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“Direct to Drug” screening as a precision medicine tool in multiple myeloma

ABSTRACT: “Direct to Drug” screening as a precision medicine tool in multiple myeloma

PROVIDER: PRJNA627346 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11586900_1.fastq.gz	Fastqsanger.gz
	SRR11586900_2.fastq.gz	Fastqsanger.gz
	SRR11586901_1.fastq.gz	Fastqsanger.gz
	SRR11586901_2.fastq.gz	Fastqsanger.gz
	SRR11586902_1.fastq.gz	Fastqsanger.gz

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“Direct to Drug” screening as a precision medicine tool in multiple myeloma

Project description:Seventy-six FDA approved oncology drugs and emerging therapeutics were evaluated in 25 multiple myeloma (MM) and 15 non-Hodgkin’s lymphoma cell lines and in 113 primary MM samples. Ex vivo drug sensitivities were mined for associations with clinical phenotype, cytogenetic, genetic mutation and transcriptional profiles. We investigated the predictive value of anti-apoptotic BCL2 family member transcriptomic ratios as biomarkers of venetoclax sensitivity. RNA-seq analysis was available in 38 primary patient samples, from which we identified the 9 most (median AUC 0.09409) and least (median AUC 0.7195) sensitive samples to venetoclax.

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"Direct to Drug" screening as a precision medicine tool in multiple myeloma.

Project description:Seventy-six FDA-approved oncology drugs and emerging therapeutics were evaluated in 25 multiple myeloma (MM) and 15 non-Hodgkin's lymphoma cell lines and in 113 primary MM samples. Ex vivo drug sensitivities were mined for associations with clinical phenotype, cytogenetic, genetic mutation, and transcriptional profiles. In primary MM samples, proteasome inhibitors, dinaciclib, selinexor, venetoclax, auranofin, and histone deacetylating agents had the broadest cytotoxicity. Of interest, newly diagnosed patient samples were globally less sensitive especially to bromodomain inhibitors, inhibitors of receptor tyrosine kinases or non-receptor kinases, and DNA synthesis inhibitors. Clustering demonstrated six broad groupings of drug sensitivity linked with genomic biomarkers and clinical outcomes. For example, our findings mimic clinical observations of increased venetoclax responsiveness in t(11;14) patients but also identify an increased sensitivity profile in untreated patients, standard genetic risk, low plasma cell S-Phase, and in the absence of Gain(1q) and t(4;14). In contrast, increased ex vivo responsiveness to selinexor was associated with biomarkers of poor prognosis and later relapse patients. This "direct to drug" screening resource, paired with functional genomics, has the potential to successfully direct appropriate individualized therapeutic approaches in MM and to enrich clinical trials for likely responders.

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