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SUMOylation inhibition overcomes dexamethasone resistance in multiple myeloma

ABSTRACT: SUMOylation inhibition overcomes dexamethasone resistance in multiple myeloma

PROVIDER: PRJNA687056 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13284569.fastq.gz	Fastqsanger.gz
	SRR13284570.fastq.gz	Fastqsanger.gz
	SRR13284571.fastq.gz	Fastqsanger.gz
	SRR13284572.fastq.gz	Fastqsanger.gz
	SRR13284573.fastq.gz	Fastqsanger.gz

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SUMOylation inhibition overcomes dexamethasone resistance in multiple myeloma

Project description:SUMOylation, a posttranslational modification, regulates proteins by covalent attachment of small ubiquitin-like modifier (SUMO) proteins to a lysine (Lys) residue on target proteins. Here we use TAK-981, a selective SUMO-activating enzyme (SAE) inhibitor, to inhibit global SUMOylation in glucocorticoid sensitive and resistant multiple myeloma cell lines.

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Impact of CEBPβ depletion on enhancer responses to dexamethasone in Multiple Myeloma cells

Project description:Multiple myeloma (MM) is the second most common hematological cancer. While MM is considered treatable, it remains incurable due to the eventual drug resistance in nearly all patients. A cornerstone therapeutic for MM is dexamethasone, a synthetic glucocorticoid with anti-inflammatory and anti-myeloma properties. In this study, we investigate the role of CEBPβ in modulating enhancer activities, measured by H3K27ac, in response to dexamethasone in MM cells.

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Translational profiling in multiple myeloma to identify novel therapeutic targets

Project description:The goal of this study is to identify translationally-regulated mRNAs in multiple myeloma following treatment with dexamethasone The overall design is to treat the multiple myeloma cell line MM1.S with 1uM dexamethasone for 0 or 4 hours and collect total RNA and fractionated polysome pooled RNA (in 3 fractions)

2014-07-04 | E-GEOD-59080 | biostudies-arrayexpress

Transcription profiling of human samples from multiple myeloma patients treated with bortezomib or dexamethasone

Project description:The aims of this study were to assess the feasibility of prospective pharmacogenomics research in multicenter international clinical trials of bortezomib in multiple myeloma and to develop predictive classifiers of response and survival with bortezomib. Patients with relapsed myeloma enrolled in phase 2 and phase 3 clinical trials of bortezomib and consented to genomic analyses of pretreatment tumor samples. Bone marrow aspirates were subject to a negative-selection procedure to enrich for tumor cells, and these samples were used for gene expression profiling using DNA microarrays. Data quality and correlations with trial outcomes were assessed by multiple groups. Gene expression in this dataset was consistent with data published from a single-center study of newly diagnosed multiple myeloma. Response and survival classifiers were developed and shown to be significantly associated with outcome via testing on independent data. The survival classifier improved on the risk stratification provided by the International Staging System. Predictive models and biologic correlates of response show some specificity for bortezomib rather than dexamethasone. Informative gene expression data and genomic classifiers that predict clinical outcome can be derived from prospective clinical trials of new anticancer agents. Experiment Overall Design: Purified myeloma samples were collected prior to enrolment in clinical trials of bortezomib (PS-341). Samples were subject to replicate gene expression profiling using the Affymetrix 133A/B microarray. Data was normalized in MAS5.0 and the median of replicates is reported. Data was normalized to a Ttimmed mean of 15o and is NOT log transformed. Various patient parameters are reported as well as response, TTP and survival upon treatment with bortezomib or dexamethasone.

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