1 ing conditioning regimens that are minimally myelotoxic.

2      When treated with a cell cycle-specific myelotoxic agent, the animals reconstituted with PrP-nul

3  could potentially avoid the requirement for myelotoxic agents altogether.

4  stimulation with differentiating cytokines, myelotoxic agents and inflammatory substances.

5 ential role for FAK in regulating hemolytic, myelotoxic, as well as acute inflammatory stress respons

6 tologic malignancy (P <.001), total previous myelotoxic chemotherapy (P <.001), T-cell dose (P =.03),

7 ading cause of morbidity and mortality after myelotoxic chemotherapy or radiation exposure.

8 e, and leucovorin (ProMACE-CytaBOM) when the myelotoxic drugs cyclophosphamide, doxorubicin, etoposid

9  both drugs failed to mitigate hydroxyurea's myelotoxic effects and caused loss of HbF induction.

10 /wk for 8 weeks to nonhuman primates was not myelotoxic, hypomethylated DNA in the gamma-globin gene

11                                              Myelotoxic injury in the bone marrow (BM) as a consequen

12  Exposing the animals to cell cycle-specific myelotoxic injury resulted in premature death due to hem

13 owed accelerated hematopoietic recovery from myelotoxic injury, and HO-1(+/-) HSCs repopulated lethal

14 al for hematopoiesis and for protection from myelotoxic injury.

15  cells have shown that 100 cGy, although not myelotoxic, is stem cell toxic, and indicate that the fi

16  allograft survival, it was not nephrotoxic, myelotoxic, or lipotoxic and did not increase CsA-induce

17 ot impact HSC function under steady-state or myelotoxic stress conditions (such as arsenic or radiati

18 ogenitor cells during steady state and after myelotoxic stress in vivo.

19  who had received fewer than three cycles of myelotoxic therapy for chronic myeloid leukemia or myelo

20 neutropenia even during periods of full-dose myelotoxic therapy.

21                                              Myelotoxic treatments for oncologic diseases are often c