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1 MDS and acute myeloid leukemia patient samples harboring
2 MDS stem and progenitor cells are characterized by key f
3 MDS-UPDRS Part I total mean (SD) scores increased from b
4 and its variant myelodysplastic syndrome 1 (MDS)/EVI encode zinc-finger proteins that have been reco
5 poietic neoplasm (4 MDS, 1 AML, 1 MPN, and 2 MDS/MPN) and 3 patients (1.1%) developed BM failure char
6 (2.9%) developed a hematopoietic neoplasm (4 MDS, 1 AML, 1 MPN, and 2 MDS/MPN) and 3 patients (1.1%)
8 responsiveness of LEN-resistant non-del(5q) MDS cells and AML cells, providing an explanation for th
9 next-generation sequencing in 94 non-del(5q) MDS patients randomized in the GFM-Len-Epo-08 clinical t
11 ata link Rps14 haploinsufficiency in del(5q) MDS to activation of the innate immune system and induct
13 encoded by a gene (CAST) deleted in del(5q) MDS, correlated with LEN responsiveness in patients with
20 cognition emerges as a molecular theme among MDS-relevant mutations of pre-mRNA splicing factors.
25 min walk ES=0.20 (95% CI -0.44 to 0.45) and MDS-UPDRS III ES=-0.30 (95% CI 0.07 to 0.54)) in favour
29 cerebral organoids derived from control and MDS-induced pluripotent stem cells (iPSCs) using time-la
30 technology, we have knocked out both EVI and MDS/EVI and have shown that EVI and MDS/EVI are not esse
31 el, we show here that high levels of EVI and MDS/EVI are expressed in the intestine at the climax of
32 EVI and MDS/EVI and have shown that EVI and MDS/EVI are not essential for embryogenesis and premetam
34 alis On the other hand, knocking out EVI and MDS/EVI causes severe retardation in the growth and deve
35 contrast to the established role of EVI and MDS/EVI in cancer development, their potential function
38 hematopoietic neoplasms (MDS, AML, MPN, and MDS/MPN) was calculated and adjusted for sex, age, and f
41 d significant replication of higher baseline MDS-UPDRS motor score, male sex, and increased age, as w
42 d with female sex (p=0.008), higher baseline MDS-UPDRS Part II scores (p<0.001) and more severe motor
43 There was a weak trend (P = 0.1) between MDS and large drusen; those in the highest category of M
44 (</=4 score), those in the highest category MDS adherence (>6 score) showed lower odds of nvAMD (odd
46 gous for either SAMD9L mutation, 3 developed MDS upon loss of the mutated SAMD9L allele following int
50 equivalent dose, sex, age, disease duration, MDS-UPDRS III score at the first assessment, duration of
53 pean Working Group of MDS in Childhood (EWOG-MDS) conducted in Germany over a period of 15 years.
57 sk and lower risk subjects were compared for MDS-UPDRS part III score (and derivations of this) to id
58 cytes are found, but diagnostic criteria for MDS or other hematologic diseases are not fulfilled, a c
60 hematopoietic stem-cell transplantation for MDS may inform prognostic stratification and the selecti
64 ectories (n = 39) in patients suffering from MDS (n = 52) and chronic myelomonocytic leukemia-1 (n =
66 [SD] age, 72.3 [15.6] years), 55 (64.0%) had MDS, 21 (24.4%) had de novo AML, and 10 (11.6%) had AML
67 ) or placebo (n=47); similar proportions had MDS (50 [51%] patients to eltrombopag, 22 (47%) patients
69 lso seen in a stage-specific manner in human MDS samples as well as in murine models of the disease.
72 These novel findings may help to identify MDS patients with a high risk of disease progression who
73 d Parkinson's Disease Rating Scale Part III (MDS-UPDRS III) score at the last assessment as the outco
75 equisite steps for induction of apoptosis in MDS cells and in acute myeloid leukemia (AML) cells.
78 ression (as assessed by the annual change in MDS-UPDRS score) into the final models of treatment effe
83 signaling pathways has been demonstrated in MDS HSPCs and is being targeted therapeutically in precl
86 ugh CRBN and IKZF1, has cytotoxic effects in MDS and AML that depend on a calcium- and calpain-depend
88 ates with UPDRS part III scores (increase in MDS-UPDRS per doubling of odds 0.52, 95% CI 0.31 to 0.72
89 Also, dyserythropoiesis was increased in MDS patients with the deletion of chromosome 11q23, wher
90 major contributor to cell-free DNA levels in MDS patients as a result of ineffective hematopoiesis.
91 first time, aberrantly expressed lncRNAs in MDS and further prioritize biologically relevant lncRNAs
92 The median number of aKIR genes was lower in MDS patients than healthy controls (2 vs 3 genes; P = .0
96 mphomyeloid HSC origin of SF3B1 mutations in MDS-RS patients and provide a novel in vivo platform for
98 ng System by enumerating blasts from NECs in MDS-E and in the overall MDS population reclassified app
101 blasts (RAEB)-2 diagnosis is not possible in MDS-E, as patients with 10% to < 20% BM blasts from TNCs
102 y role of the BMME to disease progression in MDS and support a therapeutic strategy whereby manipulat
115 ic cells, and we surmised that the malignant MDS genome would be a major contributor to cell-free DNA
116 N), myelodysplastic syndrome (MDS), or mixed MDS/MPN overlap syndrome (including chronic myelomonocyt
117 features of a pediatric unclassifiable mixed MDS/MPN and mimics many clinical manifestations of JMML
119 ia (AML), myeloproliferative neoplasm (MPN), MDS/MPN, or otherwise unexplained cytopenia (for >6 mo).
120 expression profiling of HSPCs from the MSI2 MDS mice identifies a signature that correlates with poo
121 (K700E) myeloid progenitors and SF3B1-mutant MDS patient samples demonstrate aberrant 3' splice-site
122 on into immune-deficient mice, SF3B1 mutated MDS-RS HSCs differentiated into characteristic ring side
125 ound in 10% of patients with myelodysplasia (MDS) and 30% of patients with acute myeloid leukemia (AM
127 expected number of hematopoietic neoplasms (MDS, AML, MPN, and MDS/MPN) was calculated and adjusted
132 rge drusen; those in the highest category of MDS had 20% reduced odds compared with those in the lowe
134 is sufficient to prevent the development of MDS in Apc(del/+) mice and that altered canonical WNT si
137 In this study, to investigate the effects of MDS on human progenitor subtypes that control neuronal o
138 nical vignettes showing specific features of MDS and AML in FA patients, this paper summarizes our pr
141 B1 in stromal cells from a high frequency of MDS/AML patients, a finding that together with our resul
142 ive studies of the European Working Group of MDS in Childhood (EWOG-MDS) conducted in Germany over a
146 understanding of the molecular landscape of MDS, coupled with the emergence of cost- and time-effect
147 ouse model of MDS results in a rapid loss of MDS haematopoietic stem and progenitor cells (HSPCs) and
149 itional deletion of Msi2 in a mouse model of MDS results in a rapid loss of MDS haematopoietic stem a
150 S in vivo using a transgenic murine model of MDS with hematopoietic expression of the translocation p
153 mutated genes central to the pathogenesis of MDS, which can be organized into a limited number of cel
157 udy, therefore, deepens our understanding of MDS cellular pathogenesis and highlights the broad utili
158 ent advances in our genetic understanding of MDS, with a particular focus on the emerging role for mu
160 trioxide (ATO) have demonstrated synergy on MDS treatment, but the treatment can cause significant s
161 We enrolled 84 adult patients with AML or MDS in a single-institution trial of decitabine to ident
162 on for thrombocytopenic patients with AML or MDS who are ineligible for other treatment and who are n
163 e findings reveal a novel role of EVI and/or MDS/EVI in regulating the formation and/or proliferation
164 d with the prognosis of patients with MDS or MDS/MPN, the role of ASXL1 in erythropoiesis remains unc
165 ults with low- or intermediate 1-risk MDS or MDS/myeloproliferative neoplasm (MPN), including chronic
166 ce develop myelodysplastic syndrome (MDS) or MDS and myeloproliferative neoplasms (MPN) overlapping d
167 blasts from NECs in MDS-E and in the overall MDS population reclassified approximately 9% of lower-ri
168 centre, open-label, dose-finding study (PACE-MDS), with long-term extension, eligible patients were a
170 Our data confirm that adult and pediatric MDS are separate diseases with disparate mechanisms, and
171 PK pathway mutations are common in pediatric MDS (45% of primary cohort), while mutations in RNA spli
172 he somatic and germline changes of pediatric MDS using whole exome sequencing, targeted amplicon sequ
174 on germline defect predisposing to pediatric MDS with a very high prevalence in adolescents with mono
175 cording to karyotype, 108 additional primary MDS patients registered with EWOG-MDS were studied.
176 ed for 15% of advanced and 7% of all primary MDS cases, but were absent in children with MDS secondar
177 MD9 or SAMD9L were present in 17% of primary MDS patients, and these variants were routinely lost in
179 t methylation and DNMTi treatment of primary MDS stroma enhanced its ability to support erythroid dif
183 ine GATA2 mutations in children with primary MDS was 7%, and 15% in those presenting with advanced di
185 +/-63% to +/-10% (tissue to background ratio MDS mean of 1.55, bias -0.05, limits of agreement -0.20
187 e common among patients with therapy-related MDS than those with primary MDS (15% vs. 3%, P<0.001).
188 ons a Hi-C dataset, performs high-resolution MDS separately on each partition, and then reassembles t
192 s or older, with intermediate-2 or high-risk MDS or AML, with bone marrow blasts of 50% or less, and
193 d leukemia (sAML; in comparison to high-risk MDS), FLT3, PTPN11, WT1, IDH1, NPM1, IDH2 and NRAS mutat
195 randomly assigned patients with higher-risk MDS and chronic myelomonocytic leukemia (CMML) 1:1:1 to
197 in high-risk MDS (in comparison to low-risk MDS), TP53, GATA2, KRAS, RUNX1, STAG2, ASXL1, ZRSR2 and
200 hort of patients with non-del(5q) lower-risk MDS treated with ESAs, none of the most commonly used se
202 ty Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor subscale (part 3) in the practically de
203 ty Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Part I score and other validated NMS scales a
204 ty Unified Parkinson's Disease Rating Scale (MDS-UPDRS) part III, of 208 individuals who had previous
206 ty Unified Parkinson's Disease Rating Scale, MDS-UPDRS III), fitness, health and well-being measured.
207 JAY to the popular multidimensional scaling (MDS) approach for visualization of small data sets drawn
208 n approximation of multidimensional scaling (MDS) that partitions a Hi-C dataset, performs high-resol
209 eviously published Mediterranean Diet Score (MDS) was used to classify participants according to thei
210 screened >600 cases of primary or secondary MDS in children and adolescents who were enrolled in the
211 c syndrome (MDS) and 82 cases with secondary MDS enrolled in 2 consecutive prospective studies of the
215 cents with primary myelodysplastic syndrome (MDS) and 82 cases with secondary MDS enrolled in 2 conse
220 athogenesis of the myelodysplastic syndrome (MDS) and are closely associated with clinical phenotype.
221 miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an e
223 nts diagnosed with myelodysplastic syndrome (MDS) and monosomy 7 harbor germline mutations in GATA2.
225 ases of late onset myelodysplastic syndrome (MDS) and/or acute myeloid leukemia (AML), suggesting tha
226 el(5q)) subtype of myelodysplastic syndrome (MDS) has been linked to heterozygous deletion of RPS14,
227 oblasts subtype of myelodysplastic syndrome (MDS) have mutations in Splicing Factor 3B, Subunit 1 (SF
231 (+/-) mice develop myelodysplastic syndrome (MDS) or MDS and myeloproliferative neoplasms (MPN) overl
232 low/intermediate-1 myelodysplastic syndrome (MDS) patients achieve an erythroid response with lenalid
233 stromal cells from myelodysplastic syndrome (MDS) patients and observed widespread aberrant cytosine
235 high-risk cases of myelodysplastic syndrome (MDS) showed far greater suppression of TEs than low-risk
236 f individuals with myelodysplastic syndrome (MDS) with deletion of chromosome 5q (del(5q)) to treatme
238 ed as diagnosis of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), myeloproliferative n
239 nal hematopoiesis, myelodysplastic syndrome (MDS), and acute myeloid leukemia (AML) and are associate
240 ing diseases, like myelodysplastic syndrome (MDS), develop preferentially in elderly individuals.
241 s with non-del(5q) myelodysplastic syndrome (MDS), lenalidomide promotes erythroid lineage competence
242 ve neoplasm (MPN), myelodysplastic syndrome (MDS), or mixed MDS/MPN overlap syndrome (including chron
246 e (aCML) is a rare myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) for which no curr
247 eukemia (JMML) are myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) overlap disorders
254 hematopoiesis of myelodysplastic syndromes (MDS) and its impact on response to drug therapy remain p
255 ng of genomics in myelodysplastic syndromes (MDS) and leukemias and the limitations of precision-medi
259 ted 5q lower-risk myelodysplastic syndromes (MDS) are treated with erythropoiesis-stimulating agents
262 with higher-risk myelodysplastic syndromes (MDS) but are less well-studied in lower-risk disease.
263 eukemia (CML) and myelodysplastic syndromes (MDS) either sensitive or resistant to their respective t
264 genetic basis of myelodysplastic syndromes (MDS) is heterogeneous, and various combinations of somat
265 acute leukemias, myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPNs), non-Hodgkin l
266 s of mutations in myelodysplastic syndromes (MDS), we investigated clonal dynamics using whole-exome
270 EEG/fMRI and multivariate dynamical systems (MDS) analysis to characterize network relationships betw
271 gether, these studies have demonstrated that MDS stem cells are functionally critical for the initiat
273 efect that was rescued when we corrected the MDS causative chromosomal deletion and severe apoptosis
274 apeutic strategy whereby manipulation of the MDS microenvironment may improve hematopoietic function
275 s used to investigate the association of the MDS score and AMD, taking account of potential confounde
276 eeks, off-medication scores on part 3 of the MDS-UPDRS had improved by 1.0 points (95% CI -2.6 to 0.7
279 ological presentation, and predisposition to MDS with -7/del(7q), whereas hematopoietic revertant mos
280 2 families with cytopenia, predisposition to MDS with chromosome 7 aberrations, immunodeficiency, and
281 ECs, 22% of patients with MDS-E and 12% with MDS from the whole series diagnosed within WHO categorie
282 We have used SF3b1 mutations associated with MDS to interrogate the role of the yeast ortholog, Hsh15
284 MDS cases, but were absent in children with MDS secondary to therapy or acquired aplastic anemia.
286 ))-which commonly occurs in individuals with MDS and AML-in an inducible, hemizygous manner in hemato
289 ll survival after HSCT in both patients with MDS and patients with MDS/AML (P values ranging from .00
291 sociated with the prognosis of patients with MDS or MDS/MPN, the role of ASXL1 in erythropoiesis rema
294 fore transplantation from 1514 patients with MDS who were enrolled in the Center for International Bl
296 stematically from NECs, 22% of patients with MDS-E and 12% with MDS from the whole series diagnosed w
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