The effect of IM and MSC treatment on gene expression in CML CD34+ cells

ABSTRACT: Tyrosine kinase inhibitors (TKI) are highly effective in treatment of chronic myeloid leukemia (CML) but do not eliminate leukemia stem cells (LSC), which remain a potential source of relapse. TKI treatment effectively inhibits BCR-ABL kinase activity in CML LSC, suggesting that additional kinase-independent mechanisms contribute to LSC preservation. We investigated whether signals from the bone marrow (BM) microenvironment protect CML LSC from TKI treatment. Coculture with human BM mesenchymal stromal cells (MSC) significantly inhibited apoptosis and preserved CML stem/progenitor cells following TKI exposure, maintaining colony forming ability and engraftment potential in immunodeficient mice. We found that the N-Cadherin receptor plays an important role in MSC-mediated protection of CML

ORGANISM(S): Homo sapiens

SUBMITTER: Ravi Bhatia 

PROVIDER: E-GEOD-43225 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress