Post-transplantation lymphoproliferative disorders: Current concepts and future therapeutic approaches

Table 1 Epstein-Barr virus-positive vs Epstein-Barr virus-negative post-transplant lymphoproliferative disorders[25]

	EBV-positive PTLD	EBV-negative PTLD
Molecular-genomic studies	Fewer genomic abnormalities	Share many genomic/ transcriptmic features with diffuse large B-cell lymphoma in IC patients
Origin	Mostly B-cell proliferative lesions	Mostly T-cell proliferative lesions
Gene-expression	“Non-germinal” center B-cell	“Germinal center B-cell type”[4]
Prevalence	More common (first peak)	Less common (second peak)
Risk of PTLD	Less risk compared to seronegative TR	Seronegative SOT pediatric TR are more vulnerable to develop PTLD with increased estimated risk of 10-75[16,17]
SOT vs HSCT	Almost all cases of HSCT (100%) are EBV positive	In SOT, both EBV positive and negative are present
Clinical consequences of EBV status	Less clear	Less clear
Prognosis/response to therapy in adults.	Not prognostic/predictive of response to therapy[21,23]
Common criteria	A considerable proportion of both EBV+ve and -ve PTLD respond to RI as a sole intervention[24]
Future studies	Whole-exome/genome wide sequencing and studies of role of EBV-associated microRNAs, may further define PTLD pathogenesis with more precise molecular-genomic classification of both EBV+ve and EBV-ve PTLD

RI: Reduction of immunosuppression; IC: Immunocompetent; PTLD: Post-transplant lymphoproliferative disorders; EBV: Epstein-Barr virus; HSCT: Haplo-identical allogeneic hematopoietic stem-cell transplant; KTR: Kidney transplant recipients; TR: Transplant recipients; SOT: Solid organ transplantation.