ライフサイエンスコーパス: hematological

1 including cutaneous (4%), psychiatric (4%), hematological (6%), and other AEs (6%).

2 s and tubular aggregate myopathy but without hematological abnormalities.

3 Hematological analyses indicated a drop in platelet coun

4 are associated with substantially different hematological and clinical features and define a distinc

5 followed by laboratory evaluation of routine hematological and hepato-renal parameters, abdomino-pelv

6 y functions and harbors mutations underlying hematological and immunological diseases.

7 niche and loss of HSCs, contributing to the hematological and immunological dysfunctions and reduced

8 ith no new vascular events and resolution of hematological and immunological phenotype at a median fo

9 ne marrow fibrosis (BMF) develops in various hematological and non-hematological conditions and is a

10 nesis as a promoter of cell survival in both hematological and nonhematological malignancies.

11 ion of vitamin C deficiency in patients with hematological and other cancers may improve responses to

12 activated inappropriately in a wide range of hematological and solid cancers, but clinically availabl

13 tch signaling is known to be associated with hematological and solid cancers.

14 A handful of trials are targeting non-CD19 hematological and solid malignancies and represent the v

15 of CARs and reviews the clinical studies in hematological and solid malignancies that are beginning

16 us immune escape pathways are shared between hematological and solid malignancies, several unique pat

17 itors (HDACis) have demonstrated activity in hematological and solid malignancies.

18 ion 3 (STAT3) is dysregulated in a number of hematological and solid malignancies.

19 generally expressed at low levels on various hematological and solid tissues, while plasma cells expr

20 y of cell lines in the NCI panel of 60 human hematological and solid tumor cell lines.

21 d peptide that is an immunotherapy target in hematological and solid tumor malignancies.

22 antitumor activity in a broad range of both hematological and solid tumor models.

23 d has the potential to treat various B7H6(+) hematological and solid tumors.

24 n significant therapeutic potential for both hematological and solid tumors.

25 simulation tool over a range of hemodynamic, hematological, and anticoagulation conditions could assi

26 to their established systemic pigmentation, hematological, and lung phenotypes.

27 Parasitological, hematological, and micronutrient data were obtained from

28 Post-HSCT hematological autoimmunity (cytopenias) was reported in

29 Medical records, hematological, biochemical, and anthropometric measureme

30 h global BMF, and one individual developed a hematological cancer (acute myeloid leukemia) in childho

31 hly specific and selective identification of hematological cancer cells and for detection of minimal

32 genes, and the viability of STAT3-dependent hematological cancer cells.

33 Multiple myeloma (MM) is a hematological cancer for which immune-based treatments a

34 prostate, thyroid, non-Hodgkin lymphoma, or hematological cancer in either group.

35 tigated whether mLOY was associated with non-hematological cancer in three prospective cohorts (8,679

36 terval (CI) = 1.17-3.13; 637 events) and non-hematological cancer mortality (HR = 3.62, 95% CI = 1.56

37 l-but not maternal-age at birth and sporadic hematological cancer risk.

38 Acute Myeloid Leukemia (AML) is a fatal hematological cancer.

39 002).There were no differences by subtype of hematological cancer.

40 pound currently in human clinical trials for hematological cancers and solid tumors.

41 ric antigen receptor (CAR) T cells targeting hematological cancers has yielded impressive clinical re

42 ention Study-II participants, 2,532 incident hematological cancers were identified between 1992 and 2

43 In hematological cancers, the relevance of ongoing DNA dama

44 ) represent a valid treatment option in some hematological cancers, triggering clinically relevant im

45 However, for hematological cancers, which develop and disseminate qui

46 so be relevant for clinical imaging of other hematological cancers.

47 Two compounds are already approved to treat hematological cancers.

48 gnized as an important therapeutic target in hematological cancers.

49 gents for treating inflammatory diseases and hematological cancers.

50 sferase 3A (DNMT3A) is frequently mutated in hematological cancers; however, the underlying oncogenic

51 armacological profiling across more than 100 hematological cell line models identified a subset of MC

52 AK-STAT and HDAC pathway blockade in several hematological cell lines, inhibition of colony formation

53 ion of JAK-STAT and HDAC pathway blockade in hematological cell lines.

54 New reports of hematological changes associated with altitude and cold

55 Mouse and rat studies showed hematological changes with elevations of plasma EPO and

56 tcomes were improvement in immunological and hematological characteristics and evidence of safety thr

57 lusion of leukemia epigenomes in the healthy hematological chromatin sample space gives us insights o

58 F) develops in various hematological and non-hematological conditions and is a central pathological f

59 index (RMI) have shown value in a variety of hematological conditions.

60 cy encourage clinical studies to explore the hematological consequences of HNF1A deficiency in human

61 signaling during embryogenesis leads to the hematological defects seen later in life in FA.

62 s with high-risk hematopoietic malignancies, hematological deficiencies, and other immune diseases.

63 Hematological diagnosis was monoclonal gammopathy of ren

64 Myelodysplastic syndrome is a rare, chronic hematological disease characterized by heterogeneous cli

65 ical IGF1R inhibitory strategies prevent the hematological disease found in AIRAPL-deficient mice as

66 e transfusion requirement is an indicator of hematological disease severity and predictor of decrease

67 A hematological disease transcriptomic signature and incre

68 solid organ tolerance, cure of non-malignant hematological disease, and HIV reservoir clearance.

69 ht serve as an early indicator of underlying hematological disease.

70 Acute hematological diseases (leukemias and aggressive lymphom

71 involved in the pathogenesis of a variety of hematological diseases and in regulating the function of

72 ture of risk factors for cardiometabolic and hematological diseases and provide additional functional

73 eived an allogeneic BMT for the treatment of hematological diseases developed liver dysfunction with

74 Triapine showed anticancer activity against hematological diseases, however, studies on solid tumors

75 e exploited for therapeutic applications for hematological diseases, including anemia.

76 In various in vivo models of hematological diseases, loss of STAT3 in NK cells enhanc

77 system for modeling a wide variety of human hematological diseases.

78 splantation (HSCT) is a common treatment for hematological diseases.

79 dely used in the diagnosis and monitoring of hematological diseases.

80 with sickle cell disease (SCD), an inherited hematological disorder associated with vascular inflamma

81 Sickle cell disease (SCD) is a hematological disorder leading to blood vessel occlusion

82 data implicate hnRNP K in the development of hematological disorders and suggest hnRNP K acts as a tu

83 be used effectively for in silico studies of hematological disorders based on first principles and pa

84 However, in many hematological disorders the spectrin network and lipid b

85 Patients with various hematological disorders who underwent splenectomy betwee

86 There were 30 cancers, 9 malignant hematological disorders, 14 chronic inflammatory disease

87 development of expansion strategies to treat hematological disorders.

88 ting, focusing on its potential for treating hematological disorders.

89 represents a curative treatment for various hematological disorders.

90 owledge implicating the shelterin complex in hematological disorders.

91 marrow, as well as the relationship between hematological disturbances and gametocyte development in

92 ofluidic devices for studying and diagnosing hematological dysfunctions and the clinical impact made

93 ive phenotypic descriptions, biochemical and hematological effects, associated pathology and ethnic o

94 The disorder is a dangerous urological and hematological emergency since it is associated with isch

95 edictors of survival in both sexes; no other hematological factor was retained in the model.

96 oach to assess the kinetic, rheological, and hematological factors involved in vasoocclusive events a

97 The following hematological factors were investigated and correlated w

98 and protects mice from chemotherapy-induced hematological failure and death.

99 Herein we describe the clinical and hematological features of a consanguineous family with a

100 n by comparing the proteome, metabolome, and hematological features of blood from hibernating and act

101 onged inflammatory stress can exacerbate the hematological impairment, leading to an additional decre

102 e remission + partial remission + trilineage hematological improvement).

103 time, mice were killed and investigated for hematological, inflammatory, and histological changes.

104 r indicate that several complex quantitative hematological, lipid, and cardiovascular traits share ge

105 al and laboratory data from 11 patients with hematological malignances or autoimmune diseases who wer

106 rrently undergoing human clinical trials for hematological malignancies (CPI-0610).

107 In contrast, the function of heparanase in hematological malignancies (except myeloma) was not inve

108 m exposure (OR: 3.23; 95% CI: 1.67-6.25) and hematological malignancies (OR: 2.85; 95% CI: 1.10-7.41)

109 their cancer management: 15 of 28 (54%) with hematological malignancies and 27 of 63 (43%) with solid

110 in all calculations, including 28 (31%) with hematological malignancies and 63 (69%) with solid tumor

111 ted mortality and morbidity in patients with hematological malignancies and bone marrow transplants.

112 ine samples from 71 patients with underlying hematological malignancies and found that the urine GM/c

113 ising therapeutic cell sources for high-risk hematological malignancies and immune disorders.

114 table mortality, especially in patients with hematological malignancies and in hematopoietic stem cel

115 I3Kdelta) is an appealing target for several hematological malignancies and inflammatory diseases.

116 re Food and Drug Administration-approved for hematological malignancies and inhibit class II and/or c

117 her CT imaging findings in 100 patients with hematological malignancies and possible invasive mold di

118 implicated in numerous pathologies including hematological malignancies and rheumatoid arthritis.

119 expression and regulation of TET proteins in hematological malignancies and solid tumors, and discuss

120 major mediators in the pathogenesis of both hematological malignancies and solid tumors.

121 latory elements-and in MLL3 and MLL4 in both hematological malignancies and solid tumors.

122 s stem cell transplantation for treatment of hematological malignancies and solid tumors.

123 The intercellular crosstalk between hematological malignancies and the tumor microenvironmen

124 are settings, especially among patients with hematological malignancies and those who are immunocompr

125 te for dCK-inhibitor based therapies against hematological malignancies and, potentially, other cance

126 arked activity in MM, while studies in other hematological malignancies are ongoing.

127 ase hematopoietic cell kinase (HCK) triggers hematological malignancies as a tumor cell-intrinsic onc

128 Treatment of hematological malignancies by adoptive transfer of activ

129 ere was no clear linear trend in the risk of hematological malignancies by either paternal or materna

130 ars, it has become increasingly evident that hematological malignancies can alter their microenvironm

131 The biological and clinical behaviors of hematological malignancies can be influenced by the acti

132 s (MDS) are a heterogeneous group of chronic hematological malignancies characterized by dysplasia, i

133 Hematological malignancies comprise a diverse set of lym

134 f NK cells developing in three patients with hematological malignancies given umbilical cord blood tr

135 tor interferon regulatory factor 4 (IRF4) in hematological malignancies has been increasingly recogni

136 40 years, the approach to classification of hematological malignancies has evolved from descriptive

137 Comparison of these findings to mutations in hematological malignancies identified several recurrentl

138 inked with chronic inflammatory diseases and hematological malignancies in humans.

139 h broad antitumor activity against solid and hematological malignancies in phases 2 and 3 clinical tr

140 ion of the mechanisms of immune tolerance in hematological malignancies is critical to inform the dev

141 Immunotherapy for hematological malignancies or solid tumors by administra

142 mples obtained from 33 cases with underlying hematological malignancies receiving induction chemother

143 B virus (HBV) infection who are treated for hematological malignancies remain at risk for HBV reacti

144 studied in solid cancers, their functions in hematological malignancies remain poorly understood.

145 arly important in the body's defense against hematological malignancies such as leukemia.

146 istration for the treatment of the subset of hematological malignancies that are dependent on the ext

147 ted a multicenter, phase 1 study in advanced hematological malignancies to assess the safety, efficac

148 ype 2 and in cancer immunotherapy trials for hematological malignancies using chimeric antigen recept

149 instability, and HSC aging and might promote hematological malignancies with age.

150 rms of immunotherapy, redirecting T cells to hematological malignancies with bispecific antibodies (B

151 sing therapeutic target for the treatment of hematological malignancies with DDR defects, where ATM/p

152 cell-targeted BsAbs for the immunotherapy of hematological malignancies with special focus on conduct

153 with resolved HBV receiving chemotherapy for hematological malignancies without antiviral prophylaxis

154 d clinical course, the evolution to advanced hematological malignancies, and the accessibility of neo

155 disorders, including autoimmune diseases and hematological malignancies, are at risk of developing os

156 have demonstrated promising results against hematological malignancies, but have encountered signifi

157 ntation (allo-BMT) is a curative therapy for hematological malignancies, but is associated with signi

158 the role of cytokines of the IL-1 family in hematological malignancies, chemotherapy-induced intesti

159 ingly, although there are multiple described hematological malignancies, DC cancers are rarely observ

160 urrently being tested in clinical trials for hematological malignancies, impairs PDA tumorigenesis by

161 (HSCT) is a critically important therapy for hematological malignancies, inborn errors of metabolism,

162 ells have been highly successful in treating hematological malignancies, including acute and chronic

163 r of these cells is often used for high-risk hematological malignancies, including acute myeloid leuk

164 ssive antitumor activity in various solid or hematological malignancies, including HCC.

165 e in cell survival and proliferation in many hematological malignancies, including multiple myeloma (

166 e a role in the treatment of diseases beyond hematological malignancies, including solid tumors and a

167 n has shown remarkable antitumor activity in hematological malignancies, it has been less effective i

168 athway activation in most cancers, including hematological malignancies, remains unknown.

169 no differences in the incidence of solid and hematological malignancies, serious infections, graft fa

170 preferentially induces apoptosis in various hematological malignancies, suggesting that EZH2 may be

171 antigen negative) receiving chemotherapy for hematological malignancies, we conducted a meta-analysis

172 l targeted epigenetic therapies for treating hematological malignancies.

173 s, in individuals without clear diagnosis of hematological malignancies.

174 tive for selected HIV-infected patients with hematological malignancies.

175 promising diagnostic tool for patients with hematological malignancies.

176 mal epigenetic control to the development of hematological malignancies.

177 are associated with many diseases, including hematological malignancies.

178 veral phase 1 trials of cancer patients with hematological malignancies.

179 Activating JAK2 mutants cause hematological malignancies.

180 components of the RNA splicing machinery in hematological malignancies.

181 ed compared with control samples in multiple hematological malignancies.

182 ssociation between paternal age at birth and hematological malignancies.

183 gs of invasive mold disease in patients with hematological malignancies.

184 tors could prove useful for the treatment of hematological malignancies.

185 y been approved for the treatment of several hematological malignancies.

186 protect HSC pool integrity, guarding against hematological malignancies.

187 65 (56%) had solid tumors, and 140 (47%) had hematological malignancies.

188 -mC, 5-hmC, and their enzymatic modifiers in hematological malignancies.

189 elop novel epigenetic therapies for treating hematological malignancies.

190 d be prioritized for targeting in a range of hematological malignancies.

191 t anticancer drugs against various solid and hematological malignancies.

192 in the blood of individuals without apparent hematological malignancies.

193 profiles, and expression changes underlying hematological malignancies.

194 nity in patients with bone marrow failure or hematological malignancies.

195 etic cell differentiation and causal role in hematological malignancies.

196 olic interventions in ALL and possibly other hematological malignancies.

197 with both developmental growth disorders and hematological malignancies.

198 e for the expression of CCL5 and CCR5 in non-hematological malignancies.

199 ns in a population of patients with advanced hematological malignancies.

200 arious diseases and is approved for treating hematological malignancies.

201 me, miR-22 transgenic mice developed MDS and hematological malignancies.

202 ination chemotherapies, especially targeting hematological malignancies.

203 ptional dynamics during hematopoiesis and in hematological malignancies.

204 the only treatment option for several severe hematological malignancies.

205 ave already been performed in the setting of hematological malignancies.

206 icacy of selinexor in patients with advanced hematological malignancies.

207 pathogenesis of several myeloid and lymphoid hematological malignancies.

208 tuximab, is an established means of treating hematological malignancies.

209 -HSCT) is a potentially curative therapy for hematological malignancies.

210 a promising therapeutic target for specific hematological malignancies.

211 iseases, cancer mortality, and high risk for hematological malignancies.

212 or patients with recurrent and/or refractory hematological malignancies.

213 rtant therapy for patients with a variety of hematological malignancies.

214 hosphorylation underlies the pathogenesis of hematological malignancies; however, the extent to which

215 ction (septicemia, pneumonia, tuberculosis), hematological malignancy (non-Hodgkin's lymphoma, leukem

216 In patients with a hematological malignancy admitted between 2009 and 2013,

217 cell non-Hodgkin lymphoma is the most common hematological malignancy and represents a substantial cl

218 Acute promyelocytic leukemia (APL) is a hematological malignancy driven by a chimeric oncoprotei

219 Lymphoma is the most common hematological malignancy in developed countries.

220 atients with erythema migrans and underlying hematological malignancy more often had signs of dissemi

221 Eligibility included adults with a hematological malignancy to receive myeloablative HCT fr

222 lid tumor patients and 6,652 patients with a hematological malignancy who were admitted between 2009

223 cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that deri

224 ith a solid tumor and 13,538 patients with a hematological malignancy with an unplanned ICU admission

225 ars old, had undergone allogeneic HSCT for a hematological malignancy, and had available pretransplan

226 ce for genetic susceptibility to this B-cell hematological malignancy, as well as insight into the bi

227 mong patients undergoing allogeneic HSCT for hematological malignancy, early administration of azithr

228 tes with increased mortality rates, risk for hematological malignancy, smoking behavior, telomere len

229 ts, suggesting that they might predispose to hematological malignancy.

230 ve been clinically used for the treatment of hematological malignancy.

231 Multiple myeloma (MM) is an age-dependent hematological malignancy.

232 iological model for VRE BSI in patients with hematological malignancy.

233 i-VRE antimicrobial therapy in patients with hematological malignancy.

234 y in the contexts of development, aging, and hematological malignancy.

235 tiple myeloma (MM) is the second most common hematological malignant abnormality.

236 l outcomes in thrombocytopenic patients with hematological malignant neoplasms?

237 Furthermore, we show that many patients with hematological neoplasia are markedly vitamin C deficient

238 sferase inhibitors (DNMTis) for treatment of hematological neoplasias.

239 novel therapeutic targets for these frequent hematological neoplasias.

240 are now recognized as among the most common hematological neoplasms, probably affecting >30 000 pati

241 TKIs) are used in the clinical management of hematological neoplasms.

242 logy Score (odds ratio, 1.12), admission for hematological (odds ratio, 1.48) or respiratory (odds ra

243 than 18 years, solid tumors, HIV infection, hematological or inflammatory conditions, and immunosupp

244 evere thrombocytopenia (patients treated for hematological or oncological reasons who are at risk of

245 or concomitant history of cancer (prostate, hematological, or thyroid), whereas 9 patients (60.0%) i

246 ity of nanoformulations and their effects on hematological parameters is now recognized as an importa

247 Hematological parameters remained in the reference range

248 lterations during blood flow correlated with hematological parameters, HbS level, and hydroxyurea (HU

249 lism, disturbed glucose homeostasis, altered hematological parameters, increased bone formation and l

250 ghee produced toxic effects in the liver and hematological parameters.

251 Because many hematological pathologies are strongly age-associated, s

252 relevant cause of morbidity and mortality in hematological patients and especially in hematopoietic s

253 Acute respiratory failure in hematological patients is related to a high mortality.

254 of invasive aspergillosis (IA) in high-risk hematological patients remains unclear.

255 is associated with a lower risk of death in hematological patients with respiratory failure.

256 In hematological patients, VZV-related complications occur

257 sis and a lower incidence of IA in high-risk hematological patients.

258 herapeutically targeting the IL-1 pathway in hematological patients.

259 y and in an additive fashion with respect to hematological phenotype, gene expression, chromatin stru

260 We have examined the hematological phenotype, HbF levels, and erythroid BCL11

261 We compared the hematological profile of patients with and without malar

262 nd essential thrombocythemia), prevention of hematological progression, and improved quality of life

263 d with cell type-restricted, closely related hematological quantitative traits in biologically releva

264 e added grades 3 to 4 toxicities and delayed hematological recovery.

265 by a high incidence of remission failure or hematological relapse after conventional chemotherapy.

266 analysis, the 2-year cumulative incidence of hematological relapse was 33.5% (95% CI, 27.3%-39.7%) wi

267 Late hematological relapses beyond 1 year occurred in 3 patie

268 lance across blinded groups in the number of hematological relapses, and the treatment was stopped De

269 Complete hematological remission was achieved in 153/180 (85%) pa

270 d and vascular cells remain a major topic of hematological research.

271 Patients who achieved hematological response after chemotherapy had higher ren

272 With a median follow-up of 14 months, hematological response and overall survival were 50% and

273 the setting of MIg, as rapid achievement of hematological response appears to result in improved ren

274 We report that IFNalpha treatment induces hematological responses in the model and causes depletio

275 Complete hematological (Revised European-American Lymphoma classi

276 nd sonographic lung abnormalities as well as hematological, serum biochemical, and endocrine hormone

277 n of p38alpha led to defective recovery from hematological stress and a delay in initiation of HSPC p

278 immediately phosphorylated in HSPCs after a hematological stress, preceding increased HSPC cycling.

279 No spasticity, albinism, or hematological symptoms were reported.

280 8.1%), infectious disease issues (12.4%), or hematological/thrombosis questions (9.5%).

281 side was associated with higher grade 3 to 4 hematological toxic effects compared with carboplatin-pa

282 (AEs), clinical and laboratory effects, and hematological toxicities.

283 purineme methyltransferase polymorphisms and hematological toxicity associated with thiopurine treatm

284 LA stabilized nanoemulsions manifested lower hematological toxicity than corresponding micelles sugge

285 e side effects, including nephrotoxicity and hematological toxicity.

286 The regimen was well tolerated with minimal hematological toxicity.

287 rmed genome-wide CNV association analyses of hematological trait, hematocrit, on 521 Korean family sa

288 e-wide association study of the eight common hematological traits among 7943 African-American childre

289 Hematological traits are important clinical indicators,

290 Hematological traits are important clinical parameters.

291 Common measures of hematological traits include red blood cell (RBC) count,

292 ny common variants have been associated with hematological traits, but identification of causal genes

293 of rare and low-frequency coding variants on hematological traits, we analyzed hemoglobin concentrati

294 sis with 20 quantitative cardiometabolic and hematological traits.

295 nsights into the role of genetic variants in hematological traits.

296 cause mortality and an increased risk of non-hematological tumors and that LOY could be induced by to

297 leukemia (T-ALL) is a heterogeneous group of hematological tumors composed of distinct subtypes that

298 The protein is also expressed in a subset of hematological tumors, and shows especially broad and hig

299 n in vivo xenograft models of both solid and hematological tumors.

300 and these drugs are used clinically to treat hematological tumors.