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Mutual antagonism between glucocorticoid and canonical Wnt signaling pathways impacts steroid resistance in acute lymphoblastic leukemia [CUT&RUN]

ABSTRACT: Mutual antagonism between glucocorticoid and canonical Wnt signaling pathways impacts steroid resistance in acute lymphoblastic leukemia [CUT&RUN]

PROVIDER: PRJNA889064 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21855230_1.fastq.gz	Fastqsanger.gz
	SRR21855230_2.fastq.gz	Fastqsanger.gz
	SRR21855231_1.fastq.gz	Fastqsanger.gz
	SRR21855231_2.fastq.gz	Fastqsanger.gz
	SRR21855232_1.fastq.gz	Fastqsanger.gz

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Mutual antagonism between glucocorticoid and canonical Wnt signaling pathways impacts steroid resistance in acute lymphoblastic leukemia [RNA-Seq]

Project description:Glucocorticoids (GCs) are a mainstay of contemporary, multi-drug chemotherapy in the treatment of acute lymphoblastic leukemia (ALL). Although overall survival rates of childhood ALL have improved, resistance to antileukemic agents remains a major clinical concern. In particular, resistance to GCs is predictive of ALL relapse and poor clinical outcome, and it therefore represents a major hurdle limiting further improvements in survival rates. While advances have been made in identifying genes and transcriptional signatures implicated in ALL GC resistance, there remains an insufficient understanding of the impact of glucocorticoid response element (GRE) alterations in GC resistance. In this work (which is a follow-up of our recent study- Bergeron et al. Leukemia 2022), we uncovered the genomic mechanism linking disruptions to the Wnt repressor gene TLE1 with glucocorticoid (GC) drug resistance in acute lymphoblastic leukemia. In this process we uncovered extensive crosstalk and mutual antagonism between GC signaling and canonical Wnt signaling in ALL cells at the DNA sequence, transcriptome and proteome levels.

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Mutual antagonism between glucocorticoid and canonical Wnt signaling pathways impacts steroid resistance in acute lymphoblastic leukemia [CUT&RUN]

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C/EBP Maintains Chromatin Accessibility in Liver and Facilitates Glucocorticoid Receptor Recruitment to Steroid Response Elements

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