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Cyclophosphamide - BioProject

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Last Updated: 27 January 2022

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Effect of high-dose cyclophosphamide gene expression profiles in cardiomyocytes of C57BL/6J mice

We've analyzed the genome-wide expression profiles of C57BL/6J mice to determine the causes of cyclophosphamide-induced myocardial damage, including CY, one of CY metabolites acrolein, and CY with N-acetyl cysteine. The gene expression profiles after the administration of acrolein differed from that of the CY administration. NAC did not limit the DHPR, RyR2, and TnC gene expression suppression after administration of NAC and CY, in addition, the gene expression profiles after the administration of NAC and CY did not influence gene expression during the administration of NAC and CY. Gene expression changes were found 3 hours after the second dose.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/798986


Low-temperature prevents side effects of an anti-cancer drug, cyclophosphamide, on organ development: a study of ex vivo organ culture model

This review looked at the molecular mechanism of the side effects of cyclophosphamide, a commonly used anti-cancer drug used for leukemia treatment, and found how to minimize the side effects by using an organ culture system. Cap analysis of gene expression in CPA-treated tooth germ cultured at low temperatures revealed that genes related to the G1/S cell cycle checkpoint were down-regulated in the CPA-treated tooth germ cultured at low temperatures. Our findings showed that maintaining a low temperature would prevent CPA's side effects on organ growth. After adding 2. 5 mM CPA or 37°C enamel reagent for 3 days at 25°C or 37°C, a mRNA profile was generated from cultured mouse tooth germ organ organs E14. 5 tooth germs, Cap Analysis Gene Expression RNA-sequencing generated a mRNA profile, using Illumina Hiseq1500.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/756520


Cyclophosphamide enhances the anti-tumor potency of GITR engagement by increasing oligoclonal cytotoxic T cell fitness

Cyclophosphamide, a derivative of cyclophosphamide, preferentially depletes regulatory T cells and promotes tumor-specific effector T cells by homeostatic proliferation. We therefore expected that CTX therapy prior to GITR agonism would restore potent anti-tumor immunity. In several clinically relevant mouse models, we show that the combination of CTX and GITR agonism robustly controls tumor formation. We demonstrate that chemotherapy causes tumor cell death, clonal expansion of highly active and terminally differentiated CD8+ T cells, and regulatory T cells depletion by AICD. The presence of an enlarged population of highly activated tumor-infiltrating oligoclonal CD8+ T cells that contribute to a global contracted TCR pool is also associated with tumor growth. The combination of CTX and GITR agonism, according to our reports, is a valid chemotherapeutic strategy that warrants further clinical investigation.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/755702

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions