Journal of Affective Disorders

Common genetic basis and causality between central nervous system disease and cancer

The epidemiological associations between central nervous system diseases and cancers have been widely studied, but the shared genetic basis and etiology between these joint phenotypes remain unclear. To explore this issue, we utilized genome-wide association study summary data to investigate the shared genetic architecture and causality between 10 central nervous system diseases and 14 cancers. We employed multiple statistical genetic approaches, including global and local genetic correlation, Mendelian randomization, shared loci and genes, and shared tissues and cell-types to systematically and robustly explore the common genetic basis and causal relationships between central nervous system diseases and cancers. Our results revealed genetic correlations between schizophrenia and both lung cancer and breast cancer, including estrogen receptor-positive breast cancer, as well as between neuroticism and both lung cancer and ovarian cancer, including serous ovarian cancer. We found causal relationships between schizophrenia and lung cancer (OR = 1.14, P = 0.009) and breast cancer (OR = 1.05, P = 3.00 × 10

Global burden, temporal trends and cross-national inequalities of the comorbidity between depressive disorder and hormone-dependent tumors in women of reproductive ages from 1990 to 2021: A population-based analysis with projections to 2036

This study aimed to analyze the global comorbidity burden of depressive disorder (DD) and hormone-dependent tumors (HDTs), including breast cancer (BC), ovarian cancer (OC), and uterine cancer (UC), among women of reproductive ages (WRAs) using Global Burden of Disease (GBD) 2021 data. Long-term trends between 1990 and 2021 in the incidence, prevalence, and disability-adjusted life years (DALYs) of the comorbidity burden were used Joinpoint regression analysis. Future trends to 2036 were projected via a Bayesian age-period-cohort (BAPC) model. Age-period-cohort (APC) model to dissect temporal trends, decomposition analysis to quantify the contributions of demographic changes, and cross-country inequality and frontier analyses to evaluate socio-economic disparities and improvement potential across nations. From 1990 to 2021, the age-standardized incidence rate (ASIR) and prevalence rate (ASPR) of the comorbidity burden of DD and HDTs increased globally, while the age-standardized DALYs rate (ASDALYsR) decreased. The APC model identified women aged 45-49 years as bearing the most stable and high-risk burden. Decomposition analysis revealed that population growth and epidemiological changes were the primary drivers of the increasing burden. Cross-country inequality analysis indicated that high-SDI countries shouldered a greater comorbidity burden, yet the gap with low-SDI regions was narrowing. Frontier analysis suggested that high-SDI regions possessed the largest potential for burden reduction. The comorbidity burden of DD and HDTs among WRAs is projected to continue rising over the next 15 years. Public health efforts must prioritize high-risk age groups and high-SDI regions, integrating depression screening and management into oncologic care to mitigate this growing dual burden.

Causality between 22 personal traits and cervical cancer: a two-sample Mendelian randomization study

Previous research has indicated that certain personal traits are closely related to cervical cancer; however, owing to the limitations of observational studies, causality remains unclear. This pioneering study employs Mendelian Randomization (MR) analysis to explore the genetic links between personal traits and the risk of cervical cancer. We analyzed 22 personal traits and cervical cancer data from genome-wide association study (GWAS) databases. Utilizing instrumental variables identified from significant single nucleotide polymorphism (SNP) associations, we employed the Inverse Variance Weighted (IVW) method, along with the Weighted Median (WM) method and MR-Egger regression. A sensitivity analysis was conducted to confirm the robustness of the findings. Moreover, risk factor analyses were performed to explore potential mediators. Our results demonstrate positive causal relationships for smoking status (OR = 1.006, 95%CI 1.003-1.009, P < 0.001), smoking initiation (OR = 1.002, 95%CI 1.001-1.003, P = 0.02), past tobacco smoking (OR = 0.998, 95%CI 0.996-0.999, P = 0.023), age at first birth (OR = 0.999, 95%CI 0.998-0.999, P < 0.001), time spent watching television (OR = 1.005, 95%CI 1.002-1.007, P = 0.001), and duration of moderate to vigorous physical activity (OR = 0.997, 95%CI 0.995-0.999, P = 0.003). Smoking status, smoking initiation, and time spent watching television emerged as risk factors for cervical cancer, whereas past tobacco smoking, age at first birth, and duration of moderate to vigorous physical activity were identified as protective factors. No causal relationships were found between the remaining 16 personal traits and cervical cancer. This study establishes significant causal relationships between several personal traits and cervical cancer, providing valuable insights for cervical cancer prevention strategies and guiding future research directions. Moreover, it further explores the potential links between personal traits and cervical cancer.