sgi-1776 and Leukemia--Myelogenous--Chronic--BCR-ABL-Positive

sgi-1776 has been researched along with Leukemia--Myelogenous--Chronic--BCR-ABL-Positive* in 1 studies

Other Studies

1 other study(ies) available for sgi-1776 and Leukemia--Myelogenous--Chronic--BCR-ABL-Positive

Article	Year
Pre-clinical evidence of PIM kinase inhibitor activity in BCR-ABL1 unmutated and mutated Philadelphia chromosome-positive (Ph+) leukemias. Oncotarget, 2015, Oct-20, Volume: 6, Issue:32 We investigated the efficacy of targeting the PIM kinase pathway in Philadelphia chromosome-positive (Ph+) leukemias. We provide evidence that inhibition of PIM, with the pan-PIM inhibitor SGI-1776, results in suppression of classic PIM effectors and also elements of the mTOR pathway, suggesting interplay between PIM and mTOR signals. Our data demonstrate that PIM inhibition enhances the effects of imatinib mesylate on Ph+ leukemia cells. We also found that PIM inhibition results in suppression of leukemic cell proliferation and induction of apoptosis of Ph+ leukemia cells, including those resistant to imatinib mesylate. Importantly, inhibition of PIM results in enhanced suppression of primary leukemic progenitors from patients with CML. Altogether these findings suggest that pharmacological PIM targeting may provide a unique therapeutic approach for the treatment of Ph+ leukemias. Topics: Dose-Response Relationship, Drug; Fusion Proteins, bcr-abl; Genes, abl; Humans; Imatinib Mesylate; Imidazoles; K562 Cells; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mutation; Philadelphia Chromosome; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-bcr; Proto-Oncogene Proteins c-pim-1; Pyridazines; Tumor Cells, Cultured	2015

Article

Year

Pre-clinical evidence of PIM kinase inhibitor activity in BCR-ABL1 unmutated and mutated Philadelphia chromosome-positive (Ph+) leukemias.

Oncotarget, 2015, Oct-20, Volume: 6, Issue:32

We investigated the efficacy of targeting the PIM kinase pathway in Philadelphia chromosome-positive (Ph+) leukemias. We provide evidence that inhibition of PIM, with the pan-PIM inhibitor SGI-1776, results in suppression of classic PIM effectors and also elements of the mTOR pathway, suggesting interplay between PIM and mTOR signals. Our data demonstrate that PIM inhibition enhances the effects of imatinib mesylate on Ph+ leukemia cells. We also found that PIM inhibition results in suppression of leukemic cell proliferation and induction of apoptosis of Ph+ leukemia cells, including those resistant to imatinib mesylate. Importantly, inhibition of PIM results in enhanced suppression of primary leukemic progenitors from patients with CML. Altogether these findings suggest that pharmacological PIM targeting may provide a unique therapeutic approach for the treatment of Ph+ leukemias.

Topics: Dose-Response Relationship, Drug; Fusion Proteins, bcr-abl; Genes, abl; Humans; Imatinib Mesylate; Imidazoles; K562 Cells; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mutation; Philadelphia Chromosome; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-bcr; Proto-Oncogene Proteins c-pim-1; Pyridazines; Tumor Cells, Cultured

2015