We investigated this issue using genomically related, clonal subsets from the same methylcholanthrene-induced sarcoma: a highly immunogenic subset that is spontaneously eliminated in vivo by adaptive immunity and a less immunogenic subset that forms tumors in immunocompetent mice, but is sensitive to PD-1/PD-L1 blockade therapy.
In this review, we provide a brief overview of the mechanisms of action of immune checkpoint inhibitors and discuss the proposed biomarkers of therapy response, such as lymphocytic infiltration, intratumoral PD-L1 expression, and mutational load in sarcomas.
Expression and clinical association of programmed cell death-1, programmed death-ligand-1 and CD8<sup>+</sup> lymphocytes in primary sarcomas is subtype dependent.
However, the unprecedented clinical activity and excellent safety profile of checkpoint inhibitors targeting programmed death-1 receptor and its ligand (PD-1/PD-L1) have galvanized the field and generated much enthusiasm to harness the power of immunotherapy in pursuit of cures in patients with advanced sarcomas.
Finally, we found that SARC-L1 is sensitive to several drugs commonly used to treat sarcoma and also susceptible to anti-PD-L1 monoclonal antibody therapy in vivo.
Our meta-analysis indicated that high PD-L1 expression is likely to be a negative factor for patients with sarcomas and that it predicts worse survival outcomes.
Stata 12.0 software was applied to calculate the strength of association between PD-L1 expression and sarcoma.In total, 14 articles containing 15 independent studies and 1,451 patients were included in this meta-analysis.