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Mice Lacking the Serotonin Transporter do not Respond to the Behavioural Effects of Psilocybin.

Eur J Pharmacol

January 2025

Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, Australia; Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Parkville, Australia. Electronic address:

Background And Purpose: Psilocybin is a serotonergic psychedelic with therapeutic potential for several neuropsychiatric disorders, including depression and anxiety disorders. Serotonin-transporter (5-HTT) knockout mice (KO) are a well-validated mouse model of anxiety/depression and are relevant to both chronic treatment with serotonin transporter reuptake inhibitors (SSRIs) and polymorphisms in the serotonin transporter-linked polymorphic region (5-HTTLPR) associated with depression/anxiety and resistance to classic antidepressant treatments. However, there is yet to be a study assessing the effect of psilocybin in 5-HTT KO mice.

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Response to azathioprine treatment in autoimmune hepatitis is dependent on glutathione transferase genotypes.

Dig Liver Dis

January 2025

Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden; Department of Laboratory Medicine, Region Jönköping County, Jönköping, Sweden. Electronic address:

Background: Azathioprine (AZA) is part of the standard treatment for autoimmune hepatitis (AIH). The first step in the complex bioconversion of AZA to active metabolites is mediated by glutathione transferases (GSTs).

Aims: Elucidate the association between GSTM1 and GSTT1 copy number variation (CNV), genetic variation in GSTA2, GSTP1, and inosine-triphosphate-pyrophosphatase, and the response to AZA in AIH.

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Pharmacogenetic Testing in Admixed Populations: Frequency of the AMR PGx Working Group Tier 1 Variant Alleles in Brazilians.

J Mol Diagn

January 2025

Clinical Research and Technological Development Division (Divisão de Pesquisa Clínica e Desenvolvimento Tecnológico), Brazilian National Cancer Institute (Instituto Nacional de Câncer), Rio de Janeiro, Brazil. Electronic address:

This article examines the frequency distribution of Tier 1 pharmacogenetic variants of the Association for Molecular Pathology Pharmacogenomics Working Group Recommendations in two large (>1.000 individuals) cohorts of the admixed Brazilian population, and in patients from the Brazilian Public Health System enrolled in pharmacogenetic trials. Three Tier 1 variants, all in DPYD, were consistently absent, which may justify their non-inclusion in genotyping panels for Brazilians; 13 variants had frequency < 1.

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CircKIAA0182 Enhances Lung Cancer Progression and Chemoresistance through Interaction with YBX1.

Cancer Lett

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Department of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, P. R. China; Institute of Clinical Pharmacology, Central South University, Changsha 410078, P. R. China. Electronic address:

Lung cancer, particularly non-small cell lung cancer (NSCLC), remains a leading cause of cancer-related mortality. Resistance to platinum-based chemotherapy, such as cisplatin, significantly limits treatment efficacy. Circular RNAs (circRNAs) have emerged as key regulators of cancer progression and chemotherapy resistance due to their stable structure, which protects them from degradation.

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Genetic polymorphism of the dihydropyrimidine dehydrogenase gene () is responsible for the variability found in the metabolism of fluoropyrimidines such as 5-fluorouracil (5-FU), capecitabine, or tegafur. The genotype is linked to variability in enzyme activity, 5-FU elimination, and toxicity. Approximately 10-40% of patients treated with fluoropyrimidines develop severe toxicity.

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