Introduction
NSCLC, tumor, T-cell apoptosis, Tumor
TUMOR, CANCER PROGRESSION, TUMOR, PROLIFERATION, DISEASE, NSCLC, IMMUNE TOLERANCE, TUMOR GROWTH
Tumor cells can evade host immune responses by exploiting immune checkpoint pathways [The mechanisms responsible for resistance to immune checkpoint inhibition are not fully defined, but treatment responsiveness has been associated with the presence of an inflamed tumor microenvironment [Immunotherapy strategies targeting indoleamine 2,3-dioxygenase 1 (IDO1), a tryptophan-catabolizing enzyme, may enhance the efficacy of immune checkpoint blockade. IDO1 contributes to tumor immune tolerance by inhibiting T-cell proliferation, inducing T-cell apoptosis, promoting the differentiation of naïve T cells into regulatory T cells, and regulating the pool of peptides available for antigen presentation [In preclinical studies, inhibition of both IDO1 and an immune checkpoint pathway provided greater control of tumor growth than immune checkpoint inhibition alone [Epigenetics refers to alterations in gene expression that occur independently of changes to inherited gene sequences. Epigenetic changes in malignant cells can lead to the upregulation of genes that promote cancer progression [Clinical data on the antitumor activity of combination treatment with an epigenetic modulator and an immune checkpoint inhibitor were limited at the time when the current study was designed. However, in a prior study, five patients with NSCLC previously treated with azacitidine and the histone deacetylase inhibitor entinostat exhibited durable (>6 months) disease control [