ライフサイエンスコーパス: CFU-GM

1 CFU-GM were also reduced in these patients, but with con

2 ls, 1.4 x 10(6) CD34+ cells, and 1.3 x 10(4) CFU-GM per kilogram patient weight.

3 ntration of 0.25 mmol/L, SNAP did not affect CFU-GM.

4 nts; including CFU-GEMM (12), BFU-E (8), and CFU-GM (6).

5 ed that rhG-CSF-recruited CFU-Meg(blood) and CFU-GM(blood) were considerably more radiosensitive than

6 antly positively associated with CD34(+) and CFU-GM.

7 milar numbers of PMF and mPB CD34+ cells and CFU-GM homed to their spleens.

8 e expansion of total cells, CD34+ cells, and CFU-GM and enhances the pool of early CD34+ CD33(dim) ce

9 Pre-CFU and CFU-GM levels were not related to the interval posttrans

10 Trauma plasma inhibits bone marrow BFU-E and CFU-GM colony growth for up to 2 weeks after injury.

11 ors showed that this inhibition of BFU-E and CFU-GM colony growth was mediated by bone marrow stroma.

12 environment, we compared growth of BFU-E and CFU-GM from 7-14-wk-old FL, 11-20-wk-old fetal bone marr

13 The fraction of BFU-E and CFU-GM retrieved from the marrow and spleen of the recip

14 BFU-E and CFU-GM values did not increase in the femur but expanded

15 2 antibody reduced femoral CFU-E, BFU-E, and CFU-GM content to less than half that found in phenylhyd

16 In addition, platelet, reticulocyte, and CFU-GM regeneration were significantly accelerated in mi

17 o control levels after 5 days treatment, and CFU-GM were significantly reduced (65%) after 7 days tre

18 n addition to osteoclast progenitors such as CFU-GM, earlier hematopoietic progenitors are also uniqu

19 reshly isolated CD34(+) cells; chemo-attract CFU-GM- and CFU-Meg-derived cells as well as other CD34(

20 significantly reduced while peripheral blood CFU-GM, BFU-E, and CFU-E was increased in the trauma pat

21 TBI caused a dose-dependent decrease of both CFU-GM(femur) (D0, 136 cGy) and CFU-Meg(femur) (D0, 148

22 and chemokines are expressed and secreted by CFU-GM-, CFU-Meg-, and BFU-E-derived cells.

23 mediator that augments colony forming cell (CFU-GM) formation in the presence of CSFs.

24 granulocyte-macrophage colony-forming cells (CFU-GM) is reduced.

25 -macrophage colony-forming progenitor cells (CFU-GM); in contrast, only Mll(PTD/WT) FLC had increased

26 Circulating CFU-GM and CFU-Meg in the blood were decreased in a dose

27 ent pairs, donor CD56(+) cells inhibited CML CFU-GM comparably to effectors from 14 HLA-mismatched un

28 eferentially suppresses amplification of CML CFU-GM to varying degrees.

29 tor(CSF; CFU-M), granulocyte-macrophage-CSF (CFU-GM), and stem cell factor (CFU-SCF).

30 yeloid lineages, including functional BFU-E, CFU-GM, and CFU-MIX progenitors.

31 -Meg(blood) D0 values for CI were 90 cGy for CFU-GM(blood) and 140 cGy for CFU-Meg(blood).

32 Average D0 values for TBI were 53 cGy for CFU-GM(blood) and 40 cGy for CFU-Meg(blood) D0 values fo

33 potent as synergistic growth stimulants for CFU-GM.

34 However, colony formation from CFU-GM was relatively resistant to the cytotoxic effects

35 a cell line CEM and the normal hematopoietic CFU-GM.

36 crease in BFU-E and CFU-G, but a decrease in CFU-GM in FL-HSCs from the H-PFOS group, indicating alte

37 +)CD38(-) (P = 0.005), and a 94% increase in CFU-GM (P = 0.01).

38 The increase in CFU-GM following ovariectomy was abrogated in animals th

39 age [CFU-GM]) showed a threefold increase in CFU-GM from ARH-77 marrow versus controls (185 +/- 32 v

40 A significant increase in CFU-GM number was observed as early as 7 days following

41 ated mice exhibited significant increases in CFU-GM compared with the saline-treated control groups.

42 th IFN-alpha showed a threefold reduction in CFU-GM amplification in responders (P = 0.03) but no sig

43 fect on BM CFU over time, FL alone increased CFU-GM and CFU-GEMM threefold and fivefold, respectively

44 lines, as determined by ELISA; and increased CFU-GM formation and osteoclastogenesis as determined ex

45 NK]) and CD56(+)CD3(+)(NK-T) cells inhibited CFU-GM growth of CML but not normal CD34(+) cells.

46 Elastase inhibited CFU-GM in methylcellulose culture.

47 concentration used, the Vav AS ODN inhibited CFU-GM colony formation from 66% to 81% when compared wi

48 Vav-targeted AS ODN inhibited CFU-GM colony formation in a sequence-specific and dose-

49 that NK-A (10(-7) to 10(-12) mol/L) inhibits CFU-GM proliferation but stimulates erythroid progenitor

50 neic T cells preferentially inhibit leukemic CFU-GM based on overexpression of proteinase 3, and that

51 Low pre-CFU but not low CFU-GM levels were associated with reduced peripheral bl

52 ed on c-kit fluorescence, over 88% of CFU-M, CFU-GM, and CFU-SCF were found in the c-kithigh populati

53 colony-forming unit-granulocyte macrophage (CFU-GM) derived from transduced CD34+ cells was shown po

54 colony-forming unit-granulocyte macrophage (CFU-GM) formation by 34% to 100%.

55 colony-forming unit-granulocyte macrophage (CFU-GM) formation in HLA-A2(+) healthy controls and CML

56 colony-forming unit-granulocyte macrophage (CFU-GM) infused was 27 x 10(4)/kg, and the number of CD3

57 colony forming unit-granulocyte macrophage (CFU-GM) level.

58 colony-forming unit-granulocyte macrophage (CFU-GM) were essentially unaffected.

59 igher numbers of CFU-granulocyte macrophage (CFU-GM), and greater than 10-fold higher numbers of burs

60 olony-forming unit-granulocyte, -macrophage (CFU-GM), burst-forming unit-erythroid (BFU-E), and colon

61 old increases in CFU-granulocyte-macrophage (CFU-GM) and CFU-granulocyte, erythrocyte, monocyte, mega

62 colony-forming unit-granulocyte-macrophage (CFU-GM) and colony-forming unit granulocyte, erythroid,

63 colony-forming unit-granulocyte-macrophage (CFU-GM) assay to quantitate the level of hematopoietic c

64 colony-forming unit-granulocyte-macrophage (CFU-GM) by the CD8+,CD57+ subset was shown by 1 FS patie

65 colony-forming unit-granulocyte-macrophage (CFU-GM) colonies, whereas Flt3low cells produced mostly

66 colony-forming unit granulocyte-macrophage (CFU-GM) from normal and leukemic individuals.

67 colony-forming unit-granulocyte-macrophage (CFU-GM) from the CD34+CD38dim fraction by 14.5- +/- 5.6-

68 colony-forming unit granulocyte-macrophage (CFU-GM) myeloid progenitors to differentiate into cells

69 colony-forming unit-granulocyte-macrophage (CFU-GM) or CFU-megakaryocyte colony formation was observ

70 tial (CFU-GEMM), and granulocyte-macrophage (CFU-GM) progenitor-derived colony formation.

71 colony-forming unit-granulocyte-macrophage (CFU-GM) recovery 23%, and estimated tumor-cell depletion

72 colony-forming unit granulocyte-macrophage (CFU-GM) were relatively resistant to these treatments.

73 colony-forming unit-granulocyte-macrophage (CFU-GM), and a 12-fold to 17-fold increase of cobbleston

74 colony-forming unit-granulocyte-macrophage (CFU-GM)-derived, burst forming unit-erythroid (BFU-E)-de

75 colony-forming unit-granulocyte/macrophage (CFU-GM) and burst-forming unit-erythroid derived from CM

76 colony-forming units-granulocyte/macrophage (CFU-GM) in the graft products for the three dose levels

77 colony-forming unit-granulocyte/macrophage (CFU-GM), burst-forming unit-erythroid (BFU-E), and CFU-e

78 colony-forming unit-granulocyte-macrophage [CFU-GM(blood)]) and megakaryocytopoietic (blood CFU-mega

79 (colony-forming unit-granulocyte-macrophage [CFU-GM] and burst-forming unit-erythroid [BFU-E]).

80 (colony-forming unit-granulocyte-macrophage [CFU-GM]) progenitor cells.

81 (colony-forming unit-granulocyte-macrophage [CFU-GM]) showed a threefold increase in CFU-GM from ARH-

82 (colony-forming unit-granulocyte-macrophage [CFU-GM], colony-forming unit-megakaryocyte [CFU-Meg], an

83 colony forming unit-granulocyte-macrophage [CFU-GM]; 17% inhibition burst forming unit-erythroid [BF

84 colony-forming units-granulocyte/macrophage [CFU-GM]), and megakaryocyte (CFU-Meg) progenitor cell gr

85 (colony-forming unit-granulocyte macrophage; CFU-GM) proliferation.

86 ming units for granulocytes and macrophages (CFU-GM), and primitive progenitors, long term culture-in

87 Bone marrow CFU-GM, BFU-E, and CFU-E colony formation was significan

88 lized fraction remaining in the bone marrow (CFU-GM(femur) and CFU-Meg(femur)).

89 ed colony-forming unit-granulocyte/monocyte (CFU-GM) cells to have a strong affinity for SBA because

90 one marrow cells, as were significantly more CFU-GM, CFU-G, and CFU-M colonies.

91 marrow erythroid (CFU-E, BFU-E) and myeloid (CFU-GM) colony growth.

92 of IFNgamma on human CD34+-derived myeloid (CFU-GM) and erythroid (BFU-E) progenitors.

93 development of erythbroid (BFU-E), myeloid (CFU-GM), and primitive progenitor (CFU-GEMM, HPP-CFC, or

94 e suppressed the growth of leukemic myeloid (CFU-GM) progenitors from such patients, whereas concomit

95 Amplification of CML, but not normal, CFU-GM in vitro was significantly inhibited by IFN-alpha

96 The maximal number CFU-GM and CFU-GEMM were seen in PB on day 10, with 537-

97 HLA-A2.1 gene was found in the DNA of 56% of CFU-GM colonies derived from lentivirus-transduced SP ce

98 Proliferative capacities of CFU-GM, BFU-E, and CFU-GEMM were intact as colonies gene

99 s was >96% and yielded 2 degrees colonies of CFU-GM, BFU-E, and CFU-GEMM.

100 brogated the IGF-II-dependent enhancement of CFU-GM and long term culture-initiating cell numbers.

101 ws, rHuMig also abrogated SCF enhancement of CFU-GM numbers in cultures of CD34+ cells stimulated wit

102 ig, inhibited the production or expansion of CFU-GM.

103 Moreover, AXII enhanced the growth of CFU-GM, the earliest identifiable OCL precursor, when bo

104 concentrations, SNAP inhibited the growth of CFU-GM.

105 3 controls studied showed >40% inhibition of CFU-GM, and all but 2 showed at least some suppression.

106 U-E]) and 3.44 micromol/L (24% inhibition of CFU-GM; 57% inhibition BFU-E) of depsipeptide for 4 hour

107 5-FU plus LSF, release of this inhibitor of CFU-GM proliferation was blocked.

108 nd p21 gene deletion accelerated the loss of CFU-GM upon growth factor deprivation, and wild-type Sur

109 ndary colony formation provides a measure of CFU-GM amplification.

110 entration range, SNP increased the number of CFU-GM by up to 94%.

111 SBA showed a small but significant number of CFU-GM cells in the SBA(-) fraction.

112 transduction was apparent in the numbers of CFU-GM colonies formed in the presence or absence of Epo

113 ic and sustained increases in the numbers of CFU-GM per kilogram collected per harvest that represent

114 dary colony numbers as well as production of CFU-GM and BFU-E.

115 t and G-CSF in stimulating the production of CFU-GM colonies in a human bone marrow-derived CD34+ col

116 id LSF stimulate or inhibit proliferation of CFU-GM.

117 M) by 1.7- to 6.2-fold and the proportion of CFU-GM in S phase, compared to vector control.

118 ffects, Survivin increased the proportion of CFU-GM in S-phase in both p21+/+ and p21-/- cells.

119 t with IFN-alpha increased the proportion of CFU-GM, which lacked BCR-ABL.

120 feline marrow yields a marked separation of CFU-GM and BFU-E progenitors, select CCE SBA(-) fraction

121 th similar kinetics and magnitude to that of CFU-GM and CFU-GEMM.

122 increased in the same time frame as those of CFU-GM and CFU-GEMM in BM, spleen, and PB, although the

123 tors exert part of the inhibition by NK-A on CFU-GM.

124 By contrast, there was little effect on CFU-GM and BFU-E formulation or on long term culture ini

125 A similar suppressive effect was observed on CFU-GM number when ovariectomized rat marrow was treated

126 d the suppressive effect of trauma plasma on CFU-GM and BFU-E colony growth during the early but not

127 Ectopic Survivin enhanced p21+/+ CFU-GM formation and expansion of c-kit+, Lin- cells, wh

128 overexpression inhibited apoptosis of p21+/+ CFU-GM and c-kit+, Lin- cells but not p21-/- cells, sugg

129 The ability of patients' CFU-GM to amplify, and suppression of this ability by IF

130 rvivin construct decreased total and S-phase CFU-GM.

131 ionships between p21 and Survivin in primary CFU-GM and c-kit+, lineage-negative (Lin-) cells and dem

132 were cultured for hematopoietic progenitors (CFU-GM, BFU-E, and CFU-E colonies).

133 Granulocyte-macrophage progenitors (CFU-GM) were present only during the first three weeks o

134 this effect by inducing RANKL and promoting CFU-GM formation and osteoclastogenesis.

135 Replating CFU-GM colonies and observing secondary colony formation

136 aximal 123- and 108-fold increase in splenic CFU-GM and CFU-GEMM, respectively.

137 ced BM progenitor expansion, whereas splenic CFU-GM/CFU-granulocyte-erythrocyte-megakaryocyte-monocyt

138 Trauma plasma suppressed CFU-GM and BFU-E colony growth by 40% to 60% at all time

139 ne, or in combination with carboplatin, than CFU-GM and BFU-E.

140 gene transfer to approximately 30-50% of the CFU GM-derived colonies.

141 The CFU-GM content of the baseline aphereses correlated with

142 CE), a differential binding to SBA among the CFU-GM forming cells was found.

143 ult bone marrow contains the majority of the CFU-GM, a proportion of the CFU-Mix, and a minor populat

144 from AIDS BM patients are more inhibitory to CFU-GM than those from peripheral blood (p < 0.05).

145 it exerts varying degrees of suppression to CFU-GM, but minimal inhibition on erythroid colonies.

146 granulocyte-macrophage colony-forming unit (CFU-GM) (median slope per day, -0.57; P = .0008), and bu

147 Granulocyte-macrophage colony-forming unit (CFU-GM) analysis demonstrated subsequent acquisition of

148 granulocyte-macrophage colony-forming unit (CFU-GM) and erythroid burst-forming unit (BFU-E) colonie

149 or granulocyte-monocyte colony-forming unit (CFU-GM) and erythroid burst-forming unit (BFU-E) growth.

150 granulocyte macrophage colony-forming unit (CFU-GM) cell cycle and proliferation and have been impli

151 granulocyte-macrophage colony-forming unit (CFU-GM) colony growth in response to granulocyte-macroph

152 granulocyte-macrophage colony-forming unit (CFU-GM) compared with mPB were detected in the marrow of

153 granulocyte-macrophage colony-forming unit (CFU-GM) content were 7.73 x 10(4)/kg and 41.6 x 10(4)/kg

154 granulocyte macrophage-colony-forming unit (CFU-GM) formation by leukemic CD34(+) cells.

155 granulocyte macrophage-colony-forming unit (CFU-GM) growth, and elastase mutations cause cyclic and

156 granulocyte-macrophage colony-forming unit (CFU-GM) growth, macrophage progenitor proliferation, and

157 granulocyte macrophage-colony-forming unit (CFU-GM) progenitors from patients with chronic myelogeno

158 by granulocyte/monocyte-colony-forming unit (CFU-GM), complete blood count (CBC), and donor chimerism

159 granulocyte-macrophage colony-forming unit (CFU-GM).

160 granulocyte-macrophage colony-forming units (CFU-GM) and erythroid burst-forming units (BFU-E) were p

161 granulocyte macrophage-colony-forming units (CFU-GM) by 1.7- to 6.2-fold and the proportion of CFU-GM

162 granulocyte/macrophage colony-forming units (CFU-GM), responsive to stimulation by granulocyte/macrop

163 body weight (r = .7, P < .005) but not with CFU-GM per kilogram or nucleated cells per kilogram.