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Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [CGH data]

ABSTRACT: Copy number and Gene expression profiling of HT-29 wild-type and bortezomib resistant cell lines Identification of mechanisms of bortezomib resistance

ORGANISM(S): Homo sapiens

PROVIDER: GSE29711 | GEO | 2011/06/04

SECONDARY ACCESSION(S): PRJNA153857

REPOSITORIES: GEO

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Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [CGH data]

Project description:Copy number and Gene expression profiling of HT-29 wild-type and bortezomib resistant cell lines Identification of mechanisms of bortezomib resistance Copy number differences between HT-29 cell line variants and a HapMap control population of 9 female samples were identified using the Agilent 1M Human CGH microarray

2011-06-04 | E-GEOD-29711 | biostudies-arrayexpress

Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [GEP data]

Project description:Copy number and Gene expression profiling of HT-29 wild-type and bortezomib resistant cell lines Identification of mechanisms of bortezomib resistance

2011-06-04 | GSE29712 | GEO

Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [GEP data]

2011-06-04 | E-GEOD-29712 | biostudies-arrayexpress

Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE29711: Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [CGH data] GSE29712: Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells [GEP data] Refer to individual Series

2011-06-04 | E-GEOD-29713 | biostudies-arrayexpress

Molecular mechanisms of bortezomib resistant adenocarcinoma cells.

Project description:Bortezomib (Velcade™) is a reversible proteasome inhibitor that is approved for the treatment of multiple myeloma (MM). Despite its demonstrated clinical success, some patients are deprived of treatment due to primary refractoriness or development of resistance during therapy. To investigate the role of the duration of proteasome inhibition in the anti-tumor response of bortezomib, we established clonal isolates of HT-29 adenocarcinoma cells adapted to continuous exposure of bortezomib. These cells were ~30-fold resistant to bortezomib. Two novel and distinct mutations in the β5 subunit, Cys63Phe, located distal to the binding site in a helix critical for drug binding, and Arg24Cys, found in the propeptide region were found in all resistant clones. The latter mutation is a natural variant found to be elevated in frequency in patients with MM. Proteasome activity and levels of both the constitutive and immunoproteasome were increased in resistant cells, which correlated to an increase in subunit gene expression. These changes correlated with a more rapid recovery of proteasome activity following brief exposure to bortezomib. Increased recovery rate was not due to increased proteasome turnover as similar findings were seen in cells co-treated with cycloheximide. When we exposed resistant cells to the irreversible proteasome inhibitor carfilzomib we noted a slower rate of recovery of proteasome activity as compared to bortezomib in both parental and resistant cells. Importantly, carfilzomib maintained its cytotoxic potential in the bortezomib resistant cell lines. Therefore, resistance to bortezomib, can be overcome with irreversible inhibitors, suggesting prolonged proteasome inhibition induces a more potent anti-tumor response.

| S-EPMC3245226 | biostudies-literature

Bortezomib resistance in CCRF-CEM cell line [CGH]

2015-11-04 | GSE74633 | GEO

Molecular Mechanisms of Bortezomib Resistant Adenocarcinoma cells

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

2011-06-04 | GSE29713 | GEO

Bortezomib resistance in CCRF-CEM cell line [CGH]

Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed comparative Genome hybridization (arrayCGH) for DNA copy number analysis on four different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compared to the parental CCRF-CEM wildtype cell line and reference DNA.

2015-11-04 | E-GEOD-74633 | biostudies-arrayexpress

A Subset of Genes Can Distinguish between Bortezomib Responsive Versus Bortezomib Resistant Myeloma

Project description:Gene expression profile (GEP) was analyzed from cultured bone marrow (BM) samples from patients with bortezomib responsive versus bortezomib resistant myeloma after 6-8 hours incubation in vitro with bortezomib 2 µg/ml or with PBS. Case D also had a fresh BM sample taken 75 minutes after IV injection of bortezomib.

2013-11-01 | GSE51940 | GEO

MicroRNA Expression Profile of serum exosomes from Bortezomib-resistant and Bortezomib-response patients in multiple myeloma

Project description:MicroRNA microarray profilling analysis was performed on exosomes derived from serum in patients with myeloma in two conditions of therapeutic efficacy, Bortezomib resistance and Bortezomib response. Bortezomib is approved and widely used treating myeloma.

2016-07-31 | GSE71435 | GEO

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