ライフサイエンスコーパス: myelosuppressive

1 It is well tolerated but more myelosuppressive.

2 in CLL, pentostatin appears to be the least myelosuppressive.

3 logs active in CLL, pentostatin may be least myelosuppressive.

4 microtubule-binding drugs might alter their myelosuppressive action, we tested their effect in cell

5 were sensitive to in vivo treatment with the myelosuppressive agent 7,12 Dimethylbenz[a]anthracene (D

6 The use of myelosuppressive agents to reduce the risk of thrombosis

7 roperty of gallium nitrate is that it is not myelosuppressive and it lacks cross-resistance to other

8 xicity studies indicated that ABDNAZ was not myelosuppressive and no dose-limiting toxicity was appar

9 ion, children received alternating blocks of myelosuppressive and non-myelosuppressive chemotherapy e

10 Clofarabine was more myelosuppressive and required more supportive care.

11 Most importantly, 26 and 30 are not myelosuppressive at therapeutically effective doses.

12 Cs in the spleen, and a mixed, predominantly myelosuppressive BM cytokine environment.

13 prophylactic levofloxacin on cycle 1 only of myelosuppressive cancer chemotherapy and on subsequent c

14 Human MCP-1/murine JE, a myelosuppressive chemokine, specifically binds C-C chemo

15 ogenitor cell (HPCs) was not inhibited by 13 myelosuppressive chemokines that normally inhibit prolif

16 HPC colony formation and for HPC response to myelosuppressive chemokines.

17 hedule of cytokine combinations after severe myelosuppressive chemotherap

18 t for the treatment of tumors in addition to myelosuppressive chemotherapeutic drugs and/or those tha

19 id cancers and lymphomas receiving cyclical, myelosuppressive chemotherapy (causing grade 4 neutropen

20 del that mimics the clinical consequences of myelosuppressive chemotherapy complicated by Pseudomonas

21 ternating blocks of myelosuppressive and non-myelosuppressive chemotherapy every 14 days for an inten

22 atients 5 years to 18 years of age receiving myelosuppressive chemotherapy for nonmyeloid malignancie

23 ministration in pediatric patients receiving myelosuppressive chemotherapy for sarcoma.

24 lso be offered to those receiving moderately myelosuppressive chemotherapy for solid tumours and lymp

25 emotherapy and in those receiving moderately myelosuppressive chemotherapy for solid tumours.

26 e mortality in the first cycle of moderately myelosuppressive chemotherapy for solid tumours.

27 First, initial intensive myelosuppressive chemotherapy is necessary to sufficient

28 ematopoietic stem cell transplantation after myelosuppressive chemotherapy is used for the treatment

29 e, administration of Mpl-L immediately after myelosuppressive chemotherapy or preparatory regimens fo

30 duration of intravenous antibiotic use after myelosuppressive chemotherapy or to enhance dose intensi

31 cycle use of pegfilgrastim with a moderately myelosuppressive chemotherapy regimen markedly reduced f

32 Recommendations: For patients undergoing myelosuppressive chemotherapy who have a hemoglobin (Hb)

33 For patients undergoing myelosuppressive chemotherapy who have a hemoglobin (Hb)

34 en the duration of febrile neutropenia after myelosuppressive chemotherapy, effectively mobilize hema

35 and expansion of HSCs and progenitors after myelosuppressive chemotherapy, inflammatory stress, and

36 ically as a platelet restorative agent after myelosuppressive chemotherapy.

37 ity of thrombocytopenia in animals receiving myelosuppressive chemotherapy.

38 ring hematopoietic organs that recover after myelosuppressive chemotherapy.

39 ematopoiesis has sufficiently recovered from myelosuppressive chemotherapy.

40 uited into cell cycle by stresses, including myelosuppressive chemotherapy.

41 /kg for pediatric sarcoma patients receiving myelosuppressive chemotherapy.

42 O may play an important role in reducing the myelosuppressive complications of naturally occurring an

43 ribed a mixed chimerism protocol that avoids myelosuppressive conditioning and permits hematopoietic

44 CD34(+) selection and reinfused after either myelosuppressive conditioning with cyclophosphamide (200

45 g hematopoietic-cell transplantation without myelosuppressive conditioning.

46 bute to the recovery of HSPCs in response to myelosuppressive conditions.

47 nt roles in signaling for IFNgamma and other myelosuppressive cytokine receptors as a common mediator

48 d hematopoietic progenitors treated with the myelosuppressive cytokine tumor necrosis factor-alpha (T

49 evidence suggests that enhanced oxidant and myelosuppressive cytokine-mediated apoptosis of hematopo

50 eneration of the inhibitory effects of these myelosuppressive cytokines on hematopoiesis.

51 pathway in the generation of the effects of myelosuppressive cytokines on human hematopoiesis.

52 Myelosuppressive cytokines, in particular IFN-gamma and

53 eudomonas aeruginosa 12.4.4 and then given a myelosuppressive dose of cyclophosphamide.

54 antation without the need for irradiation or myelosuppressive drugs was tested.

55 le should permit its use in combination with myelosuppressive drugs.

56 ders demonstrated an initial, albeit modest, myelosuppressive effect.

57 Thymidine alone had no myelosuppressive effects and produced reversible grade 1

58 lls confers multilineage protection from the myelosuppressive effects of BCNU and suggest a possible

59 G3139 may accentuate the myelosuppressive effects of doxorubicin and cyclophospha

60 The characteristics of the myelosuppressive effects of DX-8951f, paucity of severe

61 The characteristics of the myelosuppressive effects of PEG-CPT, the paucity of seve

62 tunately, the mechanisms responsible for the myelosuppressive effects of the cytokine are incompletel

63 Similarly, the myelosuppressive effects of TNF-alpha and TGF-beta were

64 indicate that myeloid cell A2ARs have direct myelosuppressive effects that indirectly contribute to t

65 The cumulative rate of severe myelosuppressive effects was unacceptably high at TMZ do

66 However, in stark contrast to hydroxyurea's myelosuppressive effects, pomalidomide augmented erythro

67 at achieves alloengraftment without toxic or myelosuppressive host conditioning.

68 tem-cell engraftment can be achieved without myelosuppressive host conditioning.

69 This requirement for potentially toxic myelosuppressive host pre-conditioning has precluded the

70 ukopenia, with risk compounded by the use of myelosuppressive immunosuppression.

71 a chemotherapeutic agent that is powerfully myelosuppressive in the model.

72 Cs enhanced hematopoietic recovery following myelosuppressive injury and restored endogenous HSC func

73 topoietic stem cell (HSC) regeneration after myelosuppressive injury are not well understood.

74 em as well as in vivo EC infusions following myelosuppressive injury in mice to demonstrate that aged

75 duced in hematopoietic vascular niches after myelosuppressive injury.

76 R signaling regulates HSC regeneration after myelosuppressive injury.

77 s HSC function at steady state and following myelosuppressive insult, in which inhibition of EC NF-ka

78 rity and duration of thrombocytopenia due to myelosuppressive irradiation, chemotherapy, or both.

79 If approved, less myelosuppressive JAK2 inhibitors such as pacritinib or N

80 m on CD34(+) cell yields and morbidity after myelosuppressive mobilization chemotherapy (MC).

81 in significantly prolonged survival without myelosuppressive or immunosuppressive effects.

82 Adverse events are predominantly myelosuppressive or respiratory.

83 ta indicates that for patients on moderately myelosuppressive out-patient chemotherapy, the greatest

84 lanning to receive cytotoxic chemotherapy or myelosuppressive radiotherapy was evaluated.

85 e, and 36 mg/m2 idarubicin [FAI]) and a more myelosuppressive, reduced-intensity regimen (100 to 150

86 The myelosuppressive regimen induced expression of p53 and t

87 c cell transplantation following a minimally myelosuppressive regimen, consisting of 100 cGy total bo

88 management of infectious complications from myelosuppressive regimens are critical.

89 that retain some toxicity, and (2) minimally myelosuppressive regimens that rely on immunosuppression

90 s and require hospitalization, and minimally myelosuppressive regimens that rely on immunosuppression

91 ical development will likely target the most myelosuppressive regimens, including those used in hemat

92 recovery in the elderly population following myelosuppressive regimens.

93 atment of haematological disorders requiring myelosuppressive regimens.

94 identified toxicities were gastrointestinal, myelosuppressive, renal, and CNS.

95 tarting dose of clofarabine (15 mg/m(2)) was myelosuppressive, requiring several dose de-escalations

96 quirement of this kinase in the induction of myelosuppressive responses.

97 in gene therapy applications to decrease the myelosuppressive side effects of TS-directed anticancer

98 yelocytic leukemia (APL) without significant myelosuppressive side effects.

99 with a key role for p38 in the generation of myelosuppressive signals by different cytokines.

100 We have previously shown that the myelosuppressive TGF-beta pathway is constitutively acti

101 T is highly effective and significantly less myelosuppressive than 1F5-SA (P < 0.0001).

102 f Tpo to speed red blood cell recovery after myelosuppressive therapy in vivo and to enhance colony-f

103 Intensive, myelosuppressive therapy is necessary to maximize outcom

104 recurrent disease and (B) pts with no prior myelosuppressive therapy or newly diagnosed tumors for w

105 Prior myelosuppressive therapy was not a determinant of toxici

106 erative status of hematopoietic organs after myelosuppressive therapy.

107 ly enhances the hematopoietic recovery after myelosuppressive therapy.

108 mpairs HSC quiescence and sensitizes mice to myelosuppressive therapy.

109 tially more constitutional, hemodynamic, and myelosuppressive toxic effects.

110 Gastrointestinal and myelosuppressive toxicities were readily managed.

111 as a means to protect against dose-limiting myelosuppressive toxicity ensuing from chemotherapy comb

112 ecessary for on-going studies evaluating non-myelosuppressive transplant regimens for the induction o

113 stimulation and display slower recovery from myelosuppressive treatment, suggesting that combinatoria

114 apeutic benefits for patients after clinical myelosuppressive treatment.