ライフサイエンスコーパス: myelodysplasia

1 ients develop late complications (especially myelodysplasia).

2 t chemotherapy regimens, developed secondary myelodysplasia.

3 and ERCC6L2 patients, mild pancytopenia with myelodysplasia.

4 genes deleted in acute myeloid leukemias and myelodysplasia.

5 g adults with acute leukemia in remission or myelodysplasia.

6 elapsed multiple myeloma, and 1 patient with myelodysplasia.

7 with a lower incidence of acute leukemia or myelodysplasia.

8 loid leukemia and the preleukemic condition, myelodysplasia.

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

10 tients with chronic granulocytic leukemia or myelodysplasia.

11 and autologous stem cell transplantation for myelodysplasia.

12 e anomalies and neutropenia, predisposing to myelodysplasia.

13 None had morphologic evidence of myelodysplasia.

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

15 partment in the bone marrow of patients with myelodysplasia.

16 with other hematologic malignancies such as myelodysplasia.

17 phedema, pulmonary alveolar proteinosis, and myelodysplasia.

18 , insertional mutagenesis led to leukemia or myelodysplasia.

19 s, such as leukocyte adhesion deficiency and myelodysplasia.

20 he only nonresponsive patient had underlying myelodysplasia.

21 a and is linked with genomic instability and myelodysplasia.

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

23 ansfusions, including sickle cell anemia and myelodysplasia.

24 atopoietic stem cell function and results in myelodysplasia.

25 ion of APC contributes to the development of myelodysplasia.

26 enitors induced bone marrow dysfunction with myelodysplasia.

27 , high podosome turnover in macrophages, and myelodysplasia.

28 oablative CB transplantation for leukemia or myelodysplasia.

29 assification; 50% of patients had underlying myelodysplasia.

30 e pathogenesis of acute myeloid leukemia and myelodysplasia.

31 evelopmental programs in the pathogenesis of myelodysplasia.

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

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

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

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

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

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

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

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

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

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

42 from 12 patients who subsequently developed myelodysplasia after HDC.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 mly assigned patients with acute leukemia or myelodysplasia and an HLA-matched donor to receive CD34-

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

59 oid-restricted cells and manifests with both myelodysplasia and autoinflammation, and could give insi

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

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

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

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

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

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

66 5q23-q31 interval are frequently observed in myelodysplasia and myeloid leukemia.

67 versy regarding diagnosis in the spectrum of myelodysplasia and myeloid leukemia.

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

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

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

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

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

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

74 Myelodysplasia and the myeloproliferative disorders are

75 In myelodysplasias and acute myeloid leukemias, abnormaliti

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

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

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

79 Myb insufficiency in mice that leads to MPN, myelodysplasia, and leukemia in later life, mirroring th

80 deficiency, infections, bone marrow failure, myelodysplasia, and monosomy 7.

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

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

83 xicity, alcohol abuse, antibiotic treatment, myelodysplasia, and VEXAS syndrome.

84 mmunodeficiency virus (SIV) infection causes myelodysplasia, anemia, and accumulation of inflammatory

85 RTANCE HIV-1 and SIV infection often lead to myelodysplasia, anemia, and accumulation of inflammatory

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

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

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

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

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

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

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

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

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

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

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

97 Recently described myelodysplasia cutis (MDS-cutis) is a cutaneous manifest

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

99 iesis in Diamond Blackfan anemia and del(5q) myelodysplasia, disorders with excessive heme in colony-

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

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

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

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

104 Secondary myelodysplasia has occurred in one patient.

105 onmyelosuppressive alternative therapies for myelodysplasia have been studied.

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

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

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

109 (MDS-cutis) is a cutaneous manifestation of myelodysplasia in which clonal myelodysplastic cells inf

110 translocations associated with leukemias and myelodysplasias in humans.

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

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

113 Myelodysplasia is a diagnostic feature of myelodysplasti

114 Myelodysplasia is a hematological disease in which genom

115 Myelodysplasia is being increasingly recognized as an im

116 w (BM) failure, developmental abnormalities, myelodysplasia, leukemia, and solid tumor predisposition

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

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

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

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

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

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

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

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

125 5, long arm, region 3, band 1, subband 1) in myelodysplasia (MDS) and acute myelogenous leukemia (AML

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

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

128 ipilimumab and decitabine for patients with myelodysplasia (MDS) and acute myeloid leukemia (AML) be

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

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

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

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

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

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

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

136 h high-risk acute myeloid leukemia (AML) and myelodysplasia (MDS) but are associated with a high risk

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

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

139 lo-SCT) for acute myeloid leukemia (AML) and myelodysplasia (MDS) remain limited, and novel treatment

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

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

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

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

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

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

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

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

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

149 d risk of developing a myeloid neoplasm with myelodysplasia (MN).

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

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

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

153 The myelodysplasia/myeloid leukemia factor 1-interacting pro

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

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

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

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

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

159 Myelodysplasia or acute myelogenous leukemia was reporte

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

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

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

163 n was lymphopenia (14%) with no incidence of myelodysplasia or leukemia.

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

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

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

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

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

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

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

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

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

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

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

175 therapy (32 R/R, 2 treatment-naive AML and 2 myelodysplasia patients) was well-tolerated and a loadin

176 myeloma patients and two of five assessable myelodysplasia patients.

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

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

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

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

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

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

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

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

185 Black patients with myelodysplasia-related AML were younger than white patie

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

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

188 ted acute myeloid leukemia (AML) or AML with myelodysplasia-related changes based on improved overall

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

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

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

192 ted acute myeloid leukemia (AML) or AML with myelodysplasia-related changes, because it improves surv

193 ), complex karyotype/monosomal karyotype, or myelodysplasia-related gene mutations with/without mutat

194 erse-risk (57.3%), mutated TP53 (14.4%), and myelodysplasia-related genetic features (65.1%).

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

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

197 eled as having idiopathic aplastic anemia or myelodysplasia represent cryptic cases of inherited BM f

198 herapy for selected patients with lower risk myelodysplasia requiring transfusion despite erythropoie

199 Myelodysplasia resulted and acute myelogenous leukaemia

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

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

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

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

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

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

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

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

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

209 Myelodysplasia syndrome (MDS) presenting as spontaneous

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

211 es at week 20 by International Working Group Myelodysplasia Syndromes/Neoplasms criteria.

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

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

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

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

216 tosis, thalassemia, sickle cell disease, and myelodysplasia that can lead to progressive fibrosis and

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

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

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

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

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

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

223 ts (median age, 68-years) with AML/high-risk myelodysplasia to GO on day 1 (GO1) or on days 1 and 4 (

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

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

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

227 e (aGVHD) in patients with acute leukemia or myelodysplasia undergoing matched sibling donor (MSD) or

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

229 Myelodysplasia was diagnosed in four patients in follow-

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

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

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

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

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

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

236 of mutant IDH2 and SRSF2 resulted in lethal myelodysplasia with proliferative features in vivo and e

237 Although Bap1KO mice develop myelodysplasia with prominent dyserythropoiesis, combine