TY - JOUR
T1 - Dysregulation of cell survival in diffuse large B cell lymphoma
T2 - Mechanisms and therapeutic targets
AU - Miao, Yi
AU - Medeiros, L. Jeffrey
AU - Xu-Monette, Zijun Y.
AU - Li, Jianyong
AU - Young, Ken H.
N1 - Funding Information:
This study is supported by The University of Texas MD Anderson Cancer Center Lymphoma Moonshot Program, Institutional Research Grant Award, Hagemeister Lymphoma Foundation, and the University Cancer Foundation via the Sister institution network Fund at The University of Texas MD Anderson Cancer.
Publisher Copyright:
Copyright © 2019 Miao, Medeiros, Xu-Monette, Li and Young.
PY - 2019
Y1 - 2019
N2 - Diffuse large B cell lymphoma (DLBCL) is the most common type of lymphoma worldwide, representing 30–40% of non-Hodgkin lymphomas, and is clinically aggressive. Although more than half of patients with DLBCL are cured by using standard first-line immunochemotherapy, the remaining patients are refractory to the first-line therapy or relapse after complete remission and these patients require novel therapeutic approaches. Understanding the pathogenesis of DLBCL is essential for identifying therapeutic targets to tackle this disease. Cell survival dysregulation, a hallmark of cancer, is a characteristic feature of DLBCL. Intrinsic signaling aberrations, tumor microenvironment dysfunction, and viral factors can all contribute to the cell survival dysregulation in DLBCL. In recent years, several novel drugs that target abnormal cell survival pathways, have been developed and tested in clinical trials of patients with DLBCL. In this review, we discuss cell survival dysregulation, the underlying mechanisms, and how to target abnormal cell survival therapeutically in DLBCL patients.
AB - Diffuse large B cell lymphoma (DLBCL) is the most common type of lymphoma worldwide, representing 30–40% of non-Hodgkin lymphomas, and is clinically aggressive. Although more than half of patients with DLBCL are cured by using standard first-line immunochemotherapy, the remaining patients are refractory to the first-line therapy or relapse after complete remission and these patients require novel therapeutic approaches. Understanding the pathogenesis of DLBCL is essential for identifying therapeutic targets to tackle this disease. Cell survival dysregulation, a hallmark of cancer, is a characteristic feature of DLBCL. Intrinsic signaling aberrations, tumor microenvironment dysfunction, and viral factors can all contribute to the cell survival dysregulation in DLBCL. In recent years, several novel drugs that target abnormal cell survival pathways, have been developed and tested in clinical trials of patients with DLBCL. In this review, we discuss cell survival dysregulation, the underlying mechanisms, and how to target abnormal cell survival therapeutically in DLBCL patients.
KW - Apoptosis
KW - BCL2
KW - BCR signaling
KW - Cell survival
KW - DLBCL
KW - EBV
KW - P53
KW - TME
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U2 - 10.3389/fonc.2019.00107
DO - 10.3389/fonc.2019.00107
M3 - Review article
C2 - 30881917
AN - SCOPUS:85063402503
SN - 2234-943X
VL - 9
JO - Frontiers in Oncology
JF - Frontiers in Oncology
IS - MAR
M1 - 107
ER -