ライフサイエンスコーパス: PTLD

1 PTLD involving the allograft, central nervous system, an

2 PTLD is associated with EBV infection and can result in

3 PTLD occurring in EBV-seronegative recipients was associ

4 PTLD, Kaposi sarcoma, and lung and bronchial cancers wer

5 756 KTX (580 PTLDs; 0.51%), 13 937 HTX (140 PTLDs; 1.0%) and 40 437 LTX (383 PTLDs; 0.95%) performed

6 37 HTX (140 PTLDs; 1.0%) and 40 437 LTX (383 PTLDs; 0.95%) performed January 2003 onward.

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 son.Our study set comprised 112 756 KTX (580 PTLDs; 0.51%), 13 937 HTX (140 PTLDs; 1.0%) and 40 437 L

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

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

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 increased occurrence of acute rejection and PTLD.

21 diagnosis, and management of EBV viremia and PTLD.

22 eported malignancy events were classified as PTLD.

23 lignant B cell lymphoproliferations, such as PTLD.

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

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

26 rophylaxis also protects from EBV-associated PTLD.

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

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

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

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

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

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

33 with Epstein-Barr virus (EBV) (+), CD20 (+) PTLD.

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

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

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

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

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

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

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

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

42 Early and late childhood PTLD have distinct characteristics.

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

44 Current PTLD treatment strategies include reduction of immunosup

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

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

47 Of 114,025 recipients, 754 developed PTLD (5-year incidence of 0.84%).

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

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

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

51 formation about patients' risk of developing PTLD.

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

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

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

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

56 posttransplant lymphoproliferative disease (PTLD) in a study of 3170 pediatric primary heart transpl

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

58 posttransplant lymphoproliferative disease (PTLD) remains problematic.

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

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

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

62 posttransplant lymphoproliferative disease (PTLD).

63 posttransplant lymphoproliferative disease (PTLD).

64 transplantation lymphoproliferative disease (PTLD).

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

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

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

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

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

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

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

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

73 Posttransplant lymphoproliferative disorder (PTLD) is a major complication of solid-organ transplanta

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

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

76 Posttransplant lymphoproliferative disorder (PTLD) is a well-established complication of immunosuppre

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

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

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

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 ost-transplant lymphoproliferative disorder (PTLD) to discover virally controlled therapeutic targets

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

85 posttransplant lymphoproliferative disorder (PTLD).

86 posttransplant lymphoproliferative disorder (PTLD).

87 ransplantation lymphoproliferative disorder (PTLD).

88 posttransplant lymphoproliferative disorder (PTLD).

89 posttransplant lymphoproliferative disorder (PTLD).

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

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

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

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

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

95 osttransplant lymphoproliferative disorders (PTLD) occurred more frequently in non-African American (

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

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

98 osttransplant lymphoproliferative disorders (PTLDs) are potentially fatal, EBV-driven B-cell malignan

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

100 osttransplant lymphoproliferative disorders (PTLDs) is limited.

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

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

103 Three patients developed early PTLD.

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

105 Most early PTLD patients experienced graft rejection before PTLD di

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

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

108 effective in treating pediatric with EBV (+) PTLD following solid-organ transplantation.

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

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

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

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

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

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

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

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

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

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

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

120 immunosuppression is a primary cause of EBV+ PTLD.

121 the implications for the development of EBV+ PTLD.

122 atening EBV lymphoproliferative disease (EBV-PTLD).

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 Strong FLC-PTLD associations were also observed at diagnosis/select

127 % confidence interval [95% CI], 2.1-3.2) for PTLD, 1.8 (95% CI, 1.4-2.4) for non-Hodgkin's lymphoma,

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

129 We assessed Medicare claims for PTLD in a retrospective cohort of 53,719 patients who un

130 ere were 719 (1.3%) patients with claims for PTLD.

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

132 -32.3), whereas HLA-B8 was a risk factor for PTLD in EBV-seropositive individuals (OR = 3.29, 95% CI

133 onor EBV status was a strong risk factor for PTLD in the seronegative recipient, but risk magnitude w

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

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

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

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

138 No risk factors for PTLD were identified.

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

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

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

142 Might this represent a separate pathway for PTLD development?

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

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

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

146 The overall risk for PTLD declined in the most recent transplant era (2001-20

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

148 18 years) with children at highest risk for PTLD with a relative risk of 2.4 compared to infants and

149 transplant recipients were at lower risk for PTLD, irrespective of the recipient EBV IgG serostatus.

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

151 ssive therapies also influences the risk for PTLD.

152 ent potential new therapeutic strategies for PTLD through targeting of EBV-driven survival signals.

153 esent a novel immunotherapeutic strategy for PTLD and other Gal1-expressing tumors.

154 rvention for prevention of and treatment for PTLD.

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

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

157 nfections while receiving therapy and 7 from PTLD.

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

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

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

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

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

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

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

165 sented with complications associated with GI-PTLD requiring emergency surgery.

166 tcome were observed between patients with GI-PTLD who required surgery and those who did not (P=0.371

167 Thirty-six patients presented with GI-PTLD.

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

169 nt recipients and associated with heightened PTLD risk.

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

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

172 In PTLD, the expression of EBV proteins, including latent m

173 tems and developed recommendations to aid in PTLD prevention.

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

175 To assess the role of B-cell dysfunction in PTLD, we measured circulating FLCs among Canadian transp

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

177 gnificantly different between early and late PTLD.

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

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

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

181 5 patients developed PTLD after 1 year (late PTLD).

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

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

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

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

186 (0.82%), and kidney (0.79%) cancers; in LT, PTLD (2.44%), lung and bronchial (2.18%), primary hepati

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

188 ll as the minimization of toxicity in milder PTLDs.

189 lactic and preemptive strategies to minimize PTLD development, including modulation of immunosuppress

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

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

192 e with functioning original allograft and no PTLD) was 71% (95% CI: 57%-82%) and overall survival was

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

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

195 duces proliferation and induces apoptosis of PTLD-derived EBV+ B cell lines.

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

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

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

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

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

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

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

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

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

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

206 of racial differences in the development of PTLD has not been reported.

207 re important variables in the development of PTLD in the pediatric heart transplant recipient.

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

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

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

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

212 -7 at transplantation developed some form of PTLD.

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

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

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

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

217 resulted in a significant lower incidence of PTLD.

218 al Cancer Registry to determine incidence of PTLD.

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

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

221 herapy was associated with increased risk of PTLD in EBV IgG-negative recipients, regardless of race.

222 status was associated with a higher risk of PTLD in the non-AF population.

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

224 lly help identify recipients at high risk of PTLD.

225 fect modifier for EBV IgG status and risk of PTLD.

226 5) were associated with an increased risk of PTLD.

227 ant were associated with a decreased risk of PTLD.

228 nt were associated with an increased risk of PTLD.

229 Adjusted risks of PTLD, rejection, death, and graft failure were examined

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

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

232 In addition to the surgery, treatment of PTLD consisted of reduction of immunosuppression, use of

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

234 he pathogenesis, diagnosis, and treatment of PTLD.

235 d reporting and improve our understanding of PTLD.

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

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

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

239 e included in this retrospective analysis on PTLD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

255 gistered in the German multicenter pediatric PTLD registry.

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

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

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

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

260 mphoblastoid B-cell lines (LCLs) and primary PTLDs overexpress galectin-1 (Gal1), a carbohydrate-bind

261 The German prospective PTLD registry D2006-2012 records baseline features, trea

262 ine features, treatment, and outcome of rare PTLD subtypes in adults after solid organ transplantatio

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

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

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

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

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

268 3 (FoxP3) in biopsies of PTLDs and survival, PTLD subtype, and clinical characteristics.

269 In total, 69.4% patients survived PTLD.

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

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

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

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

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

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

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

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

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

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

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

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

282 Mortality subsequent to PTLD did not differ by race.

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

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

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

286 84 PCNS PTLD patients, median time of SOT-to-PTLD was 54 months, 79% had kidney SOT, histology was mo

287 ts and clinicians in diagnosing and treating PTLD.

288 lack of reduction of immunosuppression upon PTLD diagnosis.

289 nd 57 matched transplant recipients who were PTLD-free.

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

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

292 nt recipients, including 29 individuals with PTLD and 57 matched transplant recipients who were PTLD-

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

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

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

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

297 ll lymphoma lines derived from patients with PTLD.

298 PTLD and clinical outcomes in patients with PTLD.

299 s do not influence survival in patients with PTLD.

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