ライフサイエンスコーパス: myelodysplasia

1 ients develop late complications (especially myelodysplasia).

2 e anomalies and neutropenia, predisposing to myelodysplasia.

3 -type mice and 23 mouse models with verified myelodysplasia.

4 genes deleted in acute myeloid leukemias and myelodysplasia.

5 elapsed multiple myeloma, and 1 patient with myelodysplasia.

6 with a lower incidence of acute leukemia or myelodysplasia.

7 loid leukemia and the preleukemic condition, myelodysplasia.

8 ns of Pebp2 can contribute to the genesis of myelodysplasia.

9 tients with chronic granulocytic leukemia or myelodysplasia.

10 and autologous stem cell transplantation for myelodysplasia.

11 None had morphologic evidence of myelodysplasia.

12 assification; 50% of patients had underlying myelodysplasia.

13 , insertional mutagenesis led to leukemia or myelodysplasia.

14 partment in the bone marrow of patients with myelodysplasia.

15 s, such as leukocyte adhesion deficiency and myelodysplasia.

16 he only nonresponsive patient had underlying myelodysplasia.

17 a and is linked with genomic instability and myelodysplasia.

18 d management of an atypical BCR-ABL positive myelodysplasia.

19 ansfusions, including sickle cell anemia and myelodysplasia.

20 atopoietic stem cell function and results in myelodysplasia.

21 ion of APC contributes to the development of myelodysplasia.

22 enitors induced bone marrow dysfunction with myelodysplasia.

23 , high podosome turnover in macrophages, and myelodysplasia.

24 and ERCC6L2 patients, mild pancytopenia with myelodysplasia.

25 oablative CB transplantation for leukemia or myelodysplasia.

26 e pathogenesis of acute myeloid leukemia and myelodysplasia.

27 evelopmental programs in the pathogenesis of myelodysplasia.

28 g adults with acute leukemia in remission or myelodysplasia.

29 t chemotherapy regimens, developed secondary myelodysplasia.

30 have balanced rearrangement than those with myelodysplasia (28% vs 4%; P <.0001).

31 ients with aplastic anemia, 39 patients with myelodysplasia, 28 patients who had recently undergone b

32 AML derived from MPNs compared with LT after myelodysplasia (4.8%) or de novo AML (5.6%), respectivel

33 A changes resulting in amino acid changes in myelodysplasia (9 in 8 controls versus 16 in 10 patients

34 agnosis of PNH in about 20% of patients with myelodysplasia (a rate similar to that seen in patients

35 In particular, it is unclear if or how myelodysplasia (abnormal blood cell morphology), a key M

36 lymphoma and development of therapy-related myelodysplasia/acute leukemia (t-MDS/AML) among patients

37 Four patients developed treatment-related myelodysplasia/acute myelogenous leukemia, and three pat

38 in is expressed in blasts from patients with myelodysplasia/acute myeloid leukemia (MDS/AML) containi

39 Myelodysplasia/acute myeloid leukemia (MDS/AML) is chara

40 from 12 patients who subsequently developed myelodysplasia after HDC.

41 phoblastic leukemia during therapy, one with myelodysplasia after therapy, and two with brain tumors

42 incidence of severe adverse events, that is, myelodysplasia, AML, stem cell transplantation, or death

43 r, sickle cell disease, aplastic anemia, and myelodysplasia, among others.

44 lating hormone levels, 5 were diagnosed with myelodysplasia and 3 with solid tumors.

45 cations, except for the unique occurrence of myelodysplasia and acute megakaryocytic leukemia type 7.

46 urring anomalies associated with preleukemic myelodysplasia and acute myelogenous leukemia with a poo

47 f static neutropenia and a predisposition to myelodysplasia and acute myelogenous leukemia.

48 uring the blast phase and in therapy-related myelodysplasia and acute myelogenous leukemia.

49 (NHL) but is associated with therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) as

50 bes the magnitude of risk of therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) in

51 tion t(2;11)(p21;q23) found in patients with myelodysplasia and acute myeloid leukemia leads to an ov

52 w that osteoblast numbers decrease by 55% in myelodysplasia and acute myeloid leukemia patients.

53 therapy, notably hypomethylating agents, in myelodysplasia and acute myeloid leukemia.

54 developmental anomalies, a high incidence of myelodysplasia and acute nonlymphocytic leukemia, and ce

55 of treatment-related complications, one from myelodysplasia and another from cyclosporine-induced ren

56 used to analyze six additional patients with myelodysplasia and chromosomal rearrangements of the 7q2

57 f myelodysplasia and that male children with myelodysplasia and disturbance of immunologic function s

58 nostic scoring systems have been devised for myelodysplasia and for primary myelofibrosis.

59 Disruption of the SRF pathway results in myelodysplasia and immune dysfunction.

60 ctive of a myeloid neoplasm characterized by myelodysplasia and monocytosis, including but not limite

61 Therapy-related myelodysplasia and myeloid leukemia (t-MDS/t-AML) is a d

62 5q23-q31 interval are frequently observed in myelodysplasia and myeloid leukemia.

63 Responders included five of 11 patients with myelodysplasia and one of four patients with aplastic an

64 studies using progenitors from patients with myelodysplasia and provide functional support for clonal

65 reports common mutations in the TET2 gene in myelodysplasia and related myeloid malignancies, suggest

66 ociated with a significant risk of secondary myelodysplasia and secondary acute myeloblastic leukemia

67 ult female conditional UTX KO mice displayed myelodysplasia and splenic erythropoiesis, whereas UTX K

68 these results also suggest a novel cause of myelodysplasia and that male children with myelodysplasi

69 Myelodysplasia and the myeloproliferative disorders are

70 In myelodysplasias and acute myeloid leukemias, abnormaliti

71 icate the p38 MAPK in the pathophysiology of myelodysplasias and suggest that p38 pharmacologic inhib

72 luding 16 cases of acute myeloid leukemia, 3 myelodysplasia, and 1 chronic myeloid leukemia.

73 rlap disorders characterized by monocytosis, myelodysplasia, and a characteristic hypersensitivity to

74 ematologic cancers like multiple myeloma and myelodysplasia, and solid tumors like lung, breast, rena

75 ole for mitochondrial genomic instability in myelodysplasia, and they fail to reproduce previous repo

76 Recurring chromosomal translocations in myelodysplasia are rare, but the most frequent are the t

77 and chronic leukemia, lymphoma, myeloma, and myelodysplasia are transplanted each year worldwide usin

78 matopoiesis but developed progressive clonal myelodysplasia as they aged, culminating in myelodysplas

79 tween the different forms of therapy-related myelodysplasia as well as their genetic associations.

80 oach, we have shown that in individuals with myelodysplasia associated with alpha-thalassemia (ATMDS)

81 acute lymphoblastic leukemia, and five with myelodysplasia at times ranging from 11 months to 9 year

82 ome children to therapy-related leukemia and myelodysplasia, but that p53 mutations otherwise are inf

83 ve generated a murine model of EVI1-positive myelodysplasia by BM infection and transplantation.

84 In contrast, the disease myelodysplasia can be confused with aplasia and can also

85 Furthermore, end-stage mice develop myelodysplasia, characterized by proliferation of atypic

86 All subtypes of myelodysplasia, chronic myelomonocytic leukemia, and acu

87 gal, and viral infections is associated with myelodysplasia, cytogenetic abnormalities, pulmonary alv

88 ominant acute myelogenous leukemia (AML) and myelodysplasia for linkage to three potential candidate

89 to be recommended for patients with low-risk myelodysplasia for similar reasons.

90 Nine of 39 (23%) patients with myelodysplasia had GPI-anchored protein-deficient cells.

91 The genetic basis of myelodysplasia has long been enigmatic, with few common

92 Secondary myelodysplasia has occurred in one patient.

93 onmyelosuppressive alternative therapies for myelodysplasia have been studied.

94 ors is associated with myeloid leukemias and myelodysplasias; however, the mechanism by which such ov

95 with novel mutations, one who presented with myelodysplasia (Ile294Thr) and the other with classic SC

96 We find that certain features indicative of myelodysplasia in humans, such as Howell-Jolly bodies an

97 translocations associated with leukemias and myelodysplasias in humans.

98 ith hematologic malignancies associated with myelodysplasia, including myelodysplastic syndromes (MDS

99 centage) can be used to divide patients with myelodysplasia into those with better (International Pro

100 Myelodysplasia is a diagnostic feature of myelodysplasti

101 Myelodysplasia is a hematological disease in which genom

102 Myelodysplasia is being increasingly recognized as an im

103 he cumulative incidence of treatment-related myelodysplasia/ leukemia (t-AML) was calculated using th

104 cies have developed in 6 patients, including myelodysplasia/leukemia in four patients and solid tumor

105 d 1 or more of the following malignancies: 9 myelodysplasia/leukemia, 1 vulvar carcinoma and metastat

106 ients (each received seven cycles) developed myelodysplasia/leukemia.

107 ed in an immunodeficiency that progresses to myelodysplasia/leukemia.

108 es characterized by mycobacterial infection, myelodysplasia, lymphedema, or aplastic anemia that prog

109 tients with acute myeloid leukemia (AML) and myelodysplasia (MDS) after nonmyeloablative compared wit

110 RUNX1 gene are found in 10% of patients with myelodysplasia (MDS) and 30% of patients with acute myel

111 5, long arm, region 3, band 1, subband 1) in myelodysplasia (MDS) and acute myelogenous leukemia (AML

112 my of chromosomes 5, 7, and 17 in refractory myelodysplasia (MDS) and acute myelogenous leukemia (AML

113 malities seen in primary and therapy-induced myelodysplasia (MDS) and acute myelogenous leukemia (AML

114 nt in malignant myeloid disorders, including myelodysplasia (MDS) and acute myeloid leukemia (AML), s

115 common cytogenetic anomalies associated with myelodysplasia (MDS) and acute myeloid leukemia (AML).

116 , deletions, or monosomy are associated with myelodysplasia (MDS) and acute myeloid leukemia both in

117 b1 have been linked to many diseases such as myelodysplasia (MDS) and cancer.

118 ution to clonal hematologic diseases such as myelodysplasia (MDS) and leukemia, which is usually asso

119 n myeloid malignancies, but in most cases of myelodysplasia (MDS) and myeloproliferative neoplasms (M

120 Aplastic anemia (AA) and myelodysplasia (MDS) are forms of bone marrow failure th

121 component of allogeneic transplantations for myelodysplasia (MDS) or acute myelogenous leukemia (AML)

122 cells might underlie the pathophysiology of myelodysplasia (MDS) or paroxysmal nocturnal hemoglobinu

123 ndrome characterized by bone marrow failure, myelodysplasia (MDS), and acute myeloid leukemia (AML).

124 mphedema, mononuclear cytopenias, infection, myelodysplasia (MDS), and acute myeloid leukemia.

125 atients with acute myeloid leukemia (AML) or myelodysplasia (MDS), and in allogeneic hematopoietic ce

126 , inv(3)/t(3;3), complex karyotype (CK), and myelodysplasia (MDS)-related cytogenetic abnormalities (

127 roxysmal nocturnal hemoglobinuria (PNH), and myelodysplasia (MDS).

128 splantation is the only curative therapy for myelodysplasia (MDS).

129 second malignancies, but none have developed myelodysplasia (MDS).

130 rnal hemoglobinuria (PNH), and some forms of myelodysplasia (MDS).

131 ed (44 with acute myelogenous leukemia [AML]/myelodysplasia [MDS], 5 with chronic myelogenous leukemi

132 Mutations that affect myelodysplasia/myeloid leukemia factor (MLF) proteins ar

133 fusion gene between nucleophosmin (NPM) and myelodysplasia/myeloid leukemia factor 1 (MLF1) is forme

134 tion of the carboxy-terminal fusion partner, myelodysplasia/myeloid leukemia factor 1 (MLF1), is unkn

135 The myelodysplasia/myeloid leukemia factor 1-interacting pro

136 ), anemia (n = 1), thrombocytopenia (n = 1), myelodysplasia (n = 1), and hypersensitivity (n = 1).

137 er solid tumors n = 20), myeloid leukemia or myelodysplasia (n = 16), and lymphoma (n = 8).

138 atients with anemia associated with low-risk myelodysplasia not receiving chemotherapy; however, ther

139 high-risk acute myeloid leukemia or advanced myelodysplasia often relapse, underscoring the need to i

140 Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML)

141 Myelodysplasia or acute myelogenous leukemia was reporte

142 or malignancy, but seven patients developed myelodysplasia or acute myelogenous leukemia, four of th

143 ated with deaths from acute myeloid leukemia/myelodysplasia or cardiovascular events.

144 oietic toxicity was minimal, and no signs of myelodysplasia or leukemia were detected.

145 Progression to myelofibrosis, myelodysplasia or leukemic transformation, and bleeding

146 nce of cancer, progression to myelofibrosis, myelodysplasia or leukemic transformation, and hemorrhag

147 arrow function were noted; in particular, no myelodysplasia or marrow exhaustion was seen.

148 in the absence of morphological features of myelodysplasia or monocytosis.

149 patients with HIV infection, liver disease, myelodysplasia, or after plateletpheresis.

150 ve on occasion resulted in clonal expansion, myelodysplasia, or leukemogenesis.

151 The epidemiology of myelodysplasia, or myelodysplastic syndrome (MDS), is in

152 Patients with aplastic anemia, myelodysplasia, or renal allografts received antithymocy

153 uman-associated MDS, including multi-lineage myelodysplasia, pancytopenia, and occasional progression

154 of secondary AML or, if possible, high-risk myelodysplasia, particularly in patients with low periph

155 in which high-risk acute myeloid leukemia or myelodysplasia patients were immunized with irradiated,

156 myeloma patients and two of five assessable myelodysplasia patients.

157 patients with treatment-related leukemia or myelodysplasia performed consecutively at the Fred Hutch

158 idence for the benefits of iron chelation in myelodysplasia, pre-stem cell transplantation, and poten

159 e of GPI-anchored protein-deficient cells in myelodysplasia predicts responsiveness to immunosuppress

160 he patient was a 6-year-old girl with FA and myelodysplasia previously treated with oxymetholone and

161 al case of Philadelphia-positive, monosomy 7 myelodysplasia progressing to acute myeloid leukaemia in

162 our patients with advanced acute leukemia or myelodysplasia received a biodistribution dose of 0.5 mg

163 Twenty-seven adult patients with leukemia or myelodysplasia received FK506 starting the day before tr

164 with de-novo AML (n=206), therapy-related or myelodysplasia-related AML (n=12), or mixed-lineage leuk

165 ients (7.4%) and BCORL1 in AML patients with myelodysplasia-related changes (9.1%).

166 odysplastic syndromes (MDSs) and to AML with myelodysplasia-related changes (AML-MRC) is not clearly

167 ic leukemia, and acute myeloid leukemia with myelodysplasia-related changes were eligible for the stu

168 on has expanded this category into "AML with myelodysplasia-related changes" (AML-MRC).

169 ulation for therapy-related AML and AML with myelodysplasia-related changes, and resurgence of an ant

170 (median age 36 years, 12 therapy-related, 8 myelodysplasia-related) transplanted with chemotherapy-s

171 ) with secondary AML (17 therapy-related, 29 myelodysplasia-related) who had not received remission i

172 Myelodysplasia resulted and acute myelogenous leukaemia

173 on and direct sequencing in 10 patients with myelodysplasia; results were compared with concomitantly

174 ients with MDS reported to the International Myelodysplasia Risk Analysis Workshop (IMRAW) who receiv

175 ive neoplasms with nonmutated JAK2, in 8% of myelodysplasia samples, in occasional samples of other m

176 oblastic leukemia (ALL), and 3 patients with myelodysplasia samples.

177 ocumented only in cases of acute leukemia or myelodysplasia secondary to therapy with drugs targeting

178 st exclusively in cases of acute leukemia or myelodysplasia secondary to therapy with drugs that targ

179 ts at risk for treatment-related leukemia or myelodysplasia should be followed closely and be conside

180 a frequent finding in myeloid leukemias and myelodysplasias, suggesting the presence of a tumor supp

181 Thirty-one of 86 patients (36%) had occult myelodysplasia suggestive of tethered cord (27% of all p

182 Myelodysplasia syndrome (MDS) presenting as spontaneous

183 with myeloma and acute myeloid leukemia and myelodysplasia syndrome, and minimal with acute lymphobl

184 Treatment-related myelodysplasia (t-MDS) occurs less frequently with the n

185 to evaluate the incidence of therapy-related myelodysplasia (t-MDS) or therapy-related acute myeloid

186 such as therapy-related myeloid leukemia or myelodysplasia (t-ML).

187 anemia of inflammation and chronic disease, myelodysplasia, thalassemia, and malarial anemia.

188 d the t(X;21)(p22.3;q22.1) in a patient with myelodysplasia that fuses AML1 in-frame to the novel par

189 oxic therapy for chronic myeloid leukemia or myelodysplasia that had evolved into leukemia.

190 th all types of imperforate anus have occult myelodysplasia that may necessitate surgical interventio

191 atopoiesis by a few residual clones) or from myelodysplasia (the dominance of a neoplastic clone).

192 to respond to immunosuppressive therapy; in myelodysplasia, the presence of a PNH population was str

193 e 5 is the most common genetic aberration in myelodysplasia, the roles of several of the deleted gene

194 Patients with advanced morphology myelodysplasia tolerated the intensified BU/CY/TBI prepa

195 with recurrent acute myelogenous leukemia or myelodysplasia treated with radiolabeled antibodies, tot

196 s (5%) experienced fatal grade 5 toxicities (myelodysplasias, two patients; infection, one patient).

197 -cell transplantation early in the course of myelodysplasia using conditioning regimens such as BUCY-

198 Myelodysplasia was diagnosed in four patients in follow-

199 Children with DS and newly diagnosed AML or myelodysplasia were prospectively enrolled on Children's

200 Nine cases of acute myelogenous leukemia or myelodysplasia were reported on the sequential regimen a

201 No patient had developed secondary myelodysplasia, whereas transformation to high-grade lym

202 d a patient with mycobacterial infection and myelodysplasia who had an uncharacterized heterozygous d

203 by neutropenia, specific granule deficiency, myelodysplasia with excess of blast cells, and various d

204 The secondary leukemia presented as myelodysplasia with monosomies of chromosomes 5 and 7 an