ライフサイエンスコーパス: thrombocytosis

1 ng paquinimod), all reduced diabetes-induced thrombocytosis.

2 es that are somatically mutated in essential thrombocytosis.

3 marrow and are reflected by neutrophilia and thrombocytosis.

4 and proliferation, resulting in reticulated thrombocytosis.

5 der, that is, polycythemia vera or essential thrombocytosis.

6 e diagnosis of ET associated with borderline thrombocytosis.

7 in JAK2-negative myelofibrosis and essential thrombocytosis.

8 topoiesis, and bone marrow fibrosis, but not thrombocytosis.

9 xpression of Mpl and a clinical phenotype of thrombocytosis.

10 changes, edema, sclerotic bone lesions, and thrombocytosis.

11 and in the other in the setting of essential thrombocytosis.

12 ant feature was the development of a chronic thrombocytosis.

13 consensus exists regarding the treatment of thrombocytosis.

14 ncy, thymic hypoplasia, megakaryocytosis and thrombocytosis.

15 guish between primary and secondary forms of thrombocytosis.

16 35.4%) were the primary agents used to treat thrombocytosis.

17 sive organomegaly, leukocytosis, anemia, and thrombocytosis.

18 muscle contractility, low blood pressure and thrombocytosis.

19 th treatment response and thrombotic risk in thrombocytosis.

20 associated with thrombotic complications in thrombocytosis.

21 ss thrombosis risk and treatment response in thrombocytosis.

22 y did not have pretreatment splenomegaly and thrombocytosis.

23 yeloproliferative disorders versus secondary thrombocytosis.

24 R) and who had pretreatment splenomegaly and thrombocytosis.

25 cytokine that is implicated in inflammatory thrombocytosis.

26 ation in JAK2V617I-positive individuals with thrombocytosis.

27 rrow compartment and the VEGF-A(165)-induced thrombocytosis.

28 as an underlying mechanism of paraneoplastic thrombocytosis.

29 the underlying mechanisms of paraneoplastic thrombocytosis.

30 iesis, resulting in lymphopenia, anemia, and thrombocytosis.

31 2-V617F-mediated polycythemia vera/essential thrombocytosis.

32 eletion syndrome characterized by anemia and thrombocytosis.

33 ion seen in 5q- syndrome, it does not affect thrombocytosis.

34 rrow trephine specimens of 183 patients with thrombocytosis-164 with essential thrombocythemia (ET),

35 brosis, but not in 4 patients with essential thrombocytosis, 3 with chronic myelogenous leukemia, 6 w

36 patients; musculoskeletal pain, 5 patients; thrombocytosis, 4 patients; edema, 3 patients; diarrhea

37 ion in 83 patients with chronic or transient thrombocytosis, 46 patients with deep vein (DVT) or arte

38 wn function, into Ldlr(-/-) mice resulted in thrombocytosis, accelerated thrombosis and atheroscleros

39 ozygous CALR(del/del) mice developed extreme thrombocytosis accompanied by features of MF, including

40 In addition to the expected thrombocytosis after 7 to 10 days of daily injection of

41 inhibition may represent a new treatment for thrombocytosis and clotting disorders.

42 zing expression patterns in 79 subjects with thrombocytosis and controls, and integrated data with tr

43 karyocytopoiesis and myelopoiesis leading to thrombocytosis and granulocytosis.

44 K2V617I mutation in a family with hereditary thrombocytosis and herein characterize the hematopoietic

45 ve disorder in JAK2 and MPL wt patients with thrombocytosis and may have prognostic and therapeutic r

46 n approximately half of those with essential thrombocytosis and myelofibrosis.

47 Thrombocytosis and platelet hyperreactivity are known to

48 between PMF and polycythemia vera/essential thrombocytosis and reveal methylomic signatures of ASXL1

49 orate the course of MPN, but rather enhanced thrombocytosis and shortened the overall survival.

50 t and haemoglobin electrophoresis to exclude thrombocytosis and sickle cell anaemia, and serum angiot

51 a define a dysregulated miRNA fingerprint in thrombocytosis and support a developmentally restricted

52 s were associated with polyclonal hereditary thrombocytosis and triple-negative MPNs.

53 ith Down syndrome (DS) display macrocytosis, thrombocytosis, and a 500-fold increased risk of develop

54 CMV/IL-33 mice also suffer from anemia, thrombocytosis, and a marked dysregulation of myelopoies

55 K2 mutations in polycythemia vera, essential thrombocytosis, and chronic idiopathic myelofibrosis.

56 in inflammation (reduction in leukocytosis, thrombocytosis, and circulating interleukin-6 levels), r

57 21-miRNA genetic fingerprint associated with thrombocytosis, and demonstrated that a 3-member subset

58 le, ring sideroblasts associated with marked thrombocytosis, and juvenile myelomonocytic leukemia, ar

59 Antibiotic-treated mice exhibited anemia, thrombocytosis, and leukopenia, with pronounced pan-lymp

60 asms, including polycythemia vera, essential thrombocytosis, and myelofibrosis, are disorders charact

61 methylation in polycythemia vera, essential thrombocytosis, and PMF samples compared with healthy co

62 ative disorders polycythemia vera, essential thrombocytosis, and primary myelofibrosis are clonal dis

63 did not compromise PLT formation but caused thrombocytosis, and resulted in expansion of MK progenit

64 ypoplasia, and megakaryocytic dysplasia with thrombocytosis, and that p53 plays a critical role in ma

65 oiesis seen in patients who develop reactive thrombocytosis, and these cytokines also are known to re

66 ing in hepatic fibrosis, transient postnatal thrombocytosis, anemia, a gene expression profile that i

67 c-Myc(-/-) mice develop a syndrome of severe thrombocytosis-anemia-leukopenia because of significant

68 The IL-6-dependent colitis-induced thrombocytosis appears to result from an enhancement of

69 ermined that polycythemia vera and essential thrombocytosis are characterized by aberrant promoter hy

70 teria for distinguishing among etiologies of thrombocytosis are limited in their capacity to delineat

71 e significantly elevated in patients who had thrombocytosis as compared with those who did not.

72 < or = PHR and pretreatment splenomegaly or thrombocytosis at 3 months had such a low major cytogene

73 he majority of patients with leukocytosis or thrombocytosis at baseline (n = 28 and n = 10, respectiv

74 s had a nadir at day 3 followed by a rebound thrombocytosis at day 21, with nadir values significantl

75 Thrombocytosis, bone marrow megakaryocytic proliferation

76 Transgene rescued mice exhibit thrombocytosis but only partial correction of the stem c

77 ase, manifesting either as erythrocytosis or thrombocytosis, can be initiated clonally from a single

78 stinct genetic biomarker subsets can predict thrombocytosis class using routine phlebotomy.

79 atelet transcriptome sequencing and extended thrombocytosis cohort analyses identified a single loss-

80 loped to assign phenotypic class between the thrombocytosis cohorts, and by JAK2 genotype.

81 unts revealed a profound reticulocytosis and thrombocytosis despite normal serum Epo levels and blood

82 -risk essential thrombocythemia (ET) address thrombocytosis, disease-related symptoms, as well as ris

83 a lesser extent, CALRins5 (type II) induced thrombocytosis due to a megakaryocyte (MK) hyperplasia.

84 We speculate that countering paraneoplastic thrombocytosis either directly or indirectly by targetin

85 lar volume overload, sclerotic bone lesions, thrombocytosis, elevated VEGF, and abnormal pulmonary fu

86 the MPN polycythemia vera (PV) and essential thrombocytosis (ET) by disrupting JAK2 protein stability

87 diopathic myelofibrosis (IMF), and essential thrombocytosis (ET).

88 as to define the contribution of IL-6 to the thrombocytosis, exaggerated agonist-induced platelet agg

89 > or = 5 cm below the costal margin (BCM) or thrombocytosis > or = 700 x 10(9)/L pretreatment added s

90 dy mass index (BMI; >/=25 kg/m(2)), ascites, thrombocytosis (>400,000 cells/mm(3)), albumin (<3.0 g/d

91 V617F transgenic mice with thrombocytosis had higher serum levels of IFNgamma than

92 Ovarian cancer patients with thrombocytosis had higher tumor proliferation indices co

93 ll 19 patients with familial polycythemia or thrombocytosis had polyclonal hematopoiesis, whereas 22

94 dic thrombocythemia (ST), 16 with hereditary thrombocytosis (HT), 11 with sporadic polycythemia (SP),

95 NF-E2 function and cause erythrocytosis and thrombocytosis in a murine model.

96 logist for evaluation of persistent isolated thrombocytosis in March 2012.

97 The mechanisms of paraneoplastic thrombocytosis in ovarian cancer and the role that plate

98 d hepatic thrombopoietin were also linked to thrombocytosis in patients.

99 g thrombopoietin and interleukin-6 abrogated thrombocytosis in tumor-bearing mice.

100 was essential for the CALR mutants to induce thrombocytosis in vivo, although Tpo contributes to dise

101 f these serious adverse events, headache and thrombocytosis, in one (2%) of 42 patients in the romipl

102 The mechanisms behind the hereditary thrombocytosis induced by the thrombopoietin (THPO) rece

103 AP1 in cancer cells in vivo protects against thrombocytosis-induced increase in metastasis.

104 Thrombocytosis is a common complication of rheumatoid ar

105 of essential thrombocythemia and hereditary thrombocytosis is acquired, and germ-line-activating mut

106 Thrombocytosis is an unexpected consequence of reduced M

107 Relative thrombocytosis is associated with a worse MICS profile,

108 Thrombocytosis is associated with inflammation, and cert

109 Paraneoplastic thrombocytosis is associated with many solid tumors and

110 Thrombocytosis is often observed in gastrointestinal, lu

111 What initiates this reactive thrombocytosis is poorly understood.

112 Thrombocytosis is present in more than 30% of patients w

113 n to their role in rheumatoid arthritis with thrombocytosis, it has been demonstrated recently that m

114 ice exhibit many features of MPNs, including thrombocytosis, leukocytosis, Epo-independent colony for

115 iculocytosis, leukocytosis, neutrophilia and thrombocytosis, marked expansion of erythroid progenitor

116 tive disease (MPD) characterized by profound thrombocytosis, megakaryocyte hyperplasia, dysplastic me

117 s of the c-Myb(M303V/M303V) mutation include thrombocytosis, megakaryocytosis, anemia, lymphopenia, a

118 leukocytes), and aberrant expression during thrombocytosis, most profound in ET.

119 current smoking, Killip class >/=2, baseline thrombocytosis, multivessel disease, symptom onset-to-ba

120 eveloped a significant MPN, characterized by thrombocytosis, neutrophilia, and splenomegaly.

121 edefined factors in the IMDC model (anaemia, thrombocytosis, neutrophilia, Karnofsky performance stat

122 stantial enlargement of the liver and marked thrombocytosis occurred in 16.1% and 22.0% of the patien

123 Eighty-two percent of physicians treated thrombocytosis only when platelet counts exceeded 1000 x

124 as a markedly worse prognosis than essential thrombocytosis or polycythemia vera, the molecular disti

125 ts presence excludes secondary polycythemia, thrombocytosis, or bone marrow fibrosis from other cause

126 ited reciprocal reductions during periods of thrombocytosis (P < .07).

127 Decreased DLCO was associated with thrombocytosis (p = 0.05), with hepatic dysfunction (ele

128 absolute RP counts than asymptomatic chronic thrombocytosis patients (98 +/- 64 x 10(9)/L [range, 54

129 0.1%, mean +/- SD) than asymptomatic chronic thrombocytosis patients (n = 23, RP% = 3.4% +/- 1.8%), h

130 y) when compared with asymptomatic transient thrombocytosis patients (n = 40, 4.5% +/- 2.7% and 35 +/

131 Chronic thrombocytosis patients presenting with thrombosis (n =

132 Follow-up studies in seven chronic thrombocytosis patients showed that successful aspirin t

133 bsolute RP counts compared with only 1 of 63 thrombocytosis patients who remained asymptomatic.

134 In addition, 7 of 8 thrombocytosis patients who were studied before developi

135 absolute counts were also noted in transient thrombocytosis patients with thrombosis (n = 6, 11.5% +/

136 Chronic thrombocytosis patients with thrombosis also had signifi

137 nts remained significantly higher in chronic thrombocytosis patients with thrombosis when patients we

138 Here, we report that the thrombocytosis phenotype induced by MPL P106L belongs to

139 d in Mpl(-/-) mice, MPL P106L could induce a thrombocytosis phenotype with high circulating THPO leve

140 ypothesized that ESRD patients with relative thrombocytosis (platelet count >300 x 10(3)/muL) have a

141 ese findings indicate that IL-6 mediates the thrombocytosis, platelet hyperreactivity, and accelerate

142 ractions between tumor growth/metastasis and thrombocytosis/platelet activation.

143 yeloproliferative neoplasms (MPNs) essential thrombocytosis, polycythemia vera, and primary myelofibr

144 ssic myeloproliferative neoplasms--essential thrombocytosis, polycythemia vera, and primary myelofibr

145 e have identified 2 families with hereditary thrombocytosis presenting novel heterozygous germ-line m

146 sideroblasts (RARS) and RARS associated with thrombocytosis (RARS-T), 2 distinct subtypes of MDS and

147 fractory anemia with ringed sideroblasts and thrombocytosis (RARS-T).

148 milial forms of nonclonal erythrocytosis and thrombocytosis, respectively.

149 The thrombocytosis response was absent in IL-6(-/-) mice.

150 ntial thrombocythemia (ET), 19 with reactive thrombocytosis (RT)-for bone marrow angiogenesis, bone m

151 rombocythemia [ET]) from nonclonal (reactive thrombocytosis [RT]) etiologies.

152 s miR-145 and miR-146a may contribute to the thrombocytosis seen in the 5q- syndrome.

153 it, increased red blood cells, leukocytosis, thrombocytosis, splenomegaly, reduced serum erythropoiet

154 icantly and modulated 5-fluorouracil-induced thrombocytosis strongly, suggesting a regulatory role fo

155 loss, and rheumatoid arthritis patients with thrombocytosis tend to have more severe disease.

156 tients with type 2 diabetes have reticulated thrombocytosis that correlates with glycated hemoglobin

157 e a germline mutation that leads to familial thrombocytosis that involves a residue other than Val617

158 s that in rheumatoid arthritis with reactive thrombocytosis, the ability of the cytokines to enhance

159 Celiac disease may also be associated with thrombocytosis, thrombocytopenia, leukopenia, venous thr

160 Thus, CALR mutants are sufficient to induce thrombocytosis through MPL activation.

161 an often indolent course, and (in essential thrombocytosis) usually a normal life span.

162 The thrombocytosis was associated with an increased risk of

163 However, the thrombocytosis was less sustained after single versus da

164 ained in JAK2V617F(+)Tpo(-/-) mice, although thrombocytosis was reduced compared with JAK2V617F(+) mi

165 Thrombocytosis was significantly associated with advance

166 To augment current diagnostic studies for thrombocytosis, we retrospectively evaluated clinical re

167 Leukocytosis and thrombocytosis were also detected in infected gerbils, i

168 ted genes in polycythemia vera and essential thrombocytosis were involved predominantly in cell signa

169 mical inhibitors could promote a paradoxical thrombocytosis when used at suboptimal doses.

170 umor and host tissue leads to paraneoplastic thrombocytosis, which fuels tumor growth.

171 a transplantable ET-like disease with marked thrombocytosis, which is associated with increased and m

172 mice displayed profound megakaryocytosis and thrombocytosis with a remarkable expansion of megakaryoc

173 DSS colitis in WT mice was associated with thrombocytosis with an elevated number of both mature an

174 Both murine models exhibited thrombocytosis with increased megakaryocytes and megakar

175 routine blood work in June 2011 to have mild thrombocytosis, with a platelet count of 405,000.

176 lungs during stimulated as well as reactive thrombocytosis without precluding observations that some