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Venetoclax resistance leads to broad resistance to standard-of-care anti-MM agents, but not to immunotherapies

ABSTRACT: Venetoclax resistance leads to broad resistance to standard-of-care anti-MM agents, but not to immunotherapies

PROVIDER: PRJNA1120802 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29306969_1.fastq.gz	Fastqsanger.gz
	SRR29306969_2.fastq.gz	Fastqsanger.gz
	SRR29306970_1.fastq.gz	Fastqsanger.gz
	SRR29306970_2.fastq.gz	Fastqsanger.gz
	SRR29306971_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Venetoclax resistance leads to broad resistance to standard-of-care anti-MM agents, but not to immunotherapies

Project description:Venetoclax is the first example of personalized medicine for multiple myeloma (MM), with meaningful clinical activity as a monotherapy and in combination in myeloma patients harboring the t(11:14) translocation. However, despite the high response rates and prolonged PFS, a significant proportion of patients eventually relapse. Here, we aimed to study adaptive molecular responses after the acquisition of venetoclax resistance in sensitive t(11:14) MM cell models. We therefore generated single-cell venetoclax-resistant t(11:14) MM cell lines and investigated the mechanisms contributing to resistance as well as the cells’ sensitivity to other treatments. Our data suggests that acquired resistance to venetoclax is characterized by reduced mitochondrial priming and changes in BCL-2 family proteins’ expression in MM cells, conferring broad resistance to standard-of-care anti-myeloma drugs. However, our results show that the resistant cells are still sensitive to immunotherapeutic treatments, highlighting the need to consider appropriate sequencing of these treatments following venetoclax-based regimens.

2024-06-06 | GSE269245 | GEO

Venetoclax resistance leads to broad resistance to standard-of-care anti-MM agents, but not to immunotherapies.

Project description:AbstactTo our knowledge, venetoclax is the first example of personalized medicine for multiple myeloma (MM), with meaningful clinical activity as a monotherapy and in combination in patients with myeloma harboring the t(11:14) translocation. However, despite the high response rates and prolonged progression-free survival, a significant proportion of patients eventually relapse. Here, we aim to study adaptive molecular responses after the acquisition of venetoclax resistance in sensitive t(11:14) MM cell models. We therefore generated single-cell venetoclax-resistant t(11:14) MM cell lines and investigated the mechanisms contributing to resistance as well as the cells' sensitivity to other treatments. Our data suggest that acquired resistance to venetoclax is characterized by reduced mitochondrial priming and changes in B-cell lymphoma-2 (BCL-2) family proteins' expression in MM cells, conferring broad resistance to standard-of-care antimyeloma drugs. However, our results show that the resistant cells are still sensitive to immunotherapeutic treatments, highlighting the need to consider appropriate sequencing of these treatments after venetoclax-based regimens.

| S-EPMC11339023 | biostudies-literature

Determinants of venetoclax resistance

Project description:Determinants of venetoclax resistance

| PRJNA558091 | ENA

Determinants of venetoclax resistance

Project description:Determinants of venetoclax resistance

| PRJNA558092 | ENA

Genetic determinants of venetoclax resistance

Project description:Genetic determinants of venetoclax resistance

| PRJNA528105 | ENA

Assessing DNA methylation differences upon aquired Venetoclax resistance

Project description:We analyzed DNA methylation alterations upon acquired Venetoclax resistance using 8 different cell line pairs

2023-11-22 | GSE166577 | GEO

Hypomethylating agents sensitize diffuse large B-cell lymphoma to venetoclax

Project description:We established acquired venetoclax resistant OCI-LY1R cell line by treating venetoclax sensitive parental OCI-Ly1 cell line with increasing doses of venetoclax up till 1µM. Parental OCI-Ly1 and venetoiclax-resistant OCI-Ly1R cells were treated with vehicle control or decitabine at 1uM for 3 days. We found that decitabine differantially regulated gene expression in venetoclax sensitive and resistant cells. With gene set enrichment analysis, we identified two pathways that were deregulated by decitabine in both cell lines.

2023-07-25 | GSE223598 | GEO

Genetic determinants of venetoclax resistance

Project description:Resistance to the first approved BCL-2 inhibitor venetoclax is emerging in lymphoid malignancies. The study aimed to identify the genetic determinants of such resistance. From genome-scale screens we determined the genes influencing the sensitivity to BCL-2 inhibition. The present set of data is related to expression changes (assessed by RNA sequencing) observed in the resistant OCI-Ly1 lymphoma cell line as well as those resulting from genetic perturbation (using CRISPR-Cas9) targeting the genes highlighted in our genome-scale screen.

2019-09-25 | GSE128563 | GEO

Assessing DNA methylation differences upon aquired Venetoclax resistance

Project description:Assessing DNA methylation differences upon aquired Venetoclax resistance

| PRJNA701295 | ENA

Effect of venetoclax, tedizolid, and combination treatment on gene expression in a venetoclax-resistant AML cell line

Project description:The goal of this study was to profile the changes in gene expression in an AML cell line with acquired resistance to venetoclax in response to treatment with venetoclax, tedizolid, or combination of the 2 drugs.

2019-08-20 | GSE136032 | GEO

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