TY - JOUR
T1 - Biological Difference Between Epstein–Barr Virus Positive and Negative Post-transplant Lymphoproliferative Disorders and Their Clinical Impact
AU - Ferla, Valeria
AU - Rossi, Francesca Gaia
AU - Goldaniga, Maria Cecilia
AU - Baldini, Luca
PY - 2020/5/8
Y1 - 2020/5/8
N2 - Epstein–Barr virus (EBV) infection is correlated with several lymphoproliferative disorders, including Hodgkin disease, Burkitt lymphoma, diffuse large B-cell lymphoma (DLBCL), and post-transplant lymphoproliferative disorder (PTLD). The oncogenic EBV is present in 80% of PTLD. EBV infection influences immune response and has a causative role in the oncogenic transformation of lymphocytes. The development of PTLD is the consequence of an imbalance between immunosurveillance and immunosuppression. Different approaches have been proposed to treat this disorder, including suppression of the EBV viral load, reduction of immune suppression, and malignant clone destruction. In some cases, upfront chemotherapy offers better and durable clinical responses. In this work, we elucidate the clinicopathological and molecular-genetic characteristics of PTLD to clarify the biological differences of EBV(+) and EBV(–) PTLD. Gene expression profiling, next-generation sequencing, and microRNA profiles have recently provided many data that explore PTLD pathogenic mechanisms and identify potential therapeutic targets. This article aims to explore new insights into clinical behavior and pathogenesis of EBV(–)/(+) PTLD with the hope to support future therapeutic studies.
AB - Epstein–Barr virus (EBV) infection is correlated with several lymphoproliferative disorders, including Hodgkin disease, Burkitt lymphoma, diffuse large B-cell lymphoma (DLBCL), and post-transplant lymphoproliferative disorder (PTLD). The oncogenic EBV is present in 80% of PTLD. EBV infection influences immune response and has a causative role in the oncogenic transformation of lymphocytes. The development of PTLD is the consequence of an imbalance between immunosurveillance and immunosuppression. Different approaches have been proposed to treat this disorder, including suppression of the EBV viral load, reduction of immune suppression, and malignant clone destruction. In some cases, upfront chemotherapy offers better and durable clinical responses. In this work, we elucidate the clinicopathological and molecular-genetic characteristics of PTLD to clarify the biological differences of EBV(+) and EBV(–) PTLD. Gene expression profiling, next-generation sequencing, and microRNA profiles have recently provided many data that explore PTLD pathogenic mechanisms and identify potential therapeutic targets. This article aims to explore new insights into clinical behavior and pathogenesis of EBV(–)/(+) PTLD with the hope to support future therapeutic studies.
KW - Epstein–Barr virus
KW - gene expression profile
KW - microRNA
KW - next-generation sequencing
KW - post-transplant lymphoproliferative disorders
KW - tumor microenvironment
UR - http://www.scopus.com/inward/record.url?scp=85085097746&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85085097746&partnerID=8YFLogxK
U2 - 10.3389/fonc.2020.00506
DO - 10.3389/fonc.2020.00506
M3 - Review article
AN - SCOPUS:85085097746
VL - 10
JO - Frontiers in Oncology
JF - Frontiers in Oncology
SN - 2234-943X
M1 - 506
ER -