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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 increasing appreciation that this regimen is myelosuppressive and associated with a higher risk of in
8 roperty of gallium nitrate is that it is not myelosuppressive and it lacks cross-resistance to other
9 xicity studies indicated that ABDNAZ was not myelosuppressive and no dose-limiting toxicity was appar
10 ion, children received alternating blocks of myelosuppressive and non-myelosuppressive chemotherapy e
11                         Clofarabine was more myelosuppressive and required more supportive care.
12          Most importantly, 26 and 30 are not myelosuppressive at therapeutically effective doses.
13 Cs in the spleen, and a mixed, predominantly myelosuppressive BM cytokine environment.
14 prophylactic levofloxacin on cycle 1 only of myelosuppressive cancer chemotherapy and on subsequent c
15                     Human MCP-1/murine JE, a myelosuppressive chemokine, specifically binds C-C chemo
16 ogenitor cell (HPCs) was not inhibited by 13 myelosuppressive chemokines that normally inhibit prolif
17 HPC colony formation and for HPC response to myelosuppressive chemokines.
18 hedule of cytokine combinations after severe myelosuppressive chemotherap
19 t for the treatment of tumors in addition to myelosuppressive chemotherapeutic drugs and/or those tha
20 id cancers and lymphomas receiving cyclical, myelosuppressive chemotherapy (causing grade 4 neutropen
21  hematological malignancies hospitalized for myelosuppressive chemotherapy are at high risk of life-t
22 del that mimics the clinical consequences of myelosuppressive chemotherapy complicated by Pseudomonas
23 arian, and non-Hodgkin lymphomas, initiating myelosuppressive chemotherapy courses were included from
24 ternating blocks of myelosuppressive and non-myelosuppressive chemotherapy every 14 days for an inten
25 atients 5 years to 18 years of age receiving myelosuppressive chemotherapy for nonmyeloid malignancie
26 ministration in pediatric patients receiving myelosuppressive chemotherapy for sarcoma.
27 lso be offered to those receiving moderately myelosuppressive chemotherapy for solid tumours and lymp
28 emotherapy and in those receiving moderately myelosuppressive chemotherapy for solid tumours.
29 e mortality in the first cycle of moderately myelosuppressive chemotherapy for solid tumours.
30                     First, initial intensive myelosuppressive chemotherapy is necessary to sufficient
31 ematopoietic stem cell transplantation after myelosuppressive chemotherapy is used for the treatment
32 e, administration of Mpl-L immediately after myelosuppressive chemotherapy or preparatory regimens fo
33 duration of intravenous antibiotic use after myelosuppressive chemotherapy or to enhance dose intensi
34 cycle use of pegfilgrastim with a moderately myelosuppressive chemotherapy regimen markedly reduced f
35 se can be successfully treated with a mildly myelosuppressive chemotherapy regimen.
36     Recommendations: For patients undergoing myelosuppressive chemotherapy who have a hemoglobin (Hb)
37                      For patients undergoing myelosuppressive chemotherapy who have a hemoglobin (Hb)
38 en the duration of febrile neutropenia after myelosuppressive chemotherapy, effectively mobilize hema
39  and expansion of HSCs and progenitors after myelosuppressive chemotherapy, inflammatory stress, and
40 ically as a platelet restorative agent after myelosuppressive chemotherapy.
41 ity of thrombocytopenia in animals receiving myelosuppressive chemotherapy.
42 ring hematopoietic organs that recover after myelosuppressive chemotherapy.
43 ematopoiesis has sufficiently recovered from myelosuppressive chemotherapy.
44 uited into cell cycle by stresses, including myelosuppressive chemotherapy.
45 /kg for pediatric sarcoma patients receiving myelosuppressive chemotherapy.
46 O may play an important role in reducing the myelosuppressive complications of naturally occurring an
47 ribed a mixed chimerism protocol that avoids myelosuppressive conditioning and permits hematopoietic
48 CD34(+) selection and reinfused after either myelosuppressive conditioning with cyclophosphamide (200
49 g hematopoietic-cell transplantation without myelosuppressive conditioning.
50 bute to the recovery of HSPCs in response to myelosuppressive conditions.
51 nt roles in signaling for IFNgamma and other myelosuppressive cytokine receptors as a common mediator
52 d hematopoietic progenitors treated with the myelosuppressive cytokine tumor necrosis factor-alpha (T
53  evidence suggests that enhanced oxidant and myelosuppressive cytokine-mediated apoptosis of hematopo
54 eneration of the inhibitory effects of these myelosuppressive cytokines on hematopoiesis.
55  pathway in the generation of the effects of myelosuppressive cytokines on human hematopoiesis.
56                                              Myelosuppressive cytokines, in particular IFN-gamma and
57 eudomonas aeruginosa 12.4.4 and then given a myelosuppressive dose of cyclophosphamide.
58 antation without the need for irradiation or myelosuppressive drugs was tested.
59 le should permit its use in combination with myelosuppressive drugs.
60 ders demonstrated an initial, albeit modest, myelosuppressive effect.
61                       Thymidine alone had no myelosuppressive effects and produced reversible grade 1
62 lls confers multilineage protection from the myelosuppressive effects of BCNU and suggest a possible
63                     G3139 may accentuate the myelosuppressive effects of doxorubicin and cyclophospha
64                   The characteristics of the myelosuppressive effects of DX-8951f, paucity of severe
65                   The characteristics of the myelosuppressive effects of PEG-CPT, the paucity of seve
66 tunately, the mechanisms responsible for the myelosuppressive effects of the cytokine are incompletel
67                               Similarly, the myelosuppressive effects of TNF-alpha and TGF-beta were
68 indicate that myeloid cell A2ARs have direct myelosuppressive effects that indirectly contribute to t
69                The cumulative rate of severe myelosuppressive effects was unacceptably high at TMZ do
70  However, in stark contrast to hydroxyurea's myelosuppressive effects, pomalidomide augmented erythro
71                 The latter cause significant myelosuppressive effects, which make it challenging to f
72 at achieves alloengraftment without toxic or myelosuppressive host conditioning.
73 tem-cell engraftment can be achieved without myelosuppressive host conditioning.
74       This requirement for potentially toxic myelosuppressive host pre-conditioning has precluded the
75 ukopenia, with risk compounded by the use of myelosuppressive immunosuppression.
76  a chemotherapeutic agent that is powerfully myelosuppressive in the model.
77 ryonic development, infectious diseases, and myelosuppressive injuries caused by irradiation and chem
78 Cs enhanced hematopoietic recovery following myelosuppressive injury and restored endogenous HSC func
79 topoietic stem cell (HSC) regeneration after myelosuppressive injury are not well understood.
80 em as well as in vivo EC infusions following myelosuppressive injury in mice to demonstrate that aged
81 R signaling regulates HSC regeneration after myelosuppressive injury.
82 duced in hematopoietic vascular niches after myelosuppressive injury.
83 s HSC function at steady state and following myelosuppressive insult, in which inhibition of EC NF-ka
84 such as systemic infection, inflammation, or myelosuppressive insults.
85 rity and duration of thrombocytopenia due to myelosuppressive irradiation, chemotherapy, or both.
86                            If approved, less myelosuppressive JAK2 inhibitors such as pacritinib or N
87                       The approval of 2 less-myelosuppressive JAKis, pacritinib and momelotinib, prov
88 m on CD34(+) cell yields and morbidity after myelosuppressive mobilization chemotherapy (MC).
89  in significantly prolonged survival without myelosuppressive or immunosuppressive effects.
90             Adverse events are predominantly myelosuppressive or respiratory.
91 ta indicates that for patients on moderately myelosuppressive out-patient chemotherapy, the greatest
92 lanning to receive cytotoxic chemotherapy or myelosuppressive radiotherapy was evaluated.
93  associated with side effects related to the myelosuppressive recipient conditioning, which makes it
94 e, and 36 mg/m2 idarubicin [FAI]) and a more myelosuppressive, reduced-intensity regimen (100 to 150
95                                          The myelosuppressive regimen induced expression of p53 and t
96 c cell transplantation following a minimally myelosuppressive regimen, consisting of 100 cGy total bo
97  management of infectious complications from myelosuppressive regimens are critical.
98 that retain some toxicity, and (2) minimally myelosuppressive regimens that rely on immunosuppression
99 s and require hospitalization, and minimally myelosuppressive regimens that rely on immunosuppression
100 ical development will likely target the most myelosuppressive regimens, including those used in hemat
101 atment of haematological disorders requiring myelosuppressive regimens.
102 recovery in the elderly population following myelosuppressive regimens.
103 identified toxicities were gastrointestinal, myelosuppressive, renal, and CNS.
104 tarting dose of clofarabine (15 mg/m(2)) was myelosuppressive, requiring several dose de-escalations
105 quirement of this kinase in the induction of myelosuppressive responses.
106 in gene therapy applications to decrease the myelosuppressive side effects of TS-directed anticancer
107 yelocytic leukemia (APL) without significant myelosuppressive side effects.
108 with a key role for p38 in the generation of myelosuppressive signals by different cytokines.
109            We have previously shown that the myelosuppressive TGF-beta pathway is constitutively acti
110 T is highly effective and significantly less myelosuppressive than 1F5-SA (P < 0.0001).
111 ng the need for therapeutic phlebotomies and myelosuppressive therapeutic options.
112          Given the paucity of effective, non-myelosuppressive therapies, these preliminary findings h
113 f Tpo to speed red blood cell recovery after myelosuppressive therapy in vivo and to enhance colony-f
114                                   Intensive, myelosuppressive therapy is necessary to maximize outcom
115  recurrent disease and (B) pts with no prior myelosuppressive therapy or newly diagnosed tumors for w
116  not be influenced by previous or concurrent myelosuppressive therapy or supportive measures.
117                                        Prior myelosuppressive therapy was not a determinant of toxici
118 mpairs HSC quiescence and sensitizes mice to myelosuppressive therapy.
119 MA-617 therapy and less than 6 wk since last myelosuppressive therapy.
120 erative status of hematopoietic organs after myelosuppressive therapy.
121 ly enhances the hematopoietic recovery after myelosuppressive therapy.
122 tially more constitutional, hemodynamic, and myelosuppressive toxic effects.
123                             The incidence of myelosuppressive toxicities (eg, neutropenia and leukope
124                         Gastrointestinal and myelosuppressive toxicities were readily managed.
125  as a means to protect against dose-limiting myelosuppressive toxicity ensuing from chemotherapy comb
126 ecessary for on-going studies evaluating non-myelosuppressive transplant regimens for the induction o
127 ion-leads to chimerism and tolerance without myelosuppressive treatment in murine models.
128 stimulation and display slower recovery from myelosuppressive treatment, suggesting that combinatoria
129 apeutic benefits for patients after clinical myelosuppressive treatment.

 
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