DOI 10.1080/01480545.2025.2496324
Application of bioinformatics techniques to discovery of mechanisms by which plasticizers promote acute myelogenous leukemia.
Аннотация
This study aims to elucidate the potential roles of commonly used plasticizers, including Diethyl Phthalate (DEP), Dimethyl Phthalate (DMP), and Dioctyl Phthalate (DOP), in the pathogenesis of Acute Myeloid Leukemia (AML). The focus is to highlight the complex interactions between these environmental chemicals and key molecular pathways involved in tumorigenesis. We employed network toxicology and molecular docking techniques to analyze the interactions between plasticizers and key proteins associated with AML. Utilizing databases such as The Cancer Genome Atlas (TCGA), we divided selected key genes from AML bone marrow samples into two groups based on gene expression and compared their survival analyses. Enrichment analysis was conducted to identify the biological pathways associated with these genes. The enrichment analysis underscored the association between the plasticizer-targeted genes and essential pathways in AML development, indicating a broad impact of plasticizers on various cancers, including hematologic malignancies. Subsequent expression analysis using TCGA data for AML demonstrated that these genes have significant statistical relevance to the survival in AML, confirming their critical roles in tumor biology. This study provides evidence that exposure to plasticizers could influence the pathogenesis of AML through interactions with key proteins and signaling pathways. By utilizing network pharmacology and protein interaction analysis, our findings emphasize the potential risks associated with plasticizers. These results highlight the necessity for further epidemiological and clinical research to fully understand the impact of plasticizer exposure on AML risk, thereby informing future preventive and therapeutic strategies.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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