, 462 adults underwent three standardized physical examinations after enrollment. Comprehensive baseline data, including demographics, anthropometrics, vital signs, laboratory parameters, and ultrasound-confirmed thyroid nodule status have been collected. variance inflation factor and Least Absolute Shrinkage and Selection Operator were used in variable selection while logistic regression was used in statistical analysis. Results A total of 302 participants were included in the final analytical cohort. In this cohort, female sex, age, BMI, and DBP were significantly associated with the occurrence of thyroid nodules. When further analyzed using a discrete-time hazard model, age, SBP, and FPSA were significantly associated with nodule occurrence at the second and third examination. In males, logistic regression identified age, BMI, and FPSA as significant risk factors, and the discrete-time hazard model confirmed age, FPSA as independent predictors. In females, however, logistic regression showed that age was a risk factor while DBP was a protective factor, findings that were replicated in the discrete-time hazard model. Conclusion Female sex, age, BMI, DBP, and FPSA show distinct associations with thyroid nodule development: FPSA is a male-specific risk marker, while DBP is protective in females. These findings point to sex-specific biological pathways and warrant mechanistic study and validation in diverse populations.
Objective To investigate the causal relationships between fibroblast growth factors (FGFs) and gastroesophageal cancers—specifically gastric cancer (GC), cardia cancer (CC), and esophageal cancer (EC)—using a two-sample Mendelian randomization (MR) approach. Methods Bidirectional two-sample MR was conducted using GWAS data of FGFs, FGFRs, and GC, with IVW as the primary method. Univariate MR (UVMR) first identified preliminary associations, followed by multivariable MR (MVMR) to estimate the direct effects of FGFs independent of confounders. Results The IVW results indicated a nominal association between FGF7 and CC (β = -0.5152, P = 0.0402, P-FDR = 0.2008); FGF21 showed a nominal association with both CC (β = -1.0245, P = 0.0175, P-FDR = 0.1750) and GC (β = 1.1361, P = 0.0473, P-FDR = 0.4730). MVMR analysis showed that, after adjusting for cigarettes smoked per day, FGF21 was significantly causally associated with CC (OR = 0.2514); after adjusting for BMI, FGF21 was significantly causally associated with GC (OR = 2.2893). The results of the reverse analysis indicated a nominal association between EC or GC and FGF21 (OR = 0.9739, P = 0.0205, P-FDR = 0.0820. In forward MR analysis, the statistical power for exposure-outcome pairs showing an association exceeded 75%. Sensitivity analyses revealed no evidence of heterogeneity, pleiotropy, or outliers affecting the results. Conclusions Our findings provide genetic evidence that FGF21 plays a causal role in gastric carcinogenesis, exhibiting a protective effect against CC while increasing the risk of GC independent of key confounders.
This review provides a focused overview of the current cancer landscape in Europe, addressing epidemiological trends, cancer-related costs, prevention and early detection, inequalities in access to care, and the implementation of therapeutic innovation. Recent studies from major European institutions were selected to illustrate key developments. Cancer incidence, mortality, direct and indirect costs vary substantially across countries, although comparisons remain limited by differences in geographical areas included, data collection, registration systems, and methodological approaches. The available evidence highlights the need for more standardized cancer data, greater investment in prevention, equitable implementation of screening programmes, broader access to multidisciplinary care, advanced diagnostic tools, clinical trials, and precision oncology. European funding programmes and collaborative networks may contribute to these objectives by promoting shared research infrastructures and cooperation.
