Melissa Holtz

TL;DR: Results indicate that inhibition of BCR/ABL tyrosine kinase activity by imatinib mesylate does not eliminate malignant primitive progenitors in CML patients.

TL;DR: Results suggest that inhibition of Bcr-Abl tyrosine kinase by imatinib mesylate restores normal hematopoiesis by removing the proliferative advantage of CML progenitors but that elimination of all CMLprogenitors may not occur.

TL;DR: It is concluded that inhibition of BCR/ABL kinase activity in CML progenitors by imatinib results in a growth factor-dependent compensatory increase in MAPK activity and in only partial inhibition of PI-3 Kinase activity.

TL;DR: It is demonstrated that CML CD34+ progenitors are sensitive to several apoptosis-inducing stimuli including the chemotherapeutic agents Ara-C and VP-16, radiation, arsenic trioxide, ceramide, growth factor withdrawal, and the death receptor activators TNFα and TRAIL.

TL;DR: The results indicate that more potent tyrosine kinase inhibitors by themselves will not be more effective in eliminating CML progenitors than imatinib and that additional mechanism required for maintenance of malignant stem cells need to be identified to improve targeting of leukemia stem cells.