Integrative causal inference illuminates gene-environment interactions linking endocrine disruptors to female infertility.

Female infertility, a global health concern affecting up to 12 % of women, is influenced by genetic, hormonal, and environmental factors. Among environmental contributors, endocrine-disrupting chemicals (EDCs), which interfere with hormonal systems, have gained attention for their potential impact on reproductive health. This study used Mendelian randomization (MR) and colocalization analyses to explore the causal relationships between gene expression influenced by EDCs and female infertility.

Genomic evidence based on eQTL data implicates endocrine disruptors as environmental risk factors for estrogen receptor-positive breast cancer.

Background: Estrogen receptor-positive (ER+) breast cancer is the most common molecular subtype of breast cancer and is strongly influenced by hormonal and environmental factors. Endocrine-disrupting chemicals (EDCs), which interfere with hormone signaling, have been suggested to contribute to ER+ breast cancer risk, but causal mechanisms remain unclear.

Methods: We integrated chemical-gene interaction data from the TEDX and CTD databases with large-scale genomic datasets to investigate the relationship between EDC-regulated gene expression and ER+ breast cancer.

Integrative in silico analysis of per- and polyfluorinated alkyl substances (PFAS)-associated molecular alterations in human cancers: a multi-cancer framework for predicting toxicogenomic disruption.

Background: Per- and polyfluorinated alkyl substances (PFAS) are persistent environmental pollutants with known bioaccumulation potential and growing evidence of an association with cancer risk. However, the molecular mechanisms potentially linking PFAS exposure to carcinogenesis remain poorly understood. This study integrates computational toxicology and bioinformatics approaches to explore how PFAS-related molecular targets and pathways may overlap with those altered in six cancer types: breast carcinoma, kidney renal clear cell carcinoma, liver hepatocellular carcinoma, prostate adenocarcinoma, thyroid cancer, and uterine corpus endometrial carcinoma, all of which have been previously implicated in PFAS-related research.

Analyzing the potential targets and mechanism of per- and polyfluoroalkyl substances (PFAS) on breast cancer by integrating network toxicology, single-cell sequencing, spatial transcriptomics, and molecular simulation.

Per- and polyfluoroalkyl substances (PFAS), particularly perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), are persistent environmental contaminants linked to adverse health effects, including an increased risk of breast cancer. However, the molecular mechanisms through which PFAS contribute to breast cancer development remain poorly understood. In this study, we employed an integrated approach combining network toxicology, single-cell sequencing, spatial transcriptomics, and molecular simulation to investigate the effects of PFAS on breast cancer.