Jose A. Cancelas

TL;DR: The deletion of both Rac1 and Rac2 murine alleles leads to a massive egress of hematopoietic stem/progenitor cells into the blood from the marrow, whereas Rac1–/– but not Rac2-/– HSC/Ps fail to engraft in the bone marrow of irradiated recipient mice.

TL;DR: It is shown that expression of MLL-AF9 in human CD34+ cells induces acute myeloid, lymphoid, or mixed-lineage leukemia in immunodeficient mice, and Targeting the Rac signaling pathway by pharmacologic or genetic means resulted in rapid and specific apoptosis of M LL-AF 9 cells, suggesting that the Rac signaled pathway may be a valid therapeutic target in Mll-rearranged AML.

TL;DR: Rac proteins thus differentially regulate engraftment and mobilization phenotypes, suggesting that these biological processes and steady-state hematopoiesis are biochemically separable and that Rac proteins may be important molecular targets for stem cell modification.

TL;DR: Peripheral nerve and tumors contain transiently proliferating Schwann cells that lose axonal contact, providing insight into early neurofibroma formation.

TL;DR: In a conditional-knockout mouse model, it is shown that CDC42−/− HSCs enter the active cell cycle, resulting in significantly increased number and frequency of the stem/progenitor cells in the BM, and Cdc42 deficiency also causes impaired adhesion, homing, lodging, and retention of H SCs, leading to massive egress from BM to distal organs and peripheral blood and to an engraftment failure.