Our data indicate that IGF2BP1 maintains leukemia stem cell properties by regulating multiple pathways of stemness through transcriptional and metabolic factors.
Here, we use Cbfb-MYH11 knock-in mice to show that IL1RL1 is expressed by cell populations with high LSC activity, and that the cell surface expression of IL1RL1 is dynamic, implying that the expression of IL1RL1 is not restricted to a specific stage of differentiation.
Here, we use Cbfb-MYH11 knock-in mice to show that IL1RL1 is expressed by cell populations with high LSC activity, and that the cell surface expression of IL1RL1 is dynamic, implying that the expression of IL1RL1 is not restricted to a specific stage of differentiation.
B-cell lymphoma 2 (BCL-2) is an antiapoptotic protein involved in the survival and maintenance of AML, and it is overexpressed in the leukemia stem cell population.
Importantly, we identified pathways involved in the leukemia stem cell interaction with the bone marrow niche, such as integrin, CXCR4, and interleukin-8, among the most upregulated signaling pathways in patients with high CD97 expression.
Here we show that triple-mutated AML is characterized by high leukemia stem cell (LSC) frequency, an aberrant leukemia-specific <i>GPR56</i><sup>high</sup>CD34<sup>low</sup> immunophenotype, and synergistic upregulation of Hepatic Leukemia Factor (<i>HLF</i>).
Furthermore, downregulation of ZEB1 by LMO2 complex results in an increased leukaemia stem cell (LSC) phenotype as well as unsensitivity in response to methotrexate (MTX) chemotherapy in T-ALL cells.
Conditional knockout models of murine acute myeloid leukemia indicate that <i>Hhex</i> maintains leukemia stem cell self-renewal by enabling Polycomb-mediated epigenetic repression of the Cdkn2a tumor suppressor locus, encoding p16<sup>Ink4a</sup> and p19<sup>Arf</sup> However, whether <i>Hhex</i> overexpression also affects hematopoietic differentiation is unknown.
In murine models of chronic myelogenous leukemia (CML), CCL3 is critical for the maintenance of a leukemia stem cell population, and leukemia progression.
We found that <i>Mef2c<sup>S222A/S222A</sup></i> knock-in mutant mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by <i>MLL-AF9</i> MEF2C phosphorylation was required for leukemia stem cell maintenance and induced by MARK kinases in cells.
To determine the role of TET2 deficiency in leukemia stem cell maintenance, we generated a reversible transgenic RNAi mouse to model restoration of endogenous Tet2 expression.