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Glutaminase inhibition in combination with azacytidine in myelodysplastic syndromes: Clinical efficacy and correlative analyses

ABSTRACT: Glutaminase inhibition in combination with azacytidine in myelodysplastic syndromes: Clinical efficacy and correlative analyses

PROVIDER: PRJNA935325 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23476120_1.fastq.gz	Fastqsanger.gz
	SRR23476120_2.fastq.gz	Fastqsanger.gz
	SRR23476121_1.fastq.gz	Fastqsanger.gz
	SRR23476121_2.fastq.gz	Fastqsanger.gz
	SRR23476122_1.fastq.gz	Fastqsanger.gz

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Glutaminase inhibition in combination with azacytidine in myelodysplastic syndromes: Clinical efficacy and correlative analyses

Project description:Malignancies can become reliant on glutamine as an alternative energy source and as a facilitator of aberrant DNA methylation, thus implicating glutaminase (GLS) as a potential therapeutic target. We demonstrate preclinical synergy of telaglenastat (CB-839), a selective GLS inhibitor, when combined with azacytidine (AZA), in vitro and in vivo, followed by a phase Ib/II study of the combination in patients with advanced MDS. Treatment with telaglenastat/AZA led to an ORR of 70% with CR/mCRs in 53% patients and a median overall survival of 11.6 months. scRNAseq and flow cytometry demonstrated a myeloid differentiation program at the stem cell level in clinical responders. Expression of non-canonical glutamine transporter, SLC38A1, was found to be overexpressed in MDS stem cells; was associated with clinical responses to telaglenastat/AZA and predictive of worse prognosis in a large MDS cohort. These data demonstrate the safety and efficacy of a combined metabolic and epigenetic approach in MDS.

2024-02-12 | GSE225352 | GEO

Glutaminase inhibition in combination with azacytidine in myelodysplastic syndromes: Clinical efficacy and correlative analyses.

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ZRSR2 mutant myelodysplastic syndromes

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ZRSR2 mutant myelodysplastic syndromes

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A hypermethylated ALOX12 gene is highly susceptible to 5-azacytidine treatment in myelodysplastic syndromes

Project description:A hypermethylated ALOX12 gene is highly susceptible to 5-azacytidine treatment in myelodysplastic syndromes

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Oxidative stress in myelodysplastic syndromes

Project description:Control of oxidative stress in the bone marrow (BM) is key for maintaining the balance between self-renewal, proliferation, and differentiation of hematopoietic cells. Breakdown of this regulation can lead to diseases characterized by BM failure such as the myelodysplastic syndromes (MDS). To better understand the role of oxidative stress in MDS development, we compared protein carbonylation as an oxidative stress marker in BM of patients with MDS and control subjects, and also patients with MDS under treatment with the iron chelator deferasirox.

2019-10-30 | PXD013609 | Pride

A hypermethylated ALOX12 gene is highly susceptible to 5-azacytidine treatment in myelodysplastic syndromes

Project description:5-azacytidine (AZA) is widely used for treatment of myelodysplastic syndromes (MDS). However, identifying predictive factors for response to AZA remains challenging. The aim in present study was to identify the genes which are susceptible to AZA in MDS and investigate the possibility of the gene for predictor for response to AZA therapy. To identify AZA-susceptible genes, we compared the gene expression changes by AZA in MDS-L cells (AZA-sensitive) with those in MDS-L/CDA cells (AZA-resistant) in culture. Of 438 AZA-susceptible genes, we searched the genes which are hypermethylated in MDS patients as compared to healthy controls by analyzing public dataset GSE152710, and found ALOX12 gene. Analysis of public dataset GSE145733 and GSE58831 revealed that ALOX12 expression was suppressed in MDS classes with excess blasts but not in other classes, and were negatively and positively correlated with bone marrow blast counts and survival, respectively, in MDS patients. Analysis of public dataset GSE152710 revealed that the methylation level of ALOX12 gene was decreased in MDS patients with complete remission but not in those with partial response and progression disease after AZA therapy. Our retrospective clinical study in which nine AZA-treated patients were enrolled suggested that ALOX12 expression was increased in patients with favorable response, while decreased in patient with poor response after AZA therapy. In conclusion, ALOX12 gene could be tumor suppressive and promising marker for predicting the response to AZA therapy in MDS.

2023-05-31 | GSE233764 | GEO

The National Myelodysplastic Syndromes (MDS) Study

Project description:The National Myelodysplastic Syndromes (MDS) Study

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The National Myelodysplastic Syndromes (MDS) Study

Project description:The National Myelodysplastic Syndromes (MDS) Study

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Genome-wide profiling of methylation identifies novel targets with aberrant hypermethylation and reduced expression in low-risk myelodysplastic syndromes.

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2012-09-28 | E-GEOD-41216 | biostudies-arrayexpress

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