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Vincristine induces spermatogenic impairment in a B-ALL PDX mouse model via downregulation of Tssk4 and Ccdc159: RNA-seq transcriptomic profiling

ABSTRACT: This dataset contains RNA sequencing (RNA-seq) data generated from testicular tissues of a B-cell acute lymphoblastic leukemia (B-ALL) patient-derived xenograft (PDX) mouse model treated with vincristine (VCR). The study aimed to elucidate the molecular mechanisms underlying VCR-induced reproductive toxicity. Samples were collected from multiple experimental groups, including normal controls (NC), leukemia-bearing controls (ALL), and VCR-treated groups with varying leukemia infiltration levels. Transcriptomic analysis revealed widespread gene expression perturbations following VCR exposure, with significant downregulation of genes crucial for spermatogenesis and sperm flagellar assembly. This data provides a comprehensive resource for understanding the genetic pathways affected by VCR in the testicular microenvironment.

ORGANISM(S): Mus musculus

PROVIDER: GSE314794 | GEO | 2025/12/26

REPOSITORIES: GEO

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Exploring the Mechanism of Resistance to vincristine in Breast Cancer Cells through Transcriptome Sequencing Technology

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Changes in Gene Expression Profile in two Multidrug Resistant Cell Lines derived from a same Drug Sensitive Cell line

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2008-06-12 | E-GEOD-2351 | biostudies-arrayexpress

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The MYC-YBX1 Circuit in Maintaining Stem-like Vincristine-Resistant Cells in Rhabdomyosarcoma

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Project description:Although intensification of chemotherapy approaches considerably increased the outcome of pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL) patients, a subgroup of them still experience treatment failure and relapse. In this context, we hypothesized that the Nrf2 signalling and its downstream effectors could be involved in sustain therapy resistance in T-ALL, as previously reported in other cancers. Indeed, in this study we identified the Aldo-Keto Reductase (AKR) enzymes AKR1C1-3, as over-expressed in T-ALL samples from therapy-resistant patients, demonstrating their fundamental role in the control of the response to vincristine (VCR) treatment. In particular, we evidence that the modulation of AKR1C1-3 gene expression and activity is sufficient to strongly affect the sensitivity of T-ALL cell lines and primary cells to VCR treatment, but not to daunorubicin, cytarabine or L-asparaginase. Moreover, we found a correlation between the degree of VCR response and the amount of AKR1Cs expression in patient-derived T-ALL xenografts. Interestingly, we show that daunorubicin and cytarabine are able to induce the over-activation of AKR1C enzymes, thus establishing a potential resistance loop generated by the combination of these drugs during T-ALL treatment. In this study, we demonstrate a clear involvement of AKR1C enzymes in controlling the response to chemotherapics in T-ALL, suggesting the possibility of considering AKR1Cs as reliable targets for the setup of novel combination treatments for T-ALL patients who do not respond to therapy

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