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Resistance to PRMT5 Inhibitor Targeted Therapy in MCL [WES]

ABSTRACT: Resistance to PRMT5 Inhibitor Targeted Therapy in MCL [WES]

PROVIDER: PRJNA1005107 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25628165_1.fastq.gz	Fastqsanger.gz
	SRR25628165_2.fastq.gz	Fastqsanger.gz
	SRR25628166_1.fastq.gz	Fastqsanger.gz
	SRR25628166_2.fastq.gz	Fastqsanger.gz
	SRR25628167_1.fastq.gz	Fastqsanger.gz

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Resistance to PRMT5 Inhibitor Targeted Therapy in MCL [WES]

Project description:To identify the genomic changes underlying PRMT5 inhibitor resistance in MCL cell lines and MCL PDX

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Resistance to PRMT5 Inhibitor Targeted Therapy in MCL [RNA-seq]

Project description:To identify the transcriptomic changes underlying acquired PRMT5 inhibitor resistance in MCL cell lines (n=3/group) and MCL PDX

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Resistance to PRMT5-targeted therapy in mantle cell lymphoma

Project description:Mantle cell lymphoma (MCL) is an incurable B-cell non-Hodgkin lymphoma, and patients who relapse on targeted therapies have poor prognosis. Protein arginine methyltransferase 5 (PRMT5), an enzyme essential for B-cell transformation, drives multiple oncogenic pathways and is overexpressed in MCL. Despite the antitumor activity of PRMT5 inhibition (PRT-382/PRT-808), drug resistance was observed in a patient-derived xenograft (PDX) MCL model. Decreased survival of mice engrafted with these PRMT5 inhibitor-resistant cells vs treatment-naive cells was observed (P = .005). MCL cell lines showed variable sensitivity to PRMT5 inhibition. Using PRT-382, cell lines were classified as sensitive (n = 4; 50% inhibitory concentration [IC50], 20-140 nM) or primary resistant (n = 4; 340-1650 nM). Prolonged culture of sensitive MCL lines with drug escalation produced PRMT5 inhibitor-resistant cell lines (n = 4; 200-500 nM). This resistant phenotype persisted after prolonged culture in the absence of drug and was observed with PRT-808. In the resistant PDX and cell line models, symmetric dimethylarginine reduction was achieved at the original PRMT5 inhibitor IC50, suggesting activation of alternative resistance pathways. Bulk RNA sequencing of resistant cell lines and PDX relative to sensitive or short-term-treated cells, respectively, highlighted shared upregulation of multiple pathways including mechanistic target of rapamycin kinase [mTOR] signaling (P < 10-5 and z score > 0.3 or < 0.3). Single-cell RNA sequencing analysis demonstrated a strong shift in global gene expression, with upregulation of mTOR signaling in resistant PDX MCL samples. Targeted blockade of mTORC1 with temsirolimus overcame the PRMT5 inhibitor-resistant phenotype, displayed therapeutic synergy in resistant MCL cell lines, and improved survival of a resistant PDX.

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PRMT5 inhibition in MCL

Project description:PRMT5 inhibition in MCL

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PRMT5 inhibition in MCL

Project description:To identify the mechanistic underpinning of the anti-tumor activity of PRMT5 inhibition in MCL, we explored transcriptomic profiles of PDX-AA cells treated in vivo for 2 weeks with PRT-382, ibrutinib, or vehicle control (n=3/group).

2023-09-27 | GSE220936 | GEO

Resistance to PRMT5 Inhibitor Targeted Therapy in MCL

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

2023-12-30 | GSE240726 | GEO

GBM stem cell lines and PRMT5 inhibitor

Project description:RNA-seq data use in a study evaluating the effect of an PRMT5 inhibitor on GSC lines.

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Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

Project description:Phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway activation contributes to mantle cell lymphoma (MCL) pathogenesis and drug resistance. However, the use of mTOR inhibitors as single agents have shown limited clinical efficacy in relation with drug activation of feedback loops. Selective PI3K inhibition or dual PI3K/mTOR catalytic inhibition are different therapeutic approaches developed to achieve effective pathway blockage. Here, we evaluated the antitumor activity of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in primary MCL cells. We found that dual PI3K/mTOR inhibitor modulated angiogenesis, tumor invasiveness and cytokine signaling compared to a mTOR inhibitor and a pan-PI3K inhibitor in MCL. We used microarrays to compare the effect of these three compounds in MCL and identified distinct classes of down-regulated genes modulated by each compound. Global RNA expression in primary cells from two MCL patients treated with a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor for 8 hours

2013-12-14 | E-GEOD-53309 | biostudies-arrayexpress

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