ライフサイエンスコーパス: HCT

1 HCT survivors had more hospitalizations or death with in

2 HCT-116 and HT-29 inhibition correlated with total pheno

3 HCT-ASCT with thiotepa and carmustine is an effective tr

4 recipient and donor harbored iciHHV-6 in 13 HCTs.

5 e tested archived BAL fluid samples from 132 HCT recipients with CMV pneumonia and 139 controls (100

6 Of 39 patients (22 SOT, 17 HCT), 15 had documented ganciclovir resistance mutations

7 The study cohort included 2609 HCT recipients and their donor pairs: 483 with proven/pr

8 d<5kDa caused cytotoxicity to Caco-2, HT-29, HCT-116 human colon cancer cells, and reduced inflammato

9 We identified 4319 HCT donor-recipient pairs (8638 subjects) who received a

10 Methods A total of 477 HCT recipients (236 autologous, 128 reduced-intensity al

11 nd HK3) in colorectal cancer (HT-29, SW 480, HCT-15, RKO, and HCT 116) and melanoma (MDA-MB-435S and

12 value within the tested range of 28.0-61.5% HCT.

13 We identified 60 HCT recipients (1.4%) and 40 donors (0.9%) with iciHHV-6

14 including telomerase-positive (HeLa, MCF-7, HCT-116, and HEK293T) and telomerase-negative cell lines

15 Thus, there were 87 HCTs (2%) in which the recipient, donor, or both harbore

16 Results: The 998 HCT survivors were a mean (SD) of 42.5 (11.6) years of a

17 After HCT, patients must be closely monitored for development

18 dpoint was complete response at day 30 after HCT-ASCT in all registered eligible patients who receive

19 optimize therapy for patients with BOS after HCT.

20 res at baseline, 2 weeks, and 3 months after HCT and caregiver-assessed QOL and mood at baseline and

21 to patients without complete response after HCT-ASCT.

22 te Cdk5 in allogeneic T-cell responses after HCT and as an important new target for therapeutic inter

23 d QOL and mood at baseline and 2 weeks after HCT.

24 and at 6 months and 1, 2, and 3 years after HCT.

25 We retrospectively analyzed all HCT recipients between 2004 and 2014, in whom real-time

26 maining patients undergoing HLA-matched allo HCT (validation cohort; n = 577) as well as to patients

27 s to patients undergoing HLA-mismatched allo HCT.

28 during 2 years of follow-up time after allo-HCT by using cause-specific proportional hazards in a re

29 Surprisingly, Ab blockade of CD70 after allo-HCT significantly increases GVHD.

30 increasingly being used off-label after allo-HCT.

31 mia, and reduced overall survival after allo-HCT.

32 nd relapse/progression of disease after allo-HCT.

33 agent in 20 HL patients relapsing after allo-HCT.

34 reased in key target organs early after allo-HCT.

35 HD, infections, and organ failure after allo-HCT.

36 vent relapse and improve survival after allo-HCT.

37 could be associated with relapse after allo-HCT.

38 pansion of recipient T reg cells before allo-HCT, exploiting the crucial role of tumor necrosis facto

39 nclusion, PD-1 blockade in relapsed cHL allo-HCT patients appears to be highly efficacious but freque

40 these major differences toward clinical allo-HCT, findings generated in animal models of GVHD have le

41 microbiota of 541 patients admitted for allo-HCT was profiled by means of 16S ribosomal sequencing of

42 In allogeneic HCT (allo-HCT), donor-derived T cells recognize host tissues as fo

43 Experimental studies in allo-HCT animal models have shown some promising results for

44 However, the role of this pathway in allo-HCT is previously unknown.

45 efficiently modulate alloreactivity in allo-HCT to either exacerbate it for a powerful antileukemic

46 ssay as an additional tool for managing allo-HCT recipients at risk for CMV reactivation needs furthe

47 prove IR to reduce these limitations of allo-HCT.

48 HL and 27 had >/=1 salvage therapy post-allo-HCT and prior to anti-PD-1 treatment.

49 PD-1 blockade post-allo-HCT should be studied further but cannot be recommended

50 ematopoietic cell transplantation (post-allo-HCT) and the success of programmed death 1 (PD-1) blocka

51 ceiving anti-PD-1 mAbs for relapse post-allo-HCT.

52 he potential of our strategy to protect allo-HCT patients from acute GvHD by expanding T reg cells vi

53 ed or refractory HL who did not receive allo-HCT.

54 1 of complications related to a second allo-HCT.

55 pectively monitored 63 CMV-seropositive allo-HCT recipients with a CMV-specific enzyme-linked immunos

56 logeneic hematopoietic cell transplant (allo-HCT) recipients at risk for cytomegalovirus (CMV) reacti

57 eic hematopoietic-cell transplantation (allo-HCT) are relapse, graft-versus-host disease (GVHD), and

58 ematopoietic stem cell transplantation (allo-HCT) by suppressing conventional T cells (Tconvs).

59 eic hematopoietic cell transplantation (allo-HCT) is a potentially curative treatment for hematologic

60 eic hematopoietic cell transplantation (allo-HCT) is indicated for patients with relapsed or refracto

61 ematopoietic stem cell transplantation (allo-HCT) recipient.

62 eic hematopoietic cell transplantation (allo-HCT).

63 eic hematopoietic cell transplantation (allo-HCT).

64 eic hematopoietic cell transplantation (allo-HCT).

65 Among 404 allogeneic HCT recipients, including 125 cord blood, 125 HLA-mismat

66 dsDNA viruses was frequent after allogeneic HCT and had a dose-dependent association with increased

67 rts, with clinical outcomes after allogeneic HCT within this prospective, multicenter study.

68 kers with clinical outcomes after allogeneic HCT.

69 e with higher risks of GVHD after allogeneic HCT.

70 s (8638 subjects) who received an allogeneic HCT and had archived pre-HCT peripheral blood mononuclea

71 L while minimizing GVHD following allogeneic HCT.

72 tested weekly plasma samples from allogeneic HCT recipients at our center from 2007 to 2014.

73 In allogeneic HCT (allo-HCT), donor-derived T cells recognize host tis

74 Reduced-intensity allogeneic HCT recipients showed evidence of delayed decline.

75 e AML who underwent myeloablative allogeneic HCT at our institution.

76 Conclusion Myeloablative allogeneic HCT recipients showed significant cognitive decline comp

77 Limited data also support use of allogeneic HCT (alloHCT) in selected HIV-infected patients who meet

78 18.7% of autologous and 35.7% of allogeneic HCT recipients.

79 ncies who underwent autologous or allogeneic HCT to inpatient palliative care integrated with transpl

80 ildren or young adults undergoing allogeneic HCT.

81 eletal complications also were greater among HCT versus non-HCT cancer survivors.

82 We evaluated supplemental oxygen use among HCT recipients with RSV infection.

83 ion fifty (IC50) for BL, SH, RG on HT-29 and HCT-116 cell proliferation ranged 0.9-2.0mg/mL.

84 associations between microbiota features and HCT outcomes.

85 ctal cancer (HT-29, SW 480, HCT-15, RKO, and HCT 116) and melanoma (MDA-MB-435S and SK-MEL-28) cell l

86 in maize plants treated with HCT as well as HCT-deficient or HCT-producing strains of C. carbonum An

87 was 95% for those who were infection-free at HCT vs 81% for those with active infection (P = .009).

88 orbidities are best captured by an augmented HCT-CI.

89 A composite model comprising augmented HCT-CI, age, and cytogenetic/molecular risks had even be

90 The augmented HCT-CI, age, and cytogenetic/molecular risks could be co

91 Autologous HCT is now the standard of care for patients with HIV-re

92 Cognitive functioning in autologous HCT recipients generally was spared.

93 r reduced-intensity allogeneic or autologous HCT remains unclear.

94 detection in the upper/lower airways before HCT and the occurrence of allo-LSs.

95 nd bronchoalveolar lavage (BAL) fluid before HCT.

96 Screening for RVs before HCT might identify patients at risk for allo-LSs.

97 standardized neuropsychologic testing before HCT and at 6 months and 1, 2, and 3 years after HCT.

98 enetically that dual SHMT1/2 knockout blocks HCT-116 colon cancer tumor xenograft formation.

99 Both HCT and non-HCT cancer survivors had significantly great

100 e MAC (n = 135) or RIC (n = 137) followed by HCT from HLA-matched related or unrelated donors.

101 Colon carcinoma HCT 116 cells were cultured and grown into three-dimensi

102 means to enhance the clinical efficacy of CB HCT.

103 rted induction treatment; 73 (92%) commenced HCT-ASCT.

104 atients with FA undergoing alternative donor HCT without radiation exposure.

105 During HCT-ASCT, the most common grade 3 toxicity was fever (50

106 Symptom burden and anxiety during HCT hospitalization partially mediated the effect of the

107 duction in symptom burden and anxiety during HCT partially accounts for the effect of the interventio

108 To assess symptom burden during HCT, we used the Edmonton Symptom Assessment Scale.

109 xamine whether symptom burden or mood during HCT mediated the effect of the intervention on 6-month o

110 care clinicians at least twice a week during HCT hospitalization; the palliative intervention was foc

111 Furthermore, the application of exogenous HCT enabled us to show that the activity of plant-encode

112 tive analysis all patients receiving a first HCT between January 2004 and September 2014 were include

113 es can influence development of IA following HCT.

114 In particular, clinicians who care for HCT survivors should be aware of their high rates of lat

115 To be considered for HCT, patients must have HIV infection that is responsive

116 age was 52 years (range, 18 to 74 years) for HCT recipients and 55 years (range, 19 to 73 years) for

117 Haplo-HCT with PT-Cy provides survival outcomes comparable to

118 t 1 year was significantly lower after Haplo-HCT (12% v 45%; P < .001), and this benefit was confirme

119 d 987 adult patients undergoing either Haplo-HCT (n = 180) or MSD-HCT (n = 807) following reduced-int

120 al hematopoietic cell transplantation (Haplo-HCT) using post-transplantation cyclophosphamide (PT-Cy)

121 body irradiation (TBI) before haploidentical HCT in a murine model.

122 icrosample collection issues and hematocrit (HCT)-related bias would facilitate more widespread use o

123 , MAF = 2.4%, p < 3 x 10(-8) for hematocrit [HCT] and HGB).

124 , based on combination of advanced age, high HCT-CI, very poor-risk cytogenetic and molecular feature

125 y, the gene coexpression profiles from human HCT recipients who developed GVHD while on immunosuppres

126 Importance ratings of identified HCT outcomes rated on a Likert scale from 1 (not importa

127 es to improve CD4 reconstitution can improve HCT outcomes, including survival, and reduce the need fo

128 Inhibition of miR-451a in HCT-116 cells significantly decreased cell proliferation

129 r natural killer (NK) cell alloreactivity in HCT can control leukemic relapse, but capturing alloreac

130 understand the appropriate role for ATLG in HCT.

131 The gut microbiota was highly dynamic in HCT recipients, with loss and appearance of taxa common

132 ssociated with prolonged shedding of HCoV in HCT recipients.

133 Infection in HCT candidates may require delay of transplantation.

134 Chemosensitivity was measured in HCT-116, a human colorectal carcinoma cell line, using i

135 acteria, particularly the gut microbiota, in HCT outcome and in GVHD development.

136 impact of frailty on subsequent mortality in HCT survivors.

137 t-transplant, a total of 694 observations in HCT recipients.

138 risk SNP of colorectal cancer, rs6983267, in HCT-116 cells.

139 o-controlled multicenter trial of Triplex in HCT patients.

140 aded according to the HCT Comorbidity Index (HCT-CI) were recognized as relevant clinical variables f

141 etic cell transplantation-comorbidity index (HCT-CI), were evaluated.

142 cores did not change after reduced-intensity HCT but declined significantly for fine motor dexterity

143 gnificantly ( P < .003) in reduced-intensity HCT recipients for executive function, verbal fluency, a

144 ontrols and autologous and reduced-intensity HCT recipients.

145 last course, patients commenced intravenous HCT-ASCT (rituximab 375 mg/m(2) [day 1], carmustine 400

146 ), high efficiency against other cell lines (HCT 116 and HeLa), and possible activation by light abov

147 but capturing alloreactivity in HLA-matched HCT has been elusive.

148 nhibition in donor selection for HLA-matched HCT may achieve superior graft versus leukemia effects,

149 ood, 125 HLA-mismatched, and 154 HLA-matched HCTs, detection of multiple viruses was common through d

150 iruses included cord blood or HLA-mismatched HCT, myeloablative conditioning, and acute graft-versus-

151 undergoing either Haplo-HCT (n = 180) or MSD-HCT (n = 807) following reduced-intensity conditioning r

152 provides survival outcomes comparable to MSD-HCT, with a significantly lower risk of chronic GVHD.

153 Myeloablative HCT recipients had significantly lower ( P < .001) post-

154 or dexterity ( P < .001) after myeloablative HCT.

155 ological malignancy to receive myeloablative HCT from an available 8/8-HLA matched URD.

156 ind trial of ATLG in unrelated myeloablative HCT, the incorporation of ATLG did not improve moderate-

157 Both HCT and non-HCT cancer survivors had significantly greater 10-year c

158 of hospitalization compared with matched non-HCT cancer survivors (280 v 173 episodes per 1,000 perso

159 ying cancer diagnosis (as applicable) to non-HCT 2-year cancer survivors, using the state cancer regi

160 tions also were greater among HCT versus non-HCT cancer survivors.

161 the risk of frailty even among nongeriatric HCT patients.

162 for iciHHV-6 and compared characteristics of HCT recipients and donors with iciHHV-6 with those of re

163 ent of reliable and objective comparisons of HCT outcomes across clinical conditions and care deliver

164 ial diversity is common during the course of HCT and is associated with GVHD development and treatmen

165 Conclusion History of HCT was associated with late morbidity and mortality amo

166 ng, C. parvum attachment to and infection of HCT-8 cells were inhibited by glycosaminoglycans and wer

167 ted C. parvum attachment to and infection of HCT-8 cells.

168 ng 3 stages was deployed to refine a list of HCT outcomes.

169 might subsequently influence the outcomes of HCT.

170 adenoviremia during the lymphopenic phase of HCT.

171 vation of HHV-6B in 25% (4/16 recipients) of HCT recipients with donor- or recipient-derived inherite

172 and those with active disease at the time of HCT support the use of treatment algorithms that use MRD

173 Host risk factors include type of HCT and degree of immunosuppression.

174 difference was observed for the viability of HCT 116 and MCF-7 cells challenged with 0.4, 4.0, and 40

175 n vitro(99m)Tc-HYNIC-TCP-1 binding assays on HCT 116 cells indicated a mean Kd of 3.04+/-0.52nM.

176 treated with HCT as well as HCT-deficient or HCT-producing strains of C. carbonum Analyses of these d

177 In the validation set, the original HCT-CI had better C statistic and AUC estimates compared

178 Augmenting the original HCT-CI with 3 independently significant comorbidities, h

179 Careful planning for the peri-HCT management of the cART can avoid risk of significant

180 Post-HCT scores were comparable between controls and autologo

181 nts had significantly lower ( P < .001) post-HCT scores than controls for executive function, verbal

182 te graft, landmark analysis at day +100 post-HCT revealed that CD3 < 300 cells/muL, CD8 < 50 cells/mu

183 day -10 and continued through day +100 post-HCT.

184 stein-Barr virus between days 0 and 100 post-HCT.

185 eg3, P = .041; ST2, P = .002) at day 30 post-HCT in vorinostat-treated subjects compared with similar

186 viruses with mortality through day 365 post-HCT with Cox models.

187 nsplantation is associated with adverse post-HCT outcome for those patients in morphologic remission.

188 ciHHV-6 could guide donor selection and post-HCT risk stratification and treatment.

189 nd to identify associated variables and post-HCT trends of cognitive impairment.

190 After a median of 285 days post-HCT, patients with PV-Haufen had an increased risk of di

191 and Cox proportional hazards models for post-HCT outcomes based on recipient and donor iciHHV-6 statu

192 targeted T-cell immunotherapy to manage post-HCT leukemic relapse.

193 Pre-HCT to 6 months post-HCT scores did not change after reduced-intensity HCT bu

194 By applying this assay to recipient post-HCT plasma and serum samples, we demonstrated reactivati

195 around the time of neutrophil recovery post-HCT is predictive of subsequent development of severe ac

196 At neutrophil recovery post-HCT, the presence of oral Actinobacteria and oral Firmic

197 We found that post-HCT dasatinib use increased the risk of cytomegalovirus

198 on on leukemia cells-upregulated in the post-HCT environment-signals for NK cell inhibition via inhib

199 cognitive reserve were associated with post-HCT cognitive impairment.

200 re, and the prognosis for patients with post-HCT relapse is poor.

201 Although 1-year post-HCT median CD4 counts and freedom from IV immunoglobulin

202 However, pre-HCT to 3 years post-HCT scores declined significantly ( P < .003) in reduced

203 At 3 years post-HCT, global cognitive impairment was present in 18.7% of

204 Pre-HCT disease staging included 10-color multiparametric fl

205 Pre-HCT to 6 months post-HCT scores did not change after red

206 Although pre-HCT patient T cells were not available, mutation effects

207 eived an allogeneic HCT and had archived pre-HCT peripheral blood mononuclear cell samples.

208 However, pre-HCT to 3 years post-HCT scores declined significantly (

209 index </= 4 and < 5% marrow myeloblasts pre-HCT were randomly assigned to receive MAC (n = 135) or R

210 This effect of pre-HCT MRD prompted us to compare outcomes in consecutive p

211 These results show that pre-HCT BAL fluid RV positivity was a predictor for allo-LSs

212 Sixty-seven (38%) patients received HCT.

213 Among patients receiving HCT, 27 (40%) had graft-versus-host disease, and most de

214 HIV-infected patients requiring HCT may also be considered for participation in trials e

215 We retrospectively reviewed HCT recipients with HCoV detected in nasal samples by po

216 Potent strategies are choosing the right HCT source (eg, donor-recipient matching, cell dose, gra

217 PE) procedure were unaffected by the blood's HCT value within the tested range of 28.0-61.5% HCT.

218 ) were associated with the need for a second HCT or death.

219 across HLA-DP disparities absent in sibling HCT.

220 Simultaneously, HCT at pH 6.6-6.7 and 7.2 increased significantly.

221 The HCT survivors were 8.4 times more likely to be frail tha

222 e the role that quality of life plays in the HCT process.

223 sence of comorbidity graded according to the HCT Comorbidity Index (HCT-CI) were recognized as releva

224 in the pH of maximum heat coagulation time (HCT) (P<.05).

225 layed Ca(2+)-dependent, saturable binding to HCT-8 and Caco-2 cells and competitively inhibited C. pa

226 re the primary difference may be exposure to HCT.

227 Shifts in gut microbiota have been linked to HCT outcomes; however, their effect on PCs is unknown.

228 ve trials to ensure that patients proceed to HCT infection free.

229 care clinics rated the importance of the top HCT outcomes identified by the Delphi process.

230 estigate how the effector molecule HC-toxin (HCT), a histone deacetylase inhibitor produced by the fu

231 Two hydroxycinnamoyl-CoA transferases (HCT/HQT) have been involved in CGA production, of which

232 s for the process of health care transition (HCT) among adolescent and young adults with special heal

233 er allogeneic hematopoietic cell transplant (HCT) conferred nearly universal mortality secondary to l

234 logeneic hematopoietic stem cell transplant (HCT) recipients and Triplex in healthy adults motivated

235 ant (SOT) and hematopoietic cell transplant (HCT) recipients at a single center over a 10-year period

236 al disease in hematopoietic cell transplant (HCT) recipients but does not lead to resolution of virem

237 (iciHHV-6) in hematopoietic cell transplant (HCT) recipients is unclear.

238 thod for hematopoietic stem cell transplant (HCT) recipients.

239 e lacking for hematopoietic cell transplant (HCT) recipients.

240 mortality in hematopoietic cell transplant (HCT) recipients.

241 n during hematopoietic stem-cell transplant (HCT).

242 rgan and hematopoietic stem cell transplant (HCT).

243 neic haemopoietic stem-cell transplantation (HCT) are at risk for CMV reactivation.

244 logeneic hematopoietic cell transplantation (HCT) are limited by incomplete understanding of their ep

245 s) after hematopoietic cell transplantation (HCT) contribute to significant morbidity and mortality.

246 eic hematopoietic stem cell transplantation (HCT) failure, and the prognosis for patients with post-H

247 logeneic hematopoietic cell transplantation (HCT) from 2010 to 2014, including 68 patients with typic

248 logeneic hematopoietic cell transplantation (HCT) from unrelated donors as compared with related dono

249 Hematopoietic cell transplantation (HCT) has been considered a curative therapy, but the pro

250 Hematopoietic cell transplantation (HCT) has now been shown to be safe and effective for sel

251 ns after hematopoietic cell transplantation (HCT) injure normal tissues and may increase the risk of

252 Hematopoietic cell transplantation (HCT) is a critical treatment of patients with high-risk

253 Hematopoietic cell transplantation (HCT) is curative for FA-related marrow failure or leukem

254 sk after hematopoietic-cell transplantation (HCT) is not known.

255 logeneic hematopoietic cell transplantation (HCT) is unknown.

256 logeneic hematopoietic cell transplantation (HCT) recently showed no difference between study arms in

257 logeneic hematopoietic cell transplantation (HCT) represents a potentially curative treatment for a v

258 es among hematopoietic cell transplantation (HCT) survivors versus a matched population of patients w

259 nrelated hematopoietic cell transplantation (HCT) were randomly assigned one to one to placebo (n =12

260 tant for hematopoietic cell transplantation (HCT), especially when HSC numbers are limited, as in the

261 for hematopoietic stem cell transplantation (HCT), patients receive high-dose chemotherapy before tra

262 After hematopoietic cell transplantation (HCT), polyoma-BK virus is associated with hemorrhagic cy

263 -matched hematopoietic cell transplantation (HCT), sibling and unrelated donors (UDs) are biologicall

264 tolerate hematopoietic cell transplantation (HCT), whereas others may not have a compatible human leu

265 logeneic hematopoietic cell transplantation (HCT), which resolved their autoimmunity.

266 logeneic hematopoietic cell transplantation (HCT).

267 ed donor hematopoietic cell transplantation (HCT).

268 logeneic hematopoietic cell transplantation (HCT).

269 logeneic hematopoietic cell transplantation (HCT).

270 logeneic hematopoietic cell transplantation (HCT).

271 ns after hematopoietic cell transplantation (HCT).

272 llogeneic haemopoietic cell transplantation (HCT).

273 rapy and hematopoietic cell transplantation (HCT).

274 (UDs) are biologically different because UD-HCT is typically performed across HLA-DP disparities abs

275 of patients with cancer who did not undergo HCT, where the primary difference may be exposure to HCT

276 young children (<10 years of age) undergoing HCT for marrow failure using low-dose busulfan-containin

277 HLA-A*0201, aged 18-75 years, and undergoing HCT from a matched-related or matched-unrelated donor.

278 , 8.2 years; range 4.3-44) with FA underwent HCT between June 2009 and May 2014.

279 .4%) with myelodysplastic syndrome underwent HCT using matched unrelated (n = 25, 55.5%), mismatched

280 y was performed on 94 patients who underwent HCT from 2009 to 2011 and who were previously enrolled i

281 act in 1,328 patients with AML who underwent HCT from 9/10 or 10/10 HLA-matched unrelated donors.

282 stool samples from 66 patients who underwent HCT, starting pre-transplantation and continuing weekly

283 that the increased GVHD risk after unrelated HCT is predominantly an effect of HLA-mismatching.

284 npermissive HLA-DPB1 mismatches in unrelated HCT.

285 ve been involved in CGA production, of which HCT reflects CGA levels.

286 However, risk associated with HCT decreased for diagnosis years 1987-1995; the hazard

287 ater well-being, and hazards associated with HCT decreased, reaching levels of significantly less ris

288 r in children and adolescents diagnosed with HCT-related adenoviremia.

289 at 2,791 sites in maize plants treated with HCT as well as HCT-deficient or HCT-producing strains of

290 However, survivors treated with HCT experienced somewhat greater well-being, and hazards

291 Among survivors, those treated with HCT had higher median Karnofsky/Lansky scores than those

292 Among patients treated with HCT, treatment at an early age is associated with improv

293 ors in the subgroup of patients treated with HCT.

294 and Methods Patients age 18 to 65 years with HCT comorbidity index </= 4 and < 5% marrow myeloblasts

295 ved between patients treated with or without HCT (P = .671).

296 ved between patients treated with or without HCT across all diagnosis years (1964-2013).

297 ll-being of patients treated with or without HCT along with clinical factors associated with mortalit

298 sky/Lansky scores than those treated without HCT (P < .001).

299 Methods Two-year HCT survivors treated at a comprehensive cancer center f

300 Results After median follow-up of 7.1 years, HCT survivors experienced significantly greater rates of