Post-Transplant Lymphoproliferative Disease (PTLD) after Allogeneic Hematopoietic Stem Cell Transplantation: Biology and Treatment Options

Clerico, Michele; Dogliotti, Irene; Consoli, C.; Giaccone, Luisa; Bruno, Benedetto; Cavallo, Federica

doi:10.3390/jcm11247542

Cited by 14 publications

(13 citation statements)

References 73 publications

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“…Rituximab +/− RIS is the first line of treatment for HSCT PTLD with escalation to EBV-directed adoptive cell immunotherapy in rituximabrefractory cases. 14 This review will highlight the treatment of non-destructive PTLD, polymorphic PTLD and monomorphic DLBCL PTLD. Treatment of non-DLBCL monomorphic PTLD follows traditional histology-based treatments in immunocompetent patients and will not be reviewed here.…”

Section: R E V I E Wmentioning

confidence: 99%

“…39 Also, RIS is often ineffective by itself due to an insufficient cytotoxic response mounted by the donor system at the time of diagnosis. 8,14 Thus, the first line of treatment in CD20+ HSCT PTLD is often rituximab +/− RIS if feasible. Complete response to frontline rituximab monotherapy in HSCT PTLD has been reported to be only 20% (ORR 60%-65%) with a 2year median OS of 50%.…”

Section: Current Practice For Treatment Of Hsct Ptldmentioning

confidence: 99%

“…The risk‐stratified sequential treatment approach does not apply to HSCT PTLD. Rituximab +/− RIS is the first line of treatment for HSCT PTLD with escalation to EBV‐directed adoptive cell immunotherapy in rituximab‐refractory cases 14 . This review will highlight the treatment of non‐destructive PTLD, polymorphic PTLD and monomorphic DLBCL PTLD.…”

Section: Introductionmentioning

confidence: 99%

“…Significant RIS may not be feasible in many cases of HSCT PTLD due to risk of GvHD 39 . Also, RIS is often ineffective by itself due to an insufficient cytotoxic response mounted by the donor system at the time of diagnosis 8,14 . Thus, the first line of treatment in CD20+ HSCT PTLD is often rituximab +/− RIS if feasible.…”

Section: Introductionmentioning

confidence: 99%

“…2,8,11 For HSCT, PTLD risk factors include EBV recipient-donor sero-mismatch, selective donor T-cell depletion, haploidentical donor, unrelated or HLA-mismatched related donor, umbilical cord transplant, use of reduced intensity conditioning regimens, age of recipient older than 50, the use of antithymocyte globulin (ATG) or anti-CD3 monoclonal antibody and chronic GvHD requiring prolonged immunosuppression. 2,8,[12][13][14] The incidence of PTLD is high in the first year after transplantation (early onset PTLD) then starts to decline. The majority of early onset PTLD are SOT and HSCT PTLD that are driven by EBV.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Post‐transplant lymphoproliferative disorder: Update on treatment and novel therapies

2023

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Post-transplant lymphoproliferative disorder (PTLD) is rare and heterogeneous lymphoid proliferations that occur as a result of immunosuppression following solid organ transplant (SOT) and haematopoietic stem cell transplant (HSCT) with the majority being driven by EBV. Although some histologies are similar to lymphoid neoplasms seen in immunocompetent patients, treatment of PTLD may be different due to difference in pathobiology and higher risk of treatment complications. The most common treatment approach in SOT PTLD after failing immunosuppression reduction (RIS) takes into consideration a risk-stratified sequential algorithm with rituximab +/− chemotherapy based on phase 2 studies. In HSCT PTLD, RIS alone and chemotherapy are usually ineffective making rituximab +/− RIS as the gold standard of frontline treatment. In this review, we give an update on the treatment of PTLD beyond RIS. We highlight the most recent studies that attempted to incorporate more aggressive chemotherapy regimens and novel treatments into the traditional risk-stratified sequential approach. We also discuss the role of EBV-cytotoxic T lymphocytes in treatment of EBV-driven PTLD. Other novel agents with potential role in PTLD will be discussed in addition to the challenges that could arise with chimeric antigen receptor T-cell therapy and immune checkpoint inhibitors in this population.

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Section: R E V I E Wmentioning

confidence: 99%

Section: Current Practice For Treatment Of Hsct Ptldmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Post‐transplant lymphoproliferative disorder: Update on treatment and novel therapies

2023

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Improving the safety of CAR‐T‐cell therapy: The risk and prevention of viral infection for patients with relapsed or refractory B‐cell lymphoma undergoing CAR‐T‐cell therapy

Qian,

Yang,

Zhang

et al. 2024

American J Hematol

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Chimeric antigen receptor (CAR) T‐cell therapy, an innovative immunotherapeutic against relapsed/refractory B‐cell lymphoma, faces challenges due to frequent viral infections. Despite this, a comprehensive review addressing risk assessment, surveillance, and treatment management is notably absent. This review elucidates immune response compromises during viral infections in CAR‐T recipients, collates susceptibility risk factors, and deliberates on preventive strategies. In the post‐pandemic era, marked by the Omicron variant, new and severe threats to CAR‐T therapy emerge, necessitating exploration of preventive and treatment measures for COVID‐19. Overall, the review provides recommendations for viral infection prophylaxis and management, enhancing CAR‐T product safety and recipient survival.

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Posttransplant complications: molecular mechanisms and therapeutic interventions

Liu,

Shen,

Yan

et al. 2024

MedComm

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Posttransplantation complications pose a major challenge to the long‐term survival and quality of life of organ transplant recipients. These complications encompass immune‐mediated complications, infectious complications, metabolic complications, and malignancies, with each type influenced by various risk factors and pathological mechanisms. The molecular mechanisms underlying posttransplantation complications involve a complex interplay of immunological, metabolic, and oncogenic processes, including innate and adaptive immune activation, immunosuppressant side effects, and viral reactivation. Here, we provide a comprehensive overview of the clinical features, risk factors, and molecular mechanisms of major posttransplantation complications. We systematically summarize the current understanding of the immunological basis of allograft rejection and graft‐versus‐host disease, the metabolic dysregulation associated with immunosuppressive agents, and the role of oncogenic viruses in posttransplantation malignancies. Furthermore, we discuss potential prevention and intervention strategies based on these mechanistic insights, highlighting the importance of optimizing immunosuppressive regimens, enhancing infection prophylaxis, and implementing targeted therapies. We also emphasize the need for future research to develop individualized complication control strategies under the guidance of precision medicine, ultimately improving the prognosis and quality of life of transplant recipients.

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Post-Transplant Lymphoproliferative Disease (PTLD) after Allogeneic Hematopoietic Stem Cell Transplantation: Biology and Treatment Options

Cited by 14 publications

References 73 publications

Post‐transplant lymphoproliferative disorder: Update on treatment and novel therapies

Post‐transplant lymphoproliferative disorder: Update on treatment and novel therapies

Improving the safety of CAR‐T‐cell therapy: The risk and prevention of viral infection for patients with relapsed or refractory B‐cell lymphoma undergoing CAR‐T‐cell therapy

Posttransplant complications: molecular mechanisms and therapeutic interventions

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