Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from a reversible dasatinib-resistant state in long-term dasatinib-treated c-KIT-mutated Kasumi-1 cell line

ABSTRACT: Long-term treatment of Kasumi-1 cells at clinically attained doses of dasatinib led to decreased drug-sensitivity by means of IC50 values (relative to treatment-naive cells). Changes were paralled by profound alterations in c-KIT expression and cell signaling signatures. Upon brief discontinuation of dasatinib treatment, these alterations reversed and drug sensitivity was restored. We used gene expression profiling to examine reversal of dasatinib-resistance at the molecular/expression level. Kasumi-1 cells were either treated with dasatinib for 12 weeks (R48) or left untreated (K). Subsequently, dasatinib was withdrawn from R48 cells for 1 week (PR48). RNA was extracted from R48 and K cells and hybridized on Affymetrix microarrays after 12 weeks and PR48 after a total time span of 13 weeks.

ORGANISM(S): Homo sapiens

SUBMITTER: Karlheinz Holzmann 

PROVIDER: E-GEOD-39073 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Transitory dasatinib-resistant states in KIT(mut) t(8;21) acute myeloid leukemia cells correlate with altered KIT expression.

Herrmann Markus D MD   Lennerz Jochen K JK   Bullinger Lars L   Bartholomae Stephan S   Holzmann Karlheinz K   Westhoff Mike-Andrew MA   Corbacioglu Selim S   Debatin Klaus-Michael KM  

Experimental hematology 20131106 2

KIT inhibition with dasatinib represents a promising approach to targeted therapy in t(8;21) acute myeloid leukemia (AML) and clinical trials are currently evaluating its clinical relevance. However, data on continuous long-term dasatinib exposure of AML cells are limited and the potential effects on KIT inhibition and dasatinib sensitivity are unexplored. Treatment-related resistance ultimately limits clinical efficacy of tyrosine kinase inhibitors (TKI), which could similarly apply to dasatini  ...[more]

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