Gene expression changes associated with progression of Irf8M-bM-^@M-^S/M-bM-^@M-^S CML-like disease into blast crisis after M-NM-2-catenin activation

ABSTRACT: Progression and disease relapse of chronic myeloid leukemia (CML) depends on leukemia-initiating cells (LIC) that resist treatment. Using mouse genetics, we observed that compound constitutive activation of M-NM-2-catenin and deletion of Irf8 results in progression of CML-like disease into fatal blast crisis, elevated leukemic potential of BCR-ABL-induced LICs, and accumulation of Imatinib-resistant LICs in GMP-like populations. We found that progression of the disease is tightly connected to the magnitude of gene expression and that activated M-NM-2-catenin enhances a pre-existing Irf8-deficient gene signature that was defined as a M-bM-^@M-^\progression specific signatureM-bM-^@M-^] (PSS). We identified M-NM-2-catenin as an amplifier of disease progression and as a critical step in the s

ORGANISM(S): Mus musculus

SUBMITTER: Marina Scheller 

PROVIDER: E-GEOD-49054 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress