SULT1A1 (Sulfotransferase Family 1A Member 1)

This study offers causal evidence supporting the protective effects of exercise against lung cancer, potentially through pathways dependent on SULT1A1.

This study demonstrates a causal relationship between circulating inflammatory proteins and cervical cancer risk in both European and Asian populations. The findings highlight both pro-cancer and protective roles of specific inflammatory proteins, offering insights for biomarkers in cervical cancer risk assessment and prevention strategies.

Gene ontology term enrichment analysis demonstrated significant enrichment in terms associated with mineralization, including ossification, bone mineralization, cartilage development, and extracellular matrix organization for these clusters of genes. This study provides a collated list of sulfate-related genes and networks that are associated with mineralization, which will facilitate future functional studies of sulfation pathways associated with bone pathology.

We also show the SAR of a smaller subset of 2-choloro-4-amino benzyl alcohols from the NCI compound collection with a similar benzyl alcohol motif. We also demonstrate the ability of key analogs to act as substrates of SULT1A1 in a colorimetric biochemical assay.

The results of the study provided possible causal evidence for the involvement of circulating inflammatory proteins in the pathogenesis of eleven hematologic malignancies. Nine proteins with cross-cancer effects were of special interest, and their potential as targets in the therapeutic intervention of blood malignancies was highlighted.

The PSO-based hybrid model effectively improved SVR performance in survival prediction for OC patients and identified key prognostic biomarkers. Despite its promising results and validation on independent datasets, limitations in generalizability and signs of overfitting suggest the model is not yet ready for clinical use. Further studies with larger, diverse datasets are recommended.

Our data indicate that a threshold level of DNA adducts is required, both in rat and human liver cells, to trigger markers of clastogenicity. These levels are unlikely to be reached in humans following chronic ES exposure through phytomedicines or the diet.

This study discovered causal associations between IL-17A, multiple serum metabolites, and LUAD occurrence, revealing the key role of inflammatory and metabolic dysregulation in LUAD pathogenesis. Our findings provide new evidence-based medical support for specific inflammatory factors and metabolites as early predictive and risk assessment biomarkers for LUAD, offering important clues for subsequent mechanistic studies and precision medicine applications.

A reverse docking analysis also showed that SULT1A1, CYP2E1, and CAT, known to play a significant role in protecting cells from harmful factors, might be potential target proteins for THB. Taken together, we suggest that THB induces non-apoptotic cell death via structural damage of intracellular organelles, especially the nuclear membrane.

IL-13, IL-18R1, TNFSF14, and TRANCE were upregulated in both lesional skin biopsies and PBMCs from AD patients. The study indicates that several cytokines, including IL-13, IL-18R1, TNFSF14, TRANCE, CXCL11, IL-33, TNF-beta, and CD5, are upstream of AD development, whereas a few circulating cytokines are potentially downstream in the development of AD.

Arg213His polymorphism of SUT1A1 gene showed a protective effect against breast cancer among Brazilian young women. More studies with different designs are needed to understand the role of PON1 and SULT1A1 polymorphisms in breast cancer development in young Brazilian women.

More detailed DFT analysis at the DSD-PBEP86/Def-TZVPP level of theory could not identify significant geometric or electronic changes which would account for this varied AhR activation. Generation of Fukui functions at the same level of theory showed that CYP1 metabolism will primarily occur at the phenyl head group of the analogues, and substituents within this ring lead to lower cytotoxicity.