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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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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.

2023-06-06 | GSE215187 | GEO

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

2023-06-06 | GSE215186 | GEO

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

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

| PRJNA889063 | ENA

Mutual antagonism between glucocorticoid and canonical Wnt signaling pathways in B-cell acute lymphoblastic leukemia

Project description:Mutual antagonism between glucocorticoid and canonical Wnt signaling pathways in B-cell acute lymphoblastic leukemia

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Mutual antagonism between glucocorticoid and canonical Wnt signaling pathways in B-cell acute lymphoblastic leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-06 | GSE215188 | GEO

Effect of glucocorticoid steroid regimens on murine dystrophic muscle

Project description:The goal of this study is to compare the effect of weekly and daily steroid regimens (prednisone) on transcriptional regulation of candidate genes for muscle repair and atrophic response in mdx mice (n=5 mice/group).

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Muscle H3K27ac landscape remodeling with glucocorticoid steroid regimens

Project description:Muscle H3K27ac landscape remodeling with glucocorticoid steroid regimens

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Muscle H3K27ac landscape remodeling with glucocorticoid steroid regimens

Project description:Duchenne muscular dystrophy is caused by genetic defects in the gene encoding dystrophin and leads to progressive muscle degeneration. Glucocorticoid steroids are current mainstay pharmacological regimen to decrease muscle inflammation and prolong the ambulatory period in these patients, but daily intake of glucocorticoids like prednisone and deflazacort causes adverse side effects like osteoporosis, adrenal suppression, insulin resistance and obesity. Intermittent steroid dosing has been proposed as alternative to maintain benefits and limit side effects, but a detailed understanding of the mechanisms underpinning the regimen-specific effects in muscle is still missing. Here we explore how once-daily versus once-weekly prednisone (4 week-long treatment) affect the epigenomic landscape in mdx mouse muscle (genetic model of Duchenne muscular dystrophy; DBA/2J background) through H3K27 acetylation profiles.

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

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2012-03-23 | GSE36726 | GEO

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