ライフサイエンスコーパス: PTLD

1 PTLD among R+ individuals occurred during the second yea

2 PTLD among R+ individuals was more likely to occur among

3 PTLD involving the allograft, central nervous system, an

4 PTLD is associated with EBV infection and can result in

5 PTLD occurring in EBV-seronegative recipients was associ

6 PTLD-related mortality did not differ between R+ and R-

7 skin cancer (SHR, 2.92; 95% CI, 2.52-3.39), PTLD (SHR, 1.93; 95% CI, 1.01-3.66), solid tumor (SHR, 1

8 Forty-seven of 74 PTLDs displayed no FoxP3 cells at all.

9 in LuT, lung and bronchial cancers (5.94%), PTLD (5.72%), and colorectal cancer (1.38%).

10 The adjusted PTLD risk was significantly decreased in the SRL group (

11 t (liver), graft dysfunction 25 months after PTLD (heart).

12 er), cytomegalovirus disease 21 months after PTLD treatment (liver), graft dysfunction 25 months afte

13 ciated with graft failure or mortality after PTLD diagnosis.

14 Patient survival after PTLD diagnosis was 64% at 1 year, 53% at 2 years, 48% at

15 Allograft survival after PTLD diagnosis was 94.4% (66.6-99.2%) at 5 years.

16 lograft survival, and patient survival after PTLD.

17 al (3.24%) and prostate (3.07%) cancers, and PTLD (2.24%); and in LuT, lung and bronchial cancers (5.

18 further improvement in outcomes with EBV and PTLD.

19 Concordance of FLCs, M-proteins, and PTLD tumor light chain restriction was imperfect.

20 diagnosis, and management of EBV viremia and PTLD.

21 lignant B cell lymphoproliferations, such as PTLD.

22 c target for the treatment of EBV-associated PTLD and that combined blockade of PI3Kdelta and mTOR pr

23 rations and patients with non-EBV-associated PTLD were refractory to IR and to chemotherapy.

24 rophylaxis also protects from EBV-associated PTLD.

25 EBV disease and its associated PTLD is more frequently seen when primary EBV infection

26 s kappa FLCs were both detected in plasma at PTLD diagnosis; although the tumor was not restricted at

27 amples obtained on average 3.5 months before PTLD diagnosis, cases were more likely to have polyclona

28 patients experienced graft rejection before PTLD diagnosis (P=0.0081).

29 roversial treatment of Burkitt lymphoma (BL)-PTLD.

30 ncreased risk of posttransplant skin cancer, PTLD, solid organ cancer, death and graft failure.

31 id organ transplant recipients, with CD20(+) PTLD unresponsive to immunosuppression reduction, were t

32 were diagnosed with severe B-lineage, CD20+, PTLD after a median of 37 months (range, 5-93) from live

33 In multivariate analysis, B-cell PTLD and hepatitis C infection were independent predicto

34 utcomes for adults with biopsy-proven B-cell PTLD treated initially with R-Mono or Rituximab plus CHO

35 Conclusion In B-cell PTLD, treatment stratification into rituximab or rituxim

36 Due to the rarity of monomorphic T-cell PTLD (T-PTLD), knowledge about pathogenesis, risk factor

37 rous membranes, monomorphic PTLD, and T-cell PTLD were independent prognostic indicators of poor surv

38 involvement, bone marrow involvement, T-cell PTLD, and age were associated with increased mortality.

39 another case with an M-protein had a T-cell PTLD.

40 Early and late childhood PTLD have distinct characteristics.

41 Compared with controls, PTLD cases had higher kappa FLCs (median 1.53 vs. 1.07 t

42 ge, serum creatinine, lactate dehydrogenase, PTLD localization, and histology), we constructed a prog

43 A total of 18 patients (1.5%) developed PTLD of B cell origin.

44 ation (early PTLD) and 85 patients developed PTLD after 1 year (late PTLD).

45 Forty-two patients developed PTLD within the first year after transplantation (early

46 ive transplant recipients (R+) who developed PTLD and compare survival outcomes with EBV-seronegative

47 ll all adult kidney recipients who developed PTLD between January 1, 1998, and December 31, 2007.

48 formation about patients' risk of developing PTLD.

49 ansfer of EBV-CTL in SOT patients developing PTLD without the need for reduction in immunosuppressive

50 At diagnosis, PTLD patients had similar numbers of EBV-specific CD4 an

51 Three children died, PTLD-free, from different transplant-related complicatio

52 posttransplant lymphoproliferative disease (PTLD) arising after solid organ transplant remains conte

53 posttransplant lymphoproliferative disease (PTLD) diagnosis (p = 0.006), while low DNAemia rates wer

54 transplantation lymphoproliferative disease (PTLD) is an often Epstein-Barr virus (EBV)-associated ma

55 posttransplant lymphoproliferative disease (PTLD) remains problematic.

56 posttransplant lymphoproliferative disease (PTLD) remains to be defined due to heterogeneity of this

57 posttransplant lymphoproliferative disease (PTLD), and EBV load measurement is an important tool to

58 posttransplant lymphoproliferative disease (PTLD), nasopharyngeal carcinoma (NPC), and AIDS-associat

59 posttransplant lymphoproliferative disease (PTLD), on EBV I latency tumors like BL, could improve th

60 posttransplant lymphoproliferative disease (PTLD).

61 posttransplant lymphoproliferative disease (PTLD).

62 transplantation lymphoproliferative disease (PTLD).

63 (posttransplant lymphoproliferative disease [PTLD] or symptomatic EBV infection, defined as flu-like

64 ransplantation lymphoproliferative diseases (PTLD) are mainly Epstein-Barr virus (EBV)-associated dis

65 posttransplant lymphoproliferative disorder (PTLD) after a rituximab-based treatment in the allogenei

66 ost-transplant lymphoproliferative disorder (PTLD) and identified response to rituximab induction as

67 posttransplant lymphoproliferative disorder (PTLD) are those who acquire primary Epstein-Barr virus (

68 posttransplant lymphoproliferative disorder (PTLD) cases after month 18.

69 Posttransplant lymphoproliferative disorder (PTLD) continues to be a devastating and potentially life

70 ransplantation lymphoproliferative disorder (PTLD) from EBV(+)PTLD in remission and EBV(-)PTLD.

71 ransplantation lymphoproliferative disorder (PTLD) in a pediatric population and explore its feasibil

72 ransplantation lymphoproliferative disorder (PTLD) incidence and presentation with both recipient Eps

73 Posttransplant lymphoproliferative disorder (PTLD) is a potentially fatal disorder arising after soli

74 Posttransplant lymphoproliferative disorder (PTLD) is a serious complication in organ transplant reci

75 ransplantation lymphoproliferative disorder (PTLD) is a well-recognized complication after solid-orga

76 Posttransplant lymphoproliferative disorder (PTLD) is an infrequent but serious complication of solid

77 ransplantation lymphoproliferative disorder (PTLD) is associated with significant mortality in kidney

78 posttransplant lymphoproliferative disorder (PTLD) is reported in the pediatric small bowel transplan

79 ost-transplant lymphoproliferative disorder (PTLD) is reported in the pediatric small bowel transplan

80 posttransplant lymphoproliferative disorder (PTLD) may be related with the Epstein-Barr virus (EBV) r

81 posttransplant lymphoproliferative disorder (PTLD) remains a major cause of morbidity and mortality a

82 ost-transplant lymphoproliferative disorder (PTLD) that occurs in pediatric organ recipients, is not

83 ransplantation lymphoproliferative disorder (PTLD), a complication of lung transplantation with an in

84 posttransplant lymphoproliferative disorder (PTLD).

85 ransplantation lymphoproliferative disorder (PTLD).

86 posttransplant lymphoproliferative disorder (PTLD).

87 posttransplant lymphoproliferative disorder (PTLD).

88 posttransplant lymphoproliferative disorder (PTLD, 1.58%), followed by lung (1.12%), prostate (0.82%)

89 Posttransplant Lymphoproliferative Disorder (PTLD-1) trial established sequential treatment with four

90 osttransplant lymphoproliferative disorders (PTLD) and Kaposi's sarcoma remain important complication

91 osttransplant lymphoproliferative disorders (PTLD) are a common malignancy after renal transplantatio

92 osttransplant lymphoproliferative disorders (PTLD) in liver transplants (LTX), at variance with prior

93 ansplantation lymphoproliferative disorders (PTLD) present a major cause of mortality and morbidity a

94 ansplantation lymphoproliferative disorders (PTLD), and first and subsequent primary occurrences of N

95 osttransplant lymphoproliferative disorders (PTLD).

96 osttransplant lymphoproliferative disorders (PTLDs) are associated with significant morbidity and mor

97 ansplantation lymphoproliferative disorders (PTLDs) are rare compared with EBV(+) PTLDs, occur later

98 osttransplant lymphoproliferative disorders (PTLDs) is limited.

99 Early PTLD development was associated with younger age (P=0.00

100 Early PTLD was often of B-cell lymphoma histology (P=0.024) an

101 Three patients developed early PTLD.

102 specific T cells tended to be lower in early PTLD compared with late PTLD.

103 Most early PTLD patients experienced graft rejection before PTLD di

104 the first year after transplantation (early PTLD) and 85 patients developed PTLD after 1 year (late

105 Whereas early PTLD appears mainly as an Epstein-Barr virus-driven dise

106 ew insights into the role of EphA4 in EBV(+) PTLD and DLBCL.

107 detected in EBV(-) tonsils but not in EBV(+) PTLD.

108 orders (PTLDs) are rare compared with EBV(+) PTLDs, occur later after transplantation, and have a poo

109 mphoproliferative disorder (PTLD) from EBV(+)PTLD in remission and EBV(-)PTLD.

110 EBV(-) PTLD developed 9-22 months (median, 15) after transplant

111 In contrast to reports of EBV(-) PTLD in adults, these plasma cell lesions occurred early

112 We describe 5 cases of EBV(-) PTLD in recipients of combined liver and small bowel all

113 Few studies have reported EBV(-) PTLD in pediatric solid-organ transplantation recipients

114 PTLD) from EBV(+)PTLD in remission and EBV(-)PTLD.

115 EBV+ PTLD can arise after primary EBV infection, or because o

116 The incidence of EBV+ PTLD is variable depending on the organ transplanted and

117 the implications for the development of EBV+ PTLD.

118 immunosuppression is a primary cause of EBV+ PTLD.

119 atening EBV lymphoproliferative disease (EBV-PTLD).

120 n = 33) or SOT (n = 13) with established EBV-PTLD, who had failed rituximab therapy, with third-party

121 fe, immediately accessible treatment for EBV-PTLD.

122 can eradicate EBV-associated lymphomas (EBV-PTLD) after transplantation of hematopoietic cell (HCT)

123 ilitates the diagnosis and management of EBV/PTLD as well as being used to inform preemptive therapy

124 also useful in the treatment of established PTLD.

125 Five PTLD cases manifested elevated FLCs with an abnormal kap

126 factors associated with mortality following PTLD were SBTx (odds ratio [OR], 12.00; 95% confidence i

127 factors associated with mortality following PTLD were SBTx (OR 12.00,95CI:2.34-61.45;p=0.003), monom

128 % confidence interval [95% CI], 2.1-3.2) for PTLD, 1.8 (95% CI, 1.4-2.4) for non-Hodgkin's lymphoma,

129 on centers were retrospectively analyzed for PTLD, either biopsy-proven or probable disease.

130 The HLA-B40 group was a risk factor for PTLD in EBV-seronegative individuals (OR = 8.38, 95% CI

131 -32.3), whereas HLA-B8 was a risk factor for PTLD in EBV-seropositive individuals (OR = 3.29, 95% CI

132 Hazards were used to model risk factors for PTLD and clinical outcomes in patients with PTLD.

133 study highlights the prognostic factors for PTLD and enables the development of a new prognostic sco

134 entified as novel susceptibility factors for PTLD in EBV-seropositive and EBV-seronegative individual

135 sed to identify independent risk factors for PTLD in our population.

136 No risk factors for PTLD were identified.

137 The prognostic factors for PTLD were investigated using Kaplan-Meier and Cox analys

138 HLA) type as risk and prognostic factors for PTLD.

139 The unadjusted hazard ratio (HR) for PTLD if recipient EBV seronegative was 5.005 for KTX, 6.

140 Might this represent a separate pathway for PTLD development?

141 Kaplan-Meier analysis was performed for PTLD-free survival, allograft survival, and patient surv

142 In EBV- recipients, hazard ratio for PTLD was 1.98 (95% CI: 1.28-3.07) for mTORi+TAC, 0.45 (9

143 Adjusted hazard ratio for PTLD was 4.39 (95% CI: 3.60-5.37) for EBV- versus EBV+ r

144 still significantly associated with risk for PTLD in LTX, though less so because of higher baseline r

145 18 years) with children at highest risk for PTLD with a relative risk of 2.4 compared to infants and

146 sensitivity to identify patients at risk for PTLD, it lacks specificity.

147 ssive therapies also influences the risk for PTLD.

148 r data support R-Mono as initial therapy for PTLD arising after renal or liver transplantation.

149 rvention for prevention of and treatment for PTLD.

150 The FoxP3 PTLDs were associated with hepatitis C seropositivity (P

151 The FoxP3 PTLDs were more frequently of T-cell phenotype (P = 0.04

152 Overall freedom from PTLD was 98.5% at 1 year, 94% at 5 years and 90% at 10 y

153 Freedom from PTLD was lowest in children (ages 1 to < 10 years) versu

154 ht were in CR 28 weeks later without further PTLD therapy.

155 s poor specificity as a biomarker for future PTLD risk.

156 ence of surgical treatment of complicated GI-PTLD after liver transplantation (LTx).

157 Most GI-PTLD occurred in the small bowel or right colon (81%).

158 In summary, GI-PTLD requiring surgical intervention is an extremely rar

159 ic stem cell and 18 liver recipients; 12 had PTLD).

160 A review was undertaken to identify PTLD cases treated at our institution over the past 25 y

161 In PTLD patients, central nervous system (CNS) involvement,

162 ndividuals, in transplant recipients, and in PTLD patients.

163 There was no difference in PTLD site between R+ and R- patients.

164 FoxP3 Tregs are rare in PTLD, possibly because of heavy immunosuppression.

165 gnificantly different between early and late PTLD.

166 The majority occurred as late PTLD in male heart transplant recipients.

167 red by insufficient immunosurveillance, late PTLD often resembles tumors with distinct pathogenetic a

168 to be lower in early PTLD compared with late PTLD.

169 5 patients developed PTLD after 1 year (late PTLD).

170 disease (P=0.016) were only observed in late PTLDs, which are more likely to present with nodal disea

171 Severe B-lineage PTLD after solid organ transplantation may be classified

172 ression tapering was associated with a lower PTLD mortality (16% vs 39%), and a decrease of EBV DNAem

173 trend to increased risk of rejection, lower PTLD risk, and similar risk for graft failure when compa

174 (0.82%), and kidney (0.79%) cancers; in LT, PTLD (2.44%), lung and bronchial (2.18%), primary hepati

175 us (EBV)-associated posttransplant lymphoma (PTLD) is a major cause of morbidity/mortality after hema

176 decreased risk of all de novo malignancies, PTLD, and subsequent primary occurrences of NMSC after H

177 inadequate as a single strategy in managing PTLD in SBTx and prompt escalation to rituximab and CTL

178 inadequate as a single strategy in managing PTLD in SBTx and prompt escalation to rituximab and/or C

179 ll as the minimization of toxicity in milder PTLDs.

180 Monomorphic PTLD made up 64% of SBTx and 43% of LTx cases.

181 = 1); polymorphic PTLD (n = 1); monomorphic PTLD (n = 27), Hodgkin disease (n = 2).

182 n, invasion of serous membranes, monomorphic PTLD, and T-cell PTLD were independent prognostic indica

183 ecreased in patients who developed non-NMSC, PTLD, or non-PTLD compared with patients who did not dev

184 Non-PTLD mortality was 3 of 41 (7%) and 4 of 60 (7%) within

185 atients who developed non-NMSC, PTLD, or non-PTLD compared with patients who did not develop these ma

186 gan transplant patients accounted for 25% of PTLD cases in R+ patients, while accounting for only 2.1

187 M-proteins were present in 91% of PTLD cases versus 50% to 67% of other recipients with hi

188 t UK single-center, single-organ analysis of PTLD to date in a retrospective cohort study of 80 cases

189 However, current knowledge on all aspects of PTLD is limited due to its rarity, morphologic heterogen

190 This rare case of PTLD presenting as multiple renal, hepatic and splenic l

191 Seventy-four cases of PTLD after solid organ transplantation with sufficient m

192 Historically, most cases of PTLD among lung transplant recipients occurred within th

193 We identified 31 cases of PTLD during the study period.

194 One hundred six cases of PTLD were identified with 1392 solid-organ transplant re

195 One hundred forty-four cases of PTLD were identified, indicating an overall EBV-related

196 Five hundred patient cases of PTLD were referred to the French registry.

197 nal (GI) tract occurs in 25% of all cases of PTLD.

198 gative predictive value for the detection of PTLD in a 28-pediatric-patient cohort with a clinical su

199 lue of (18)F-FDG PET/CT for the detection of PTLD in children with a clinical suspicion of this disea

200 determine incidence and risk determinants of PTLD in Irish kidney transplant recipients.

201 tion at 1 and 5 years after the diagnosis of PTLD was 35% (95% confidence interval [95% CI], 18-69%)

202 - and three-year survival after diagnosis of PTLD was 50% and 38%, respectively.

203 Diagnosis of PTLD was biopsy-proven based on World Health Organizatio

204 Results: The diagnosis of PTLD was established in 14 patients (49%).

205 omes at 1 and 5 years after the diagnosis of PTLD.

206 e required to reevaluate the epidemiology of PTLD in the modern era of transplant immunosuppression.

207 e increasing reports on a late-onset form of PTLD.

208 The incidence of PTLD among patients who are EBV-seropositive before tran

209 nal transplantation with a high incidence of PTLD described in the first posttransplant year.

210 The incidence of PTLD in our center is extremely low when compared with t

211 The incidence of PTLD is highest in the late posttransplantation period.

212 The incidence of PTLD was highest during the 10th to 14th posttransplanta

213 resulted in a significant lower incidence of PTLD.

214 al Cancer Registry to determine incidence of PTLD.

215 Majority of PTLD following pediatric SBTx are of monomorphic subtype

216 ed a prospective survey of the occurrence of PTLD in a French nationwide population of adult kidney r

217 o compare the characteristics and outcome of PTLD in pediatric SBTx against LTx patients at a single

218 able analysis showed that a poor response of PTLD to rituximab was associated with an age >/=30 years

219 Ri+TAC was associated with increased risk of PTLD, death, and graft failure, while MMF+CsA use was as

220 ant were associated with a decreased risk of PTLD.

221 nt were associated with an increased risk of PTLD.

222 lly help identify recipients at high risk of PTLD.

223 arr virus (EBV) serostatus and EBV status of PTLD histology, particularly in the late posttransplanta

224 Multicentered, large prospective studies of PTLD with correlative immunologic work are needed to tes

225 DG PET/CT scans due to clinical suspicion of PTLD within an 8-y period.

226 cation of this approach for the treatment of PTLD in SOT recipients.

227 he pathogenesis, diagnosis, and treatment of PTLD.

228 d reporting and improve our understanding of PTLD.

229 These challenges include the wide variety of PTLD presentation (making treatment optimization difficu

230 orkhead box protein 3 (FoxP3) in biopsies of PTLDs and survival, PTLD subtype, and clinical character

231 re included from a population-based study of PTLDs in Sweden.

232 e included in this retrospective analysis on PTLD.

233 We considered evidence on PTLD risk factors including Epstein-Barr virus serostatu

234 r than providing another classical review on PTLD, this "How I Treat" article, based on 2 case report

235 For example, one PTLD case with an IgG lambda M-protein had a tumor that

236 We found a paucity of early onset PTLD in our cohort with no cases in the first posttransp

237 Although early-onset PTLD uniformly involved the transplanted lung, this was

238 lung, this was relatively rare in late-onset PTLD (3 of 3 vs. 1 of 7).

239 ith the development of early- and late-onset PTLD in pediatric solid organ transplant recipients.

240 contrast, the seven patients with late-onset PTLD were all EBV seropositive before transplantation an

241 ecipients demonstrates a trend of late-onset PTLD with the majority of patients who died of treatment

242 gic parameters between early- and late-onset PTLD.

243 c and adult patients with EBV viremia and/or PTLD after SCT.

244 roduced by oligoclonal B-cell populations or PTLD tumor cells and could potentially help identify rec

245 Among 84 PCNS PTLD patients, median time of SOT-to-PTLD was 54 months,

246 Altogether, PCNS PTLD appears to represent a distinct clinicopathologic e

247 In pediatric PTLD patients, pretreatment EBV-specific T-cell numbers

248 gistered in the German multicenter pediatric PTLD registry.

249 the response assessment setting of pediatric PTLD, given the observed high proportions of false-posit

250 ith or without chemotherapy on the pediatric PTLD Pilot 2005 protocol.

251 Here we report our experience with pediatric PTLD nonresponsive to immunosuppression (IS) withdrawal,

252 included: early lesions (n = 1); polymorphic PTLD (n = 1); monomorphic PTLD (n = 27), Hodgkin disease

253 el with either nondestructive or polymorphic PTLD subtypes.

254 el with either nondestructive or polymorphic PTLD.

255 Since EBV-specific T cells could prevent PTLD, cellular immunotherapy has been a promising treatm

256 to identify all patients with biopsy-proven PTLD for the period 2000-2014.

257 ew and a retrospective analysis of this rare PTLD subtype.

258 of using CAR-T therapy to manage refractory PTLD in SOT recipients and its possible complications.

259 while 2 of 3 (66%) patients with EBV-related PTLD exhibited only a low EBV load beforehand.

260 dentified, indicating an overall EBV-related PTLD frequency of 3.22%, ranging from 1.16% for matched-

261 than two-thirds of patients with EBV-related PTLD survived after rituximab-based treatment.

262 ts with a high, persistent EBV load remained PTLD-free throughout a follow-up of 5.0 +/- 1.3 years, w

263 In low-risk PTLD, outcomes were similar between therapies.

264 Thirty-seven PTLD patients were included following LTx (n = 23, incid

265 Thirty-seven PTLD patients were included following LTx (n=23, inciden

266 3 (FoxP3) in biopsies of PTLDs and survival, PTLD subtype, and clinical characteristics.

267 In total, 69.4% patients survived PTLD.

268 T-PTLD is a heterogeneous group of different aberrant T-ce

269 regimen, time between transplantation and T-PTLD manifestation, T-PTLD subtype, virus positivity, lo

270 transplantation and T-PTLD manifestation, T-PTLD subtype, virus positivity, localization, therapy, a

271 We analyzed all available articles on T-PTLD in the PubMed database as well as in our own databa

272 plantation was associated with early-onset T-PTLD, whereas late onset occurred after immunosuppressio

273 to the rarity of monomorphic T-cell PTLD (T-PTLD), knowledge about pathogenesis, risk factors, thera

274 ependent favorable prognostic factors were T-PTLD of the large granular lymphocytic leukemia subtype,

275 The PTLD biopsies were reevaluated and stained with the 236A

276 In the prognostic model, the PTLD mortality increased with the increasing number of f

277 striction was present 5 years later when the PTLD relapsed.

278 distinct clinicopathologic entity within the PTLD spectrum that is associated with renal SOT, occurs

279 of 29 FoxP3 cells per mm, most (80%) of the PTLDs were FoxP3.

280 Median time to PTLD diagnosis was 8.3 (range, 1.2-13.9) years.

281 The median time to PTLD was 3.00 (95% confidence interval, 2.12-3.26) years

282 Median (range) time from transplantation to PTLD diagnosis was 41 (4-128) months.

283 84 PCNS PTLD patients, median time of SOT-to-PTLD was 54 months, 79% had kidney SOT, histology was mo

284 ts and clinicians in diagnosing and treating PTLD.

285 lack of reduction of immunosuppression upon PTLD diagnosis.

286 rameters, and pathology of 127 children with PTLD who were registered in the German multicenter pedia

287 diatric SBTx and LTx patients diagnosed with PTLD from 1989 to 2016 was conducted.

288 diatric SBTx and LTx patients diagnosed with PTLD from 1989-2016 was conducted.

289 In this study, we report our experience with PTLD in lung transplantation with CMV Ig prophylaxis.

290 ognostic score that classified patients with PTLD as being at low, moderate, high, or very high risk

291 Patients with PTLD had a 5-year survival rate of 53% and 10-year survi

292 e-negative results occurred in patients with PTLD in the Waldeyer's ring, cervical lymph nodes, or sm

293 Patients with PTLD or chronic high viral loads after solid organ trans

294 report the outcomes for three patients with PTLD refractory to immunochemotherapy 10-20 years after

295 ere isolated from 16 pediatric patients with PTLD, 4 transplanted children with EBV reactivation, and

296 PTLD and clinical outcomes in patients with PTLD.

297 s do not influence survival in patients with PTLD.

298 ll lymphoma lines derived from patients with PTLD.

299 ere compared between R+ and R- patients with PTLD.

300 compared early (<1 year) and late (>1 year) PTLD using survival analysis.