ライフサイエンスコーパス: HCT

1 HCT at a younger age continues to be associated with sup

2 HCT outcomes have improved over time, particularly for p

3 HCT recipients with RSV infections had similar outcomes

4 HCT-116 and HT-29 50% inhibition concentrations (ug/mL)

5 HCT-CI scores of 1 to 2 did not differ relative to score

6 performance of plasma mcfDNA-Seq NGS in 114 HCT recipients with pneumonia after HCT who had stored p

7 Cohorts included 1496 HCT and 1090 SOT recipients.

8 Among 17 HCT studies, the absence of or use of antiviral prophyla

9 We followed 55 HCT recipients with low-level CMV reactivation up to 8 w

10 ith additional chart review, we identified 6 HCT recipients with BoV detected in lower respiratory tr

11 2017, and March 11, 2019, we assessed 33 982 HCTs using multivariate regression models for the role o

12 s is feasible for most patients in need of a HCT, and could lower GVHD and increase availability of H

13 e reviewed all adult patients who received a HCT from June 2014-May 2015 (pre-GI PCR, n=163) and from

14 We assessed 100 adult HCT recipients a median of 9.3 years (range: 1.7-40) aft

15 between 2011 and 2016 at four Canadian adult HCT centers.

16 After HCT, mean pre-transfusion Hb levels were 70.9 g/L in the

17 intravenous bolus on days 3, 6, and 11 after HCT; tacrolimus was given intravenously at a dose of 0.0

18 ally twice daily from day -3 to day 30 after HCT).

19 r placebo were given on days 28 and 56 after HCT.

20 m(2) intravenously on days 1, 4, and 7 after HCT); or tacrolimus, methotrexate, and maraviroc (maravi

21 e viral antibody repertoire before and after HCT using a novel serosurvey (VirScan) that detects immu

22 (GVHD), all evaluated through 100 days after HCT, and grade 3 or 4 adverse events (AEs) within 2 week

23 reduces the risk of relapse and death after HCT for FLT3-ITD-positive AML.

24 scores >=3 had increased risk of death after HCT.

25 ave donor myeloid chimerism <50% early after HCT.

26 h donor T-cell and myeloid engraftment after HCT.

27 econstitution, predict clinical events after HCT, or help refine selection of optimal donors.

28 ficity, NPV, and PPV for pulmonary IMI after HCT, particularly for non-Aspergillus.

29 lial cell entry decrease CMV infection after HCT, samples were analyzed from a randomized controlled

30 protective against CMV infection later after HCT in both study arms.

31 lapse of multiple myeloma at 30 months after HCT and died 4 years posttransplantation.

32 fore HCT and those with detectable MRD after HCT derive the strongest benefit from sorafenib.

33 inhibitor sorafenib, improves outcome after HCT.

34 S in 114 HCT recipients with pneumonia after HCT who had stored plasma obtained within 14 days of dia

35 AML in complete hematologic remission after HCT were randomly assigned to receive for 24 months eith

36 , dose fractionation, and risk of SMNs after HCT.

37 scores >=3 that had inferior survival after HCT, except for patients with hemoglobinopathies.

38 ve the potential of improving survival after HCT.

39 Screening for BKPyV viremia after HCT identifies asymptomatic patients at risk for kidney

40 R1, and REG3alpha in the first 3 weeks after HCT have prognostic value for NRM in both children and a

41 mulative incidence of SMNs by 30 years after HCT was 22.0%.

42 5FU-SLN(4) was highly cytotoxic against HCT-116 cells and significantly inhibited subcutaneous t

43 Allo-HCT patients carrying lactose-nonabsorber genotypes show

44 til 6 months posttransplantation in 241 allo-HCT recipients with positive CMV serostatus.

45 CS-CMVi occurred in 70 allo-HCT recipients (29%).

46 708 allo-HCT subjects were studied (7.5% develop gram-negative in

47 the mouse gastrointestinal tract after allo-HCT and exacerbates disease severity in gnotobiotic mode

48 testing and MRD-directed therapy after allo-HCT are lacking.

49 y, we report an excellent outcome after allo-HCT in CGD, with low incidence of graft failure and mort

50 (minimal) residual disease (MRD) after allo-HCT may be used as a predictor of impending relapse and

51 and plasma samples collected late after allo-HCT using a case-control study design.

52 ve inflammation and tissue injury after allo-HCT, supporting that TIPE confers immune homeostasis and

53 eature and driver of AML relapses after allo-HCT, which can be rapidly translated into personalized t

54 e may exert immunomodulatory effects in allo-HCT patients at least in part due to control of systemic

55 y would be useful clinically to monitor allo-HCT recipients and distinguish between those at risk of

56 preventing 2 critical complications of allo-HCT - GVHD and relapse.

57 imens were collected from recipients of allo-HCT and analyzed using 16SrRNA gene sequencing.

58 loodstream infection, in the setting of allo-HCT.

59 logeneic hematopoietic cell transplant (allo-HCT) recipients, as a result of intestinal translocation

60 logeneic hematopoietic cell transplant (allo-HCT) recipients.

61 eic hematopoietic cell transplantation (allo-HCT) can cure the disease, but the indication to transpl

62 ematopoietic stem cell transplantation (allo-HCT) have thus far largely focused on early complication

63 eic hematopoietic cell transplantation (allo-HCT) is currently the standard curative treatment of acu

64 eic hematopoietic cell transplantation (allo-HCT)) demonstrates that adoptive immunotherapy can cure

65 eic hematopoietic cell transplantation (allo-HCT), we describe a high incidence of enterococcal expan

66 eic hematopoietic cell transplantation (allo-HCT).

67 eic hematopoietic cell transplantation (allo-HCT).

68 elapse mortality in patients undergoing allo-HCT.

69 of 712 patients with CGD who underwent allo-HCT transplantation from March 1993 through December 201

70 reduced HHV-6B reactivation after allogeneic HCT in a post hoc analysis of a randomized controlled tr

71 cytomegalovirus prophylaxis after allogeneic HCT to study the effect of brincidofovir on HHV-6B react

72 or treat this complication after allogeneic HCT.

73 itudinal surveillance study among allogeneic HCT recipients, pre-HCT and weekly post-HCT nasal washes

74 consolidation strategies such as allogeneic HCT.

75 tologic malignancies treatable by allogeneic HCT.

76 to predict CMV outcomes following allogeneic HCT.

77 ealed treatment with midostaurin, allogeneic HCT, ELN favorable-risk group, and lower WBC counts as s

78 Among 4905 1-year survivors of allogeneic HCT for hematologic malignancies (N = 4500) or nonmalign

79 nd augment the curative effect of allogeneic HCT for this disease.

80 iters and seroprotection rates of allogeneic HCT recipients years after different schedules of vaccin

81 reviewed records of adult SOT or allogeneic HCT recipients from 1 January 2013 to 31 December 2017 t

82 reviewed records of adult SOT or allogeneic HCT recipients from 1/1/2013-12/31/2017 to characterize

83 ill be referred for autologous or allogeneic HCT, which carries an extremely high risk of infertility

84 our prior data, mice that undergo allogeneic HCT with Tbet-knockout donors (AlloTbet) have increased

85 ldren and young adults undergoing allogeneic HCT, we quantified BKPyV viruria and viremia (pre-HCT an

86 ldren and young adults undergoing allogeneic HCT, we quantified BKPyV viruria and viremia (pre-HCT an

87 Among HCT recipients, 355 CDI episodes were diagnosed in 265 r

88 When all frequency components of an HCT are shifted by the same amount, the pitch of the res

89 reviewed all adult patients who received an HCT from June 2014-May 2015 (pre-GI PCR, n = 163) and fr

90 r antitumor activity against A549, PC-3, and HCT-116 cancer cell lines both in normoxia and hypoxia.

91 Among 2153 SOT (65%) and HCT (35%) recipients, 634 (29%) reported any antibiotic

92 Among 2153 SOT (65%) and HCT (35%) recipients, 634 (29%) reported any antibiotic

93 In vitro assays on HeLa, MCF-7, and HCT-116 cells confirmed higher photoactivity for cationi

94 of 90 g/L and resulted in similar HRQOL and HCT outcomes with fewer transfusions.

95 ng adult hematologic malignancy patients and HCT recipients who received >=7 days of ISA primary prop

96 Median age at HCT was 1.2 years.

97 n alone as the conditioning regimen for auto-HCT in patients with newly diagnosed myeloma.

98 ients with DLBCL who are ineligible for auto-HCT or who experienced failure with auto-HCT.

99 urvival were 1.9 and 12.2 months in the auto-HCT-failed cohort and 1.4 and 5.8 months in the auto-HCT

100 t a median follow-up of 9 months in the auto-HCT-failed cohort and 6 months in the auto-HCT-ineligibl

101 ients with complete remission-3% of the auto-HCT-failed cohort-had durable response (11 or more, 14 o

102 ed cohort and 1.4 and 5.8 months in the auto-HCT-ineligible cohort respectively.

103 o-HCT-failed cohort and 6 months in the auto-HCT-ineligible cohort, independently assessed objective

104 ous hematopoietic cell transplantation (auto-HCT) or who had experienced failure with auto-HCT receiv

105 gous haemopoietic cell transplantation (auto-HCT).

106 CT) or who had experienced failure with auto-HCT received nivolumab 3 mg/kg every 2 weeks.

107 uto-HCT or who experienced failure with auto-HCT.

108 ctable minimal residual disease (MRD) before HCT and those with detectable MRD after HCT derive the s

109 The presence of ST2 before HCT is a prognostic biomarker for NRM in children age 10

110 res of 0 (HR, 1.12 [95% CI, 0.93-1.34]), but HCT-CI of 3 to 4 and >=5 posed significantly greater ris

111 1) with an IC(50) of 25 nM and colon cancer (HCT-116) with an IC(50) of 1 muM, and represents a poten

112 after transplantation of hematopoietic cell (HCT) or solid organ (SOT) but is unavailable for most pa

113 e pioneered simultaneous hematopoietic cell (HCT)/kidney transplantation from HLA-identical related d

114 on human colorectal carcinoma cancer cells (HCT 116) was used as a study model.

115 d total-body irradiation, underwent combined HCT/kidney transplantation from haploidentical donors; g

116 who received reduced-intensity conditioning HCT were randomly assigned (1:1:1) by random block sizes

117 nts with nonmalignant diseases demonstrating HCT-CI scores >=3 that had inferior survival after HCT,

118 T cell-depleted HCT recipients from January 1, 2012 through September 30

119 RD, but outcomes following alternative donor HCT continue to improve on clinical trials.

120 f 482 patients who underwent unrelated donor HCT (2005-2013) with T/S-based GvHD prophylaxis.

121 Challenges during HCT include maintaining relationships with partners and

122 omes supporting the recommendation for early HCT.

123 s with acute myeloid leukemia (AML) entering HCT with poor-risk features(1-3).

124 pared with the low biotin-receptor-expressed HCT-116 cells used as the negative control, resulting in

125 ith MHC class II deficiency undergoing first HCT at Great North Children's Hospital between 1995 and

126 Two-hundred thirty-five HCT candidates or recipients had URT and LRT RV testing

127 For HCT after 2008, OS according to donor was 100% for MFDs

128 follow-up, OS improved from 33% (46-68%) for HCT before 2008 (n = 6) to 94% (66-99%) for HCT after 20

129 HCT before 2008 (n = 6) to 94% (66-99%) for HCT after 2008 (n = 19; P = .003).

130 e feasibility of transcriptomic analyses for HCT recipients.IMPORTANCE Human herpesvirus 6B (HHV-6B)

131 The expanding indications for HCT to include benign hematologic disorders as well as a

132 e that the preparation of SCD recipients for HCT and supporting them through HCT have special nuances

133 urvival [GRFS]) was defined as the time from HCT to onset of grade 3-4 acute GvHD, chronic GvHD requi

134 TL lines from specifically consented healthy HCT donors.

135 ur designed ETPs against A549, DU 145, HeLa, HCT 116, and MCF7 human cancer cell lines provide insigh

136 neutrophil counts (P <0.001) and hematocrit (HCT) levels (P = 0.045).

137 However, higher HCT-CI scores among hemoglobinopathy patients did not in

138 Human intestinal epithelial cells (IECs) (HCT-116) were infected with a strain of CoPEC (11G5 stra

139 iveness and cellular uptake of 5FU-SLN(4) in HCT-116 cancer cells.

140 Knockdown of ATG5 in HCT-116 cells increased 11G5-induced senescence, promoti

141 Knockdown of ATG5 in HCT-116 cells increased numbers of intracellular 11G5, s

142 % CI, 2.2-32.4]; P = .001), and aztreonam in HCT (IRR, 9.7 [95% CI, 3.3-35.0]; P < .001), and fluoroq

143 rtality by preventing or delaying CS-CMVi in HCT recipients.

144 QSTM1 (also called p62) were knocked down in HCT-116 cells using small interfering RNAs.

145 tracts decreased PD-L1 protein expression in HCT-116 cells.

146 cases/1000 patient-years and were highest in HCT, followed by hematologic malignancies, SOT, and soli

147 ases/1,000 patient-years and were highest in HCT, followed by hematologic malignancies, SOT, solid tu

148 seful in guiding clinical decision making in HCT recipients.

149 I and progression to CS-CMVi was observed in HCT recipients.

150 the outcome of low-level CMV reactivation in HCT recipients.

151 sal wash samples from acutely RSV-A-infected HCT recipients who recovered early (<14 days of RSV shed

152 elopmental stages were obtained by infecting HCT-8 cells cultured in vitro.

153 tect-seq on the human colon cancer cell line HCT-116 and observed overlap with previously curated LAD

154 that the human colorectal cancer cell line, HCT-116, displayed reduced expression of Raf1-tr, and re

155 uced to <70% in HLA class I or II mismatched HCT.

156 ellent following matched-related donor (MRD) HCT, leading to significantly expanded application of th

157 a T-cell-replete, MHC-haploidentical, murine HCT model (B6C3F1->B6D2F1) to test the putative underlyi

158 nt of IL-1R and TLR4 signaling in two murine HCT models.

159 nd 30, 100, and 365 days after myeloablative HCT from 37 donor-recipient pairs.

160 artial remission (PR) was achieved in 68% of HCT recipients and 54% of SOT recipients.

161 ould lower GVHD and increase availability of HCT therapy.

162 An in silico screen and characterization of HCT 116 cells lacking p300 suggested that the histone ac

163 lective pressures in the clinical context of HCT.

164 The effect of HCT-CI differed by disease indication.

165 is and possibly more effective management of HCT recipients.

166 of specific antibiotics on the microbiota of HCT patients.

167 ea were identified in a higher proportion of HCT recipients after replacing conventional stool testin

168 We treated 46 recipients of HCT (n = 33) or SOT (n = 13) with established EBV-PTLD,

169 tely, we conducted a retrospective review of HCT recipients with BoV detected in lower respiratory tr

170 Among 17 studies of HCT patients, absent or <1 year of post-transplant antiv

171 tients <5 vs >=5 years of age at the time of HCT (94% vs 66%; overall P = .0008).

172 cluded patients randomized within 2 weeks of HCT and who received at least 6 consecutive doses of stu

173 GA), were tested alone or in combination, on HCT-116 and HT-29 human colorectal cancer cells (100-600

174 The frequency of post HCT AIC in our cohort was 9%, and the most significant r

175 Post-HCT biomarker analysis showed that ST2 (>26 ng/mL), TNFR

176 ed pre-HCT and at days +7, +14, and +21 post-HCT: stimulation-2 (ST2), tumor necrosis factor receptor

177 re-HCT and at months 1-4, 8, 12, and 24 post-HCT) and tested associations of peak viremia >=10 000 or

178 re-HCT and at Months 1-4, 8, 12, and 24 post-HCT) and tested associations of peak viremia >=10 000 or

179 HHV-6B plasma detection through day 42 post-HCT was significantly lower among patients receiving bri

180 l-status data available through week 48 post-HCT at trial completion (101 deaths, 20.4%).

181 of all-cause mortality through week 48 post-HCT in the letermovir group was similar in patients with

182 (95% CI, 0.49-1.11; P = .14) at week 48 post-HCT versus placebo.

183 o group, all-cause mortality at week 48 post-HCT was higher in patients with versus those without CS-

184 tested plasma for HHV-6B through week 6 post-HCT.

185 /-) CD4 T cells from the intestine 10 d post-HCT showed lower levels of Il1rl1 (gene of ST2), Ifng, C

186 gadolinium contrast resolved by 60 days post-HCT.

187 Thirty-six patients (9%) developed post-HCT AIC, with a median onset of 6.5 months post-HCT.

188 matopoietic cell transplantation (HCT), post-HCT clones can be donor-derived and in some cases engend

189 ost disease (GVHD) prophylaxis included post-HCT cyclophosphamide, tacrolimus, and mycophenolate mofe

190 a >=109 copies/mL in the first 3 months post-HCT.

191 AIC, with a median onset of 6.5 months post-HCT.

192 109 copies/mL in the first three months post-HCT.

193 ncidence, risk factors, and outcomes of post-HCT AIC and B-lymphocyte function following rituximab.

194 The mortality of post-HCT AIC reduced from 25% (4 of 16) prior to 2011 to 5% (

195 biochemical change after initiation of post-HCT IV-ERT, but the occurrence of ADA and inhibitory ant

196 nce in individuals at increased risk of post-HCT relapse.

197 nd infused these cells prophylactically post-HCT into 12 patients ( NCT01640301 ).

198 cantly with time to contrast resolution post-HCT.

199 neic HCT recipients, pre-HCT and weekly post-HCT nasal washes and symptom surveys were collected thro

200 or IgG (200 mug/mouse) starting 2 weeks post-HCT and were sacrificed after week 5.

201 .02) was independently associated with post-HCT AIC.

202 ease were significantly associated with post-HCT AIC.

203 In 3 patients with post-HCT IRIS related to mycobacterial infection, in vitro da

204 at least every 3 months through 1 year post-HCT at the Fred Hutch (2005-2010).

205 pitopes to common viruses over the year post-HCT differed by donor and recipient pre-HCT serostatus,

206 fections (RTIs) were observed by 1 year post-HCT in 19 patients.

207 er creatinine/cystatin C eGFR two years post-HCT.

208 r creatinine/cystatin C eGFR at 2 years post-HCT.

209 On univariate analysis, pre-HCT AIC, mismatched donor, alemtuzumab, anti-thymocyte a

210 lowing 4 plasma biomarkers were assessed pre-HCT and at days +7, +14, and +21 post-HCT: stimulation-2

211 rmed VirScan on cryopreserved serum from pre-HCT and 30, 100, and 365 days after myeloablative HCT fr

212 ther clinical characteristics, including pre-HCT treatment and conditioning, did not affect antiviral

213 post-HCT differed by donor and recipient pre-HCT serostatus, with highest gains in naive donors to se

214 e study among allogeneic HCT recipients, pre-HCT and weekly post-HCT nasal washes and symptom surveys

215 of donor at day 100, but more similar to pre-HCT self by day 365.

216 we quantified BKPyV viruria and viremia (pre-HCT and at months 1-4, 8, 12, and 24 post-HCT) and teste

217 we quantified BKPyV viruria and viremia (pre-HCT and at Months 1-4, 8, 12, and 24 post-HCT) and teste

218 When pre-HCT biomarkers were included, only ST2 remained signific

219 tely enhances PC-entry nAB activity in D+/R- HCT recipients.

220 MV donor-positive/recipient-negative (D+/R-) HCT patients (33 control, 28 CMV IVIG) was tested using

221 red individuals compared with late-recovered HCT recipients.

222 ents with hematologic malignancies requiring HCT who were randomly assigned to either a restrictive (

223 til (n = 2), splenectomy (n = 2), and second HCT (n = 3).

224 ous immunoglobulin replacement, 2 had second HCT, and 3 died.

225 were conducted on mouse bearing subcutaneous HCT-116 cancer.

226 en with MPS-IH and >=2 years from successful HCT underwent IV-ERT for 2 years' duration.

227 In summary, HCT outcomes for WAS have improved since 2005, compared

228 formation to guide management in symptomatic HCT candidates and recipients.

229 In TCD HCT, peak ADV VL and ADV AAUC correlated with mortality

230 Preliminary data also show that HCT-116 colon cancer cells, in which hMATE1 is epigeneti

231 upport to reduce the long-term effect of the HCT experience on their well-being.

232 ssion to CS-CMVi occurred in 31 (56%) of the HCT recipients.

233 Our findings suggest that using the HCT-CI score, in addition to disease-specific factors, c

234 cipients for HCT and supporting them through HCT have special nuances that require awareness and clos

235 C neurons showed facilitation in response to HCT relative to pure tones, similar to cortical "harmoni

236 We recorded single-neuron responses to HCT and IHCT with varying F0 and sound level in the infe

237 Harmonic complex tones (HCTs) commonly occurring in speech and music evoke a str

238 kimate/quinate hydroxycinnamoyl transferase (HCT) or loss of function of cinnamoyl CoA reductase 1 (C

239 kimate/quinate hydroxycinnamoyl transferase (HCT), and caffeoyl shikimate esterase (CSE).

240 Hematopoietic cell transplant (HCT) and solid organ transplant (SOT) recipients are at

241 nd the use of hematopoietic cell transplant (HCT) for specific high-risk groups.

242 Only hematopoietic cell transplant (HCT) has been shown to halt neurologic progression, alth

243 cpGVHD) after hematopoietic cell transplant (HCT) manifests as progressive airway and parenchymal lun

244 Hematopoietic cell transplant (HCT) recipients are frequently infected with respiratory

245 ant (SOT) and hematopoietic cell transplant (HCT) recipients are limited.

246 ng allogeneic hematopoietic cell transplant (HCT) recipients at 3 months after transplant, giving 3 d

247 ng allogeneic hematopoietic cell transplant (HCT) recipients at 3 months after transplant, giving thr

248 infections in hematopoietic cell transplant (HCT) recipients cause substantial morbidity and mortalit

249 e outcomes of hematopoietic cell transplant (HCT) recipients treated with oral or aerosolized RBV for

250 le blood from hematopoietic cell transplant (HCT) recipients with and without HHV-6B plasma viremia,

251 rbidity among hematopoietic cell transplant (HCT) recipients, but the etiology is often not identifie

252 lignancies or hematopoietic cell transplant (HCT) recipients.

253 irus (BoV) in hematopoietic cell transplant (HCT) recipients.

254 morbidity in hematopoietic cell transplant (HCT) recipients.

255 ly after hematopoietic stem cell transplant (HCT).

256 ary IMI after hematopoietic cell transplant (HCT).

257 epleted (TCD) hematopoietic cell transplant (HCT).

258 related donor hematopoietic cell transplant (HCT).

259 Post hematopoietic cell transplantation (HCT) autoimmune cytopenia (AIC) is a potentially life-th

260 logeneic hematopoietic cell transplantation (HCT) benefits children with Hurler syndrome (MPS-IH).

261 ty after hematopoietic cell transplantation (HCT) could have potential impact on donor selection or m

262 logeneic hematopoietic cell transplantation (HCT) for difficult-to-control infections can experience

263 logeneic hematopoietic cell transplantation (HCT) for nonmalignant diseases remains a significant pro

264 logeneic hematopoietic cell transplantation (HCT) in first complete remission as a time-dependent var

265 logeneic hematopoietic cell transplantation (HCT) in the pediatric age group is lacking.

266 unrelated haemopoietic cell transplantation (HCT) is limited by graft-versus-host disease (GVHD), whi

267 on after hematopoietic cell transplantation (HCT) is poorly understood.

268 logeneic hematopoietic cell transplantation (HCT) is the leading cause of death in patients with acut

269 ity, and hematopoietic cell transplantation (HCT) is the only widely available cure, with impacts see

270 Hematopoietic cell transplantation (HCT) is the primary curative approach, with the goal of

271 mpact on hematopoietic cell transplantation (HCT) outcomes are poorly understood.

272 child's hematopoietic cell transplantation (HCT) process.

273 logeneic hematopoietic cell transplantation (HCT) recipients who underwent a BAL for evaluation of LR

274 logeneic hematopoietic cell transplantation (HCT) recipients.

275 comes in hematopoietic cell transplantation (HCT) recipients.

276 Hematopoietic cell transplantation (HCT) remains the only curative treatment for this condit

277 logeneic hematopoietic cell transplantation (HCT) utilizing the Center for International Blood and Ma

278 vHD post hematopoietic cell transplantation (HCT), its efficacy and long-term outcome in matched (MUD

279 logeneic hematopoietic cell transplantation (HCT), mediated primarily by donor T cells that become ac

280 logeneic hematopoietic cell transplantation (HCT), often fail to ablate disease-initiating MDS HSCs,

281 eic hematopoietic stem cell transplantation (HCT), patients with acute myeloid leukemia (AML) with in

282 logeneic hematopoietic cell transplantation (HCT), post-HCT clones can be donor-derived and in some c

283 is after hematopoietic cell transplantation (HCT).

284 logeneic hematopoietic cell transplantation (HCT).

285 mens for hematopoietic cell transplantation (HCT).

286 logeneic hematopoietic cell transplantation (HCT).

287 dergoing hematopoietic cell transplantation (HCT).

288 llogeneic haemopoietic cell transplantation (HCT).

289 smatched hematopoietic cell transplantation (HCT).

290 logeneic hematopoietic cell transplantation (HCT); frequency of SOS in those previously exposed to In

291 atients with hematopoietic cell transplants (HCT), cancer (hematologic and solid tumor), HIV, and sol

292 atients with hematopoietic cell transplants (HCT), cancer, human immunodeficiency virus (HIV), and so

293 daily frequency) from 18 patients undergoing HCT and determined their composition by multiparallel 16

294 In patients undergoing HCT, the use of a restrictive RBC transfusion strategy t

295 comes of 129 patients with WAS who underwent HCT at 29 Primary Immune Deficiency Treatment Consortium

296 related biomarkers in 66 males who underwent HCT.

297 of 33 982 patients who received an unrelated HCT done in Australia, Europe, Japan, North America, and

298 s GVHD risk after HLA-B-mismatched unrelated HCT and differentiates high-risk HLA-B mismatches from t

299 ism in GVHD after HLA-B-mismatched unrelated HCT.

300 d metabolites, spheroids were cultured using HCT-116 colorectal cancer cells, treated with the antica

301 oculture by 41% and 55%, and co-culture with HCT-116 and HT-29 cells by 39% and 26% (C3G) and 50% and