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Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs

ABSTRACT: Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs

PROVIDER: PRJNA1061149 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27427976_1.fastq.gz	Fastqsanger.gz
	SRR27427976_2.fastq.gz	Fastqsanger.gz
	SRR27427977_1.fastq.gz	Fastqsanger.gz
	SRR27427977_2.fastq.gz	Fastqsanger.gz
	SRR27427978_1.fastq.gz	Fastqsanger.gz

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Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs I

Project description:Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs I

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Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs II

Project description:Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs II

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Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs

Project description:Cytidine deaminase (CDA) functions in the pyrimidine salvage pathway for DNA and RNA synthesis and has been shown to protect cancer cells from deoxycytidine-based chemotherapies. In this study, we observed that CDA was overexpressed in pancreatic adenocarcinoma from patients at baseline and was essential for experimental tumor growth. Mechanistic investigations revealed that CDA localized to replication forks where it increased replication speed, improved replication fork restart efficiency, reduced endogenous replication stress, minimized DNA breaks, and regulated genetic stability during DNA replication. In cellular pancreatic cancer models, high CDA expression correlated with resistance to DNA-damaging agents. Silencing CDA in patient-derived primary cultures in vitro and in orthotopic xenografts in vivo increased replication stress and sensitized pancreatic adenocarcinoma cells to oxaliplatin. This study sheds light on the role of CDA in pancreatic adenocarcinoma, offering insights into how this tumor type modulates replication stress. These findings suggest that CDA expression could potentially predict therapeutic efficacy and that targeting CDA induces intolerable levels of replication stress in cancer cells, particularly when combined with DNA-targeted therapies

2024-01-15 | GSE252544 | GEO

Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs II

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Cytidine deaminase resolves replicative stress and protects pancreatic cancer from DNA-targeting drugs I

2024-01-24 | GSE253662 | GEO

A study of pharmacokinetic analysis of capecitabine and cytidine deaminase activity

Project description:Interventions: Blood samples(10 points) are collected after the first administration of capecitabine for pharmacokinetic analysis and cytidine deaminase activity measurement. Primary outcome(s): To evaluate the correlation AUC of 5-DFUR/AUC of 5-DFCR ratio and cytidine deaminase activity. Study Design: Single arm Non-randomized

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Cytidine Deaminase Resolves Replicative Stress and Protects Pancreatic Cancer from DNA-Targeting Drugs.

Project description:Cytidine deaminase (CDA) functions in the pyrimidine salvage pathway for DNA and RNA syntheses and has been shown to protect cancer cells from deoxycytidine-based chemotherapies. In this study, we observed that CDA was overexpressed in pancreatic adenocarcinoma from patients at baseline and was essential for experimental tumor growth. Mechanistic investigations revealed that CDA localized to replication forks where it increased replication speed, improved replication fork restart efficiency, reduced endogenous replication stress, minimized DNA breaks, and regulated genetic stability during DNA replication. In cellular pancreatic cancer models, high CDA expression correlated with resistance to DNA-damaging agents. Silencing CDA in patient-derived primary cultures in vitro and in orthotopic xenografts in vivo increased replication stress and sensitized pancreatic adenocarcinoma cells to oxaliplatin. This study sheds light on the role of CDA in pancreatic adenocarcinoma, offering insights into how this tumor type modulates replication stress. These findings suggest that CDA expression could potentially predict therapeutic efficacy and that targeting CDA induces intolerable levels of replication stress in cancer cells, particularly when combined with DNA-targeted therapies.SignificanceCytidine deaminase reduces replication stress and regulates DNA replication to confer resistance to DNA-damaging drugs in pancreatic cancer, unveiling a molecular vulnerability that could enhance treatment response.

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Base editing with a Cpf1–cytidine deaminase fusion

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ChIP-seq Analysis of Activation-Induced Cytidine Deaminase Distribution in Human B Cells: Insights for Targeting Mechanisms

Project description:We report the analysis of genome wide distribution of activation induced cytidine deaminase by ChIP-seq in Human B cells. The resultant distribution of AID has then been compared to various histone modifications and transcription factors to shed insights into the mechanisms that target this enzyme.

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High-fidelity base editing mediated by Cpf1-cytidine deaminase fusion

Project description:High-fidelity base editing mediated by Cpf1-cytidine deaminase fusion

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