@article{TCR9301,
author = {Young Kwang Chae and Ayush Arya and Jonathan Anker and Francis Giles},
title = {Another important step towards understanding tumor immune evasion—novel mechanisms of PD-L1 overexpression},
journal = {Translational Cancer Research},
volume = {5},
number = {Suppl 3},
year = {2016},
keywords = {},
abstract = {Recent advancements in the search for new treatment strategies for cancer have led to the development of therapeutic agents that target specific molecules that are critical to cancer development and/or expansion. The inhibition of the programmed cell death-1 (PD-1)/programmed cell death ligand-1 (PD-L1) pathway is one of such upcoming strategies that is being extensively explored in the field of oncology. Immunotherapy agents targeting the PD-1/PD-L1 signaling pathway have demonstrated promising anti-tumor efficacy in several malignancies, including non-small cell lung cancer (NSCLC) and melanoma, among others (1-6). Tumor cells are known to overexpress PD-L1, which aids in immune evasion by inducing T cell anergy and exhaustion within the tumor microenvironment (7). Several chromosomal alterations, most notably 9p24.1 amplification [identified in Hodgkin’s lymphoma (HL) cell lines], are reported to result in overexpression of PD-1 ligands (8,9). In addition, endogenous molecules such as interferon-γ (IFNγ) have also been identified to induce PD-L1 overexpression (10,11). The ability of tumors to suppress the host immune response is considered to be central to the clinical benefit observed with immunotherapy agents targeting the PD-1/PD-L1 signaling pathway (8,12-17). The mechanistic relationship between evasion of endogenous immunity by cancer cells and overexpression of PD-1 ligands, however, is not fully understood.},
issn = {2219-6803}, url = {https://tcr.amegroups.org/article/view/9301}
}