Background And Aims: Benzene is a group I carcinogen, which has been associated with leukemia and myelodysplastic syndrome. Moreover, it has been proposed that polymorphisms in benzene metabolizing genes influence the outcomes of benzene exposure in the human body. This systematic review aims to elucidate the existent relationship between genetic polymorphisms and the risk of developing adverse health effects in benzene-exposed workers.
Methods: Three databases were systematically searched until April 2020. The preferred reporting items for systematic reviews and meta-analyses method was used to select articles published between 2005 and 2020. Quality assessment and risk of bias were evaluated by the Newcastle-Ottawa scale.
Results: After full-text evaluation, 36 articles remained out of 645 initially screened. The most studied health effects within the reviewed papers were chronic benzene poisoning, hematotoxicity, altered urinary biomarkers of exposure, micronucleus/chromosomal aberrations, and gene methylation. Furthermore, some polymorphisms on , , , , and , among other genes, showed a statistically significant relationship with an increased risk of developing at least one of these effects on benzene-exposed workers. However, there was no consensus among the reviewed papers on which specific polymorphisms were the ones associated with the adverse health-related outcomes, except for the rs1800566 and the null genotypes. Additionally, the smoking habit was identified as a confounder, demonstrating worse health outcomes in exposed workers that smoked.
Conclusion: Though there is a positive relationship between genetic polymorphisms and detrimental health outcomes for benzene-exposed workers, broader benzene-exposed cohorts that take into account the genetic diversity of the population are needed in order to determine which specific polymorphisms incur in health risks.
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http://dx.doi.org/10.1002/hsr2.327 | DOI Listing |
Adv Sci (Weinh)
January 2025
Frontiers Science Center for Molecular Design Breeding, Beijing Key Laboratory of Crop Genetic Improvement, College of Agronomy and Biotechnology, China Agricultural University, Beijing, 100193, China.
Rice is highly sensitive to cold stress, particularly at the booting stage, which significantly threatens rice production. In this study, we cloned a gene, CTB6, encoding a lipid transfer protein involved in cold tolerance at the booting stage in rice, based on our previous fine-mapped quantitative trait locus (QTL) qCTB10-2. CTB6 is mainly expressed in the tapetum and young microspores of the anther.
View Article and Find Full Text PDFFront Plant Sci
January 2025
Department of Plant Pathology, Washington State University, Pullman, WA, United States.
Stripe rust of wheat is a serious disease caused by f. sp. ().
View Article and Find Full Text PDFFront Plant Sci
January 2025
Department of Southern Area Crop Science, National Institute of Crop Science, Rural Development Administration (RDA), Miryang, Republic of Korea.
Cold stress during the seedling stage significantly threatens rice ( L.) production, specifically in temperate climates. This study aimed to identify quantitative trait loci (QTLs) associated with cold tolerance at the seedling stage.
View Article and Find Full Text PDFFront Genet
January 2025
Molecular Bio-Computation and Drug Design Laboratory, School of Health Sciences, University of KwaZulu-Natal, Westville Campus, Durban, South Africa.
Objectives: Unlike other diseases, cancer is not just a genome disease but should broadly be viewed as a disease of the cellular machinery. Therefore, integrative multifaceted approaches are crucial to understanding the complex nature of cancer biology. Bcl-2 (B-cell lymphoma 2), encoded by the human BCL-2 gene, is an anti-apoptotic molecule that plays a key role in apoptosis and genetic variation of Bcl-2 proteins and is vital in disrupting the apoptotic machinery.
View Article and Find Full Text PDFCureus
December 2024
Internal Medicine Department, Hospital Beatriz Ângelo, ULS Loures Odivelas, Loures, PRT.
Plasminogen activator inhibitor-1 (PAI-1) is central to fibrinolysis regulation, and genetic variants such as the 4G/4G genotype predispose individuals to hypercoagulability. This case highlights a 46-year-old female patient presenting with acute mesenteric venous thrombosis, where genetic evaluation revealed homozygosity for the PAI-1 4G/4G polymorphism. Management with unfractionated heparin followed by a transition to direct oral anticoagulants led to clinical resolution.
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