Tamoxifen (TMX) is the main drug used both in pre and postmenopausal women as adjuvant treatment for hormone receptor-positive breast cancer. An important barrier to the use of TMX is the development of drug resistance caused by molecular processes related to genetic and epigenetic mechanisms, such as the actions of cytochrome P450 2D6 () polymorphisms and of its metabolites. The present study aimed to review recent findings related to the impact of polymorphisms and how they can affect the results of TMX in breast cancer treatment. The keywords , , and were searched in the PubMed, Scopus, The Cochrane Library, Scielo, and Bireme databases. Studies related to other types of neoplasms or based on other isoenzymes from cytochrome P450, but not on CYP2D6, were excluded. The impact of polymorphisms in the TMX resistance mechanism remains unclear. The gene seems to contribute to decreasing the efficacy of TMX, while the main mechanism responsible for therapy failure, morbidity, and mortality is the progression of the disease.
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http://dx.doi.org/10.1055/s-0038-1676303 | DOI Listing |
PLoS Pathog
January 2025
Department of Biology, Johns Hopkins University, Baltimore, Maryland, United States of America.
Widespread anthelmintic resistance has complicated the management of parasitic nematodes. Resistance to the benzimidazole (BZ) drug class is nearly ubiquitous in many species and is associated with mutations in beta-tubulin genes. However, mutations in beta-tubulin alone do not fully explain all BZ resistance.
View Article and Find Full Text PDFMol Oncol
January 2025
Department of Neurosciences, Reproductive Sciences and Odontostomatology, University of Naples "Federico II", Italy.
Obesity exacerbates the risk and aggressiveness of many types of cancer. Adipose tissue (AT) represents a prevalent component of the tumor microenvironment (TME) and contributes to cancer development and progression. Reciprocal communication between cancer and adipose cells leads to the generation of cancer-associated adipocytes (CAAs), which in turn foster tumor invasiveness by producing paracrine metabolites, adipocytokines, and growth factors.
View Article and Find Full Text PDFDig Dis Sci
January 2025
Provincial-Level Key Laboratory for Molecular Medicine of Major Diseases and The Prevention and Treatment With Traditional Chinese Medicine Research in Gansu Colleges and University, Gansu University of Chinese Medicine, Lanzhou, China.
Background And Aims: Alcoholic liver disease (ALD) is the leading cause of death among alcohol-related diseases, yet its pathogenesis remains incompletely understood. This article employs data mining methods to conduct an indepth study of articles on ALD published in the past three decades, aiming to elucidate the pathogenesis of ALD.
Methods: Firstly, articles related to the pathogenesis of ALD were retrieved from the Web of Science (WOS) database.
Commun Chem
January 2025
Graduate School of Engineering, Hokkaido University, N13-W8, Kita-ku, Sapporo, Hokkaido, 060-8628, Japan.
Lactacystin is an irreversible proteasome inhibitor isolated from Streptomyces lactacystinicus. Despite its importance for its biological activity, the biosynthesis of lactacystin remains unknown. In this study, we identified the lactacystin biosynthetic gene cluster by gene disruption and heterologous expression experiments.
View Article and Find Full Text PDFSci Rep
January 2025
Department of General and Transplant Surgery, Poznan University of Medical Sciences, 61-701, Poznan, Poland.
Tacrolimus is metabolized in the liver with the participation of cytochrome P450 isoforms 3A4 and 3A5 (CYP3A4, CYP3A5). Omeprazole, unlike famotidine, is a substrate and inhibitor of CYP2C19, CYP3A4, CYP3A5 enzymes. The aim of the study is to compare the effect of omeprazole and famotidine on the tacrolimus concentration and the kidney transplant function.
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