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Functional differences between healthy progenitor and cancer initiating cells may provide unique opportunities for targeted therapy approaches. Hematopoietic stem cells are tightly controlled by a network of CDK inhibitors that govern proliferation and prevent stem cell exhaustion. Loss of  Inca1  led to an increased number of short-term hematopoietic stem cells in older mice, but Inca1 seems largely dispensable for normal hematopoiesis. On the other hand,  Inca1 -deficiency enhanced cell cycling upon cytotoxic stress and accelerated bone marrow exhaustion. Moreover, AML1-ETO9a-induced proliferation was not sustained in  Inca1 -deficient cells  in vivo . As a consequence, leukemia induction and leukemia maintenance were severely impaired in  Inca1 −/−   bone marrow cells. The re-initiation of leukemia was also significantly inhibited in absence of  Inca1 −/−   in MLL—AF9- and c-myc/BCL2-positive leukemia mouse models. These findings indicate distinct functional properties of Inca1 in normal hematopoietic cells compared to leukemia initiating cells. Such functional differences might be used to design specific therapy approaches in leukemia.

Maintenance of Leukemia-Initiating Cells Is Regulated by the CDK Inhibitor Inca1