Genomics

Dataset Information

42

The BET bromodomain inhibitor CPI203 improves lenalidomide activity in in vitro and in vivo models of multiple myeloma by synergistic blockade of Ikaros and c-Myc signaling


ABSTRACT: Multiple myeloma (MM) cells were treated with the BET inhibitor CPI203 alone and in combination with lenalidomide plus dexamethasone in vitro and in vivo (mouse xenograft). We used microarrays to uncover the mechanisms underlying CPI-203 activity in MM, alone and in combination with lenalidomide plus dexamethasone (combo). Overall design: Global RNA expression was done in three MM cell lines treated in vitro with the BET inhibitor alone or with the combo for 6h.

INSTRUMENT(S): [HG-U219] Affymetrix Human Genome U219 Array

ORGANISM(S): Homo Sapiens

SUBMITTER: Patricia Pérez-Galán  

PROVIDER: GSE87403 | GEO | 2016-09-28

SECONDARY ACCESSION(S): PRJNA344666

REPOSITORIES: GEO

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Publications

The BET bromodomain inhibitor CPI203 improves lenalidomide and dexamethasone activity in <i>in vitro</i> and <i>in vivo</i> models of multiple myeloma by blockade of Ikaros and MYC signaling.

Díaz Tania T   Rodríguez Vanina V   Lozano Ester E   Mena Mari-Pau MP   Calderón Marcos M   Rosiñol Laura L   Martínez Antonio A   Tovar Natalia N   Pérez-Galán Patricia P   Bladé Joan J   Roué Gaël G   de Larrea Carlos Fernández CF  

Haematologica 20170727 10


Most patients with multiple myeloma treated with current therapies, including immunomodulatory drugs, eventually develop relapsed/refractory disease. Clinical activity of lenalidomide relies on degradation of Ikaros and the consequent reduction in IRF4 expression, both required for myeloma cell survival and involved in the regulation of MYC transcription. Thus, we sought to determine the combinational effect of an MYC-interfering therapy with lenalidomide/dexamethasone. We analyzed the potential  ...[more]

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