ライフサイエンスコーパス: hematological

1 ample was obtained from each participant for hematological analysis of leukocytes, erythrocytes and p

2 Hematological analysis, via a complete blood count (CBC)

3 logical parameters to facilitate and improve hematological analysis.

4 lopment of a low-cost, easy-to-use, and fast hematological analyzer as a point-of-care device and for

5 uence towards developing novel point-of-care hematological analyzers for resource-constrained setting

6 Hematological and biochemical analyses revealed no undes

7 dard deviation score (Z score), biochemical, hematological and clinical parameters.

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

9 matopoietic cell transplantation can correct hematological and immunological disorders by replacing a

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

11 We have applied this new approach in hematological and liver cancer cell lines and confirm th

12 ial as both iron excess and deficiency cause hematological and neurodegenerative diseases.

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

14 ita germline Npm1 mutation recapitulate both hematological and nonhematological features of dyskerato

15 Participants with hematological and solid cancer had higher relative risks

16 Hematological and solid cancers catabolize the semiessen

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

18 liver both Pt and As species to a variety of hematological and solid cancers.

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

20 ds should be able to be transferred to other hematological and solid malignancies.

21 ng their efficacy in clinical trials against hematological and solid malignancies.

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

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

24 apies in diverse preclinical mouse models of hematological and solid tumors.

25 Compound 42 also inhibited the growth of hematological and triple negative breast cancer xenograf

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

27 s to several days without any morphological, hematological, and histological complications.

28 Here we introduce a hematological assay based on label-free molecular imagin

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

30 Here, we identify a novel hematological/autoinflammatory condition (NOCARH syndrom

31 g using a comprehensive dataset of different hematological benign specimens and samples from CML pati

32 iggers various inflammatory, biochemical and hematological biomarkers.

33 d countries, with chronic steroid use (45%), hematological cancer (25%), and chemotherapy (22%) the m

34 Patients with AIDS and hematological cancer admitted with CAP may have higher p

35 reens and discovered a marked sensitivity of hematological cancer cell lines, including B-cell lympho

36 ntagonist), and dexamethasone when tested on hematological cancer cells.

37 er, zoster risk was also elevated prior to a hematological cancer diagnosis (aHR for 1-2 years prior,

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

39 Diagnosis of hematological cancer requires complete white blood cell

40 analyzed 77 noncirrhotic HBsAg carriers with hematological cancer who received rituximab-containing c

41 h fungal infections (odds ratio for AIDS and hematological cancer, 15.10 and 4.65, respectively; both

42 , and viral infections other than influenza (hematological cancer, 5.49; P < .001).

43 se included AIDS, aplastic anemia, asplenia, hematological cancer, chemotherapy, neutropenia, biologi

44 For hematological cancer, increases in zoster risk are appar

45 or solid cancer; 8.77 (95% CI 5.66-13.6) for hematological cancer; 12.0 (95% CI 6.13-23.7) for human

46 from 727 patient samples with seven forms of hematological cancers and assessed the predictivity over

47 enotype and common sensitivity profiles with hematological cancers can guide treatment options beyond

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

49 tive myeloproliferative neoplasms (MPNs) are hematological cancers that can be subdivided into entiti

50 shed therapeutic agents for the treatment of hematological cancers, as are anthracyclines such as dox

51 s been successful in clinical trials against hematological cancers, but has experienced challenges in

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

53 inically effective for managing a variety of hematological cancers.

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

55 T adult patients (n = 530), transplanted for hematological cancers.

56 immunotherapy that may be curative for some hematological cancers.

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

58 eras revealed STING-mediated MCMV control in hematological cells, similar to MyD88.

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

60 ytopenic purpura (TTP) is a life-threatening hematological condition associated with deficiency in AD

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

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

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

64 d2-/- also showed epistatic relationship for hematological defects while being not epistatic with res

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

66 tomycin C, occasional limb abnormalities and hematological deficiencies.

67 Hematological diagnosis was monoclonal gammopathy of ren

68 Hematological diagnosis was monoclonal gammopathy of ren

69 tem, manifested by an increased incidence of hematological disease in the elderly.

70 Systemic mastocytosis is a hematological disease in which aberrant mast cells accum

71 A hematological disease transcriptomic signature and incre

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

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

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

75 cal circulatory support and individuals with hematological diseases that alter physical properties of

76 (HSPCs) hold promise to cure a wide array of hematological diseases, and we previously found a role f

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

78 Like most hematological diseases, the molecular genetic basis of t

79 to T-cell deplete transplants performed for hematological diseases.

80 ese complexes are frequently dysregulated in hematological diseases.

81 etic regulator TET2 is frequently mutated in hematological diseases.

82 entral immunological organ and the origin of hematological diseases.

83 a healthy blood supply; imbalances underlie hematological diseases.

84 Sickle cell disease (SCD) is a worldwide hematological disorder causing painful episodes, anemia,

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

86 Anemia is a hematological disorder that adversely affects the health

87 ll prolymphocytic leukemia (B-PLL) is a rare hematological disorder whose underlying oncogenic mechan

88 Human parvovirus B19 (B19V) infection causes hematological disorders and is the leading cause of noni

89 o O(2) transport and their relationship with hematological disorders remain ill defined.

90 ntration, which are common manifestations of hematological disorders, can have hitherto unrecognized

91 single-step prenatal treatment of congenital hematological disorders.

92 represents a curative treatment for various hematological disorders.

93 owledge implicating the shelterin complex in hematological disorders.

94 iation between LPS levels, inflammation, and hematological dysfunction was analysed.

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

96 ood samples were taken every 2 wk to measure hematological factors.

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

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

99 2018) of these recommendations, mainly for "hematological improvement" criteria used for lower-risk

100 e leukemia or higher risk MDS] vs absence of hematological improvement) as well as on molecular and c

101 ned the relationships among gene expression, hematological indices, and relevant plasma biomarkers.

102 Routine hematological laboratory evaluation of the proposita was

103 ontribute to the development and function of hematological lineages, act as nodes for the action of m

104 y novel loci associated with anthropometric, hematological, lipid, and glycemic traits.

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

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

107 ated as a therapeutic agent for treatment of hematological malignancies and autoimmune diseases.

108 3 is frequently activated in human solid and hematological malignancies and remains a challenging the

109 oncogenic miRNA, frequently overexpressed in hematological malignancies and solid tumors.

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

111 103 clinical variables from patients with hematological malignancies and subsequent alloSCT were c

112 s to define the mutational landscape driving hematological malignancies and underscore the utility of

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

114 ffect has been understudied in patients with hematological malignancies at non-critical-care units.

115 lability of blood products for patients with hematological malignancies at Uganda Cancer Institute.

116 ls play critical roles in protection against hematological malignancies but can acquire a dysfunction

117 rative therapy for high-risk and/or advanced hematological malignancies but remains limited by graft-

118 are understood to play fundamental roles in hematological malignancies by acting as oncogenes or tum

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

120 Hematological malignancies comprise a diverse set of lym

121 40 years, the approach to classification of hematological malignancies has evolved from descriptive

122 Hematological malignancies have long been at the forefro

123 Adults with hematological malignancies hospitalized for cytotoxic ch

124 Adults with hematological malignancies hospitalized for cytotoxic ch

125 Patients with hematological malignancies hospitalized for myelosuppres

126 mples that alteration of the BMM can lead to hematological malignancies in mice, we describe, without

127 ffect has been understudied in patients with hematological malignancies in noncritical care units.

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

129 from both solid epithelial cancers and some hematological malignancies in which FAK inhibitors have

130 plicated in inflammatory diseases as well as hematological malignancies in which the AKT pathway is o

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

132 d tumors, the importance of Trk signaling in hematological malignancies is underexplored and warrants

133 ibodies are widely used for the treatment of hematological malignancies or autoimmune disease but may

134 le 84 (52.5%) individuals had a diagnosis of hematological malignancies or chronic myeloproliferative

135 Immunotherapy for hematological malignancies or solid tumors by administra

136 Patients with hematological malignancies or undergoing hematopoietic s

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

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

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

140 ymphoblastic lymphoma (T-LBL) are aggressive hematological malignancies that are currently treated wi

141 tion of tumor types in terms of solid versus hematological malignancies that can be best targeted wit

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

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

144 -line-associated bacteremia in patients with hematological malignancies who are hospitalized for cyto

145 line-associated bacteremia in patients with hematological malignancies who are hospitalized for cyto

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

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

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

149 dentical related donors for the treatment of hematological malignancies with end-stage renal failure.

150 had unprecedented impact in the treatment of hematological malignancies with few therapeutic options.

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

152 for preventing CHIP progression and treating hematological malignancies with TP53 mutations.

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

154 TET2 and DNMT3A) are frequently observed in hematological malignancies(1-3) and clonal hematopoiesis

155 Despite its success in treating melanoma and hematological malignancies, adoptive cell therapy (ACT)

156 For high-risk and refractory hematological malignancies, allogeneic hematopoietic ste

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

158 regulation of several mitotic events, and in hematological malignancies, AURKA and AURKB hyperexpress

159 eting lymphocytes has shown great promise in hematological malignancies, but clinical efficacy agains

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

161 an important curative therapy for high-risk hematological malignancies, but the development of sever

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

163 oach has been a paradigm in treating certain hematological malignancies, efforts to translate this su

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

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

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

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

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

169 topoietic stem cell donors for patients with hematological malignancies, leukemia-associated mutation

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

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

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

173 plays a profound role in the pathogenesis of hematological malignancies, which is often the result of

174 apeutic agents in the treatment of solid and hematological malignancies.

175 ibition of BTK is useful in the treatment of hematological malignancies.

176 ltiple signaling pathways, and contribute to hematological malignancies.

177 s treated with recently introduced drugs for hematological malignancies.

178 ighly expressed in multiple solid tumors and hematological malignancies.

179 ge and is associated with increased risks of hematological malignancies.

180 ears been approved for the treatment of some hematological malignancies.

181 t as potential novel therapeutic targets for hematological malignancies.

182 -round-blue cell tumors, and unexpectedly in hematological malignancies.

183 by bone marrow failure and predisposition to hematological malignancies.

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

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

186 ptional dynamics during hematopoiesis and in hematological malignancies.

187 the only treatment option for several severe hematological malignancies.

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

189 icacy of selinexor in patients with advanced hematological malignancies.

190 pathogenesis of several myeloid and lymphoid hematological malignancies.

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

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

193 a promising therapeutic target for specific hematological malignancies.

194 duced prolonged neutropenia in patients with hematological malignancies.

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

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

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

198 l targeted epigenetic therapies for treating hematological malignancies.

199 es the functional implications for different hematological malignancies.

200 or autoimmune and inflammatory disorders and hematological malignancies.

201 l blood increasingly guides clinical care in hematological malignancies.

202 transplant recommendations for melanoma and hematological malignancies.

203 ied via deep sequencing of 185 patients with hematological malignancies.

204 s a driver in many types of solid tumors and hematological malignancies.

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

206 hematopoietic stem cell transplantation for hematological malignancy at St.

207 ell leukemia/lymphoma (ATL) is an aggressive hematological malignancy caused by human T-cell leukemia

208 ation structure and reduced the incidence of hematological malignancy in miR-146a-/- mice.

209 invasive mold disease (IMD) in patients with hematological malignancy is not standardized and is a ch

210 ultiple myeloma (MM), a bone marrow-resident hematological malignancy of plasma cells, has remained l

211 Antibiotic stewardship is challenging in hematological malignancy patients.

212 phoblastic leukemia (T-ALL) is an aggressive hematological malignancy resulting from the dysregulatio

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

214 antimicrobial stewardship interventions in a hematological malignancy unit: monthly antibiotic cyclin

215 Hematological malignancy was the underlying disease in 1

216 Lymphoma is the most common type of canine hematological malignancy where the multicentric (cMCL) f

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

218 phoblastic leukemia (T-ALL) is an aggressive hematological malignancy with a dismal prognosis in pati

219 cute Myeloid Leukemia (AML) is an aggressive hematological malignancy with abnormal progenitor self-r

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

221 Treatment of hematological malignancy with antibody-drug conjugates (

222 underlying diseases (65% without underlying hematological malignancy) who had BALF galactomannan (GM

223 tion (infection, neurological condition, and hematological malignancy), nor by cumulative number of p

224 nly 9 patients (27%) had a family history of hematological malignancy, and 15 (46%) had a personal hi

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

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

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

228 resses miR-155 and develops miR-155-addicted hematological malignancy, we describe here a multi-step

229 ncer and represents the second most frequent hematological malignancy.

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

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

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

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

234 ers) were sequenced with a targeted 293-gene hematological-malignancy panel.

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

236 l outcomes in thrombocytopenic patients with hematological malignant neoplasms?

237 lored the functional relevance of volumetric hematological measures to exercise capacity.

238 ulators and transcription factor activity in hematological neoplasia, but do not confirm the putative

239 omal translocations in association with many hematological neoplasms.

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

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

242 cephalomyelitis, even at low doses devoid of hematological or neurologic toxicity.

243 assessed prediction of presence of OV using hematological parameters (HP) and Child-Turcott-Pugh (CT

244 There may be differences in hematological parameters between meat-eaters and vegetar

245 y was to perform cross-sectional analyses of hematological parameters by diet group in a large cohort

246 Specific hematological parameters included the presence of hemogl

247 Hematological parameters remained in the reference range

248 veolar shadowing on chest X-ray and clinical/hematological parameters supporting suspected ventilator

249 provide fast quantitative information of key hematological parameters to facilitate and improve hemat

250 d serious adverse events (SAEs), biochemical/hematological parameters, cell-mediated immunogenicity b

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

252 No signs of toxicity on biochemical, hematological parameters.

253 xposure on metabolism, oxidative stress, and hematological parameters.

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

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

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

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

258 ient, and cost-effective modality to improve hematological reconstitution in patients.

259 sion (CR) rate, including CR with incomplete hematological recovery (CRi) after induction therapy, wa

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

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

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

263 Late hematological relapses beyond 1 year occurred in 3 patie

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

265 Patients who achieved hematological response after chemotherapy had higher ren

266 tions because of a more rapid and persistent hematological response and acceptable safety profile.

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

268 difference between the two arms in rates of hematological response or disease progression.

269 Median time to hematological response was 1 week.

270 Overall, 22 patients had hematological response, and 19 patients (47.5%) achieved

271 62 patients (36%), all of whom had achieved hematological response.

272 onotherapy is associated with deep and rapid hematological responses in previously treated AL patient

273 effects occurred in 7 patients (8%), mostly hematological, resulting in premature drug cessation.

274 Complete hematological (Revised European-American Lymphoma classi

275 drugs have been most extensively utilized as hematological, rheumatological, and oncological therapie

276 nts with carcinoma, nonmelanoma skin cancer, hematological second cancer, and melanoma diagnosed conc

277 io, 1.03; 95% CI, 1.03-1.03; p < 0.001) with hematological, sepsis, neurologic, and pulmonary disease

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

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

280 ING also contributed to viral control in non-hematological, stromal cells.

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

282 didate loci, including genes mutated in rare hematological syndromes (ADA, GP6, IL17RA, PRF1 and SEC2

283 work associated with cell-to-cell signaling, hematological system development/function and inflammato

284 Hematological tests were performed in serum for immune b

285 was a predictive factor for SVR, while poor hematological tolerance of ribavirin requiring its dose

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

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

288 The regimen was well tolerated with minimal hematological toxicity.

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

290 by the rapid expansion of BOLA2, we assessed hematological traits and anemia prevalence in 379,385 co

291 Altogether, our results for hematological traits highlight the value of a more globa

292 In trans-ethnic meta-analyses for 15 hematological traits in 746,667 participants, including

293 In parallel, we analyzed hematological traits in mice carrying the 16p11.2 orthol

294 st whether longer telomeres cause changes to hematological traits.

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

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

297 acerbates the incidence of various solid and hematological tumors.

298 in a fractionated manner exhibited improved hematological values without sacrificing therapeutic eff

299 y cows did not induce changes in clinical or hematological variables, and gene expression profiles in

300 and grade 4 toxicity was almost exclusively hematological, which were resolved without dose reductio