PD-1/PD-L1 Inhibitors Implications in Common Human Cancers.
Lung cancer: the landscape of lung cancer treatment has been profoundly reshaped by tumor immunotherapy directed at PD-1/PD-L1. Notably, the effectiveness of PD-L1 inhibitors surpasses that of chemotherapy, particularly in advanced non-small cell lung cancer (NSCLC) patients exhibiting elevated PD-L1 levels. This potency is equally evident among patients with previously untreated metastatic squamous NSCLC. Moreover, when considering patients with NSCLC who have undergone prior treatment, a decreased rate of disease progression is more frequently observed in response to PD-1/PD-L1 inhibitors, as opposed to conventional chemotherapy. This observation holds true, particularly for patients with an extensive metastatic burden and an adverse prognosis. In current clinical therapeutics, a strategic alliance between PD-1/PD-L1 immune checkpoint inhibitors and chemotherapeutic agents has emerged as a cornerstone of treatment. This approach attests to the heightened value these inhibitors bring to the therapeutic arsenal. The rapid evolution of anti-PD-1/PD-L1 inhibitors for advanced NSCLC stands as an instrumental factor in enhancing patient outcomes, charting a promising trajectory toward improved prognosis [29,30]. In a recent study, neoadjuvant PD-1 inhibitor sintilimab was administered to individuals with NSCLC. The outcomes revealed that a notable 40.5% of participants achieved a major pathological response, while a commendable 10.8% realized a complete remission at the pathological level [14].
Prostate cancer: currently, PD-1/PD-L1 immune checkpoint inhibitors have ushered substantial clinical advantages for individuals with prostate cancer. A recent study has put forth the notion that synergizing PD-1/PD-L1 checkpoint inhibitors with radiotherapy presents a promising avenue in the management of prostate cancer [31]. However, it is noteworthy that the impact of PD-L1/PD-1 blockade in the context of prostate cancer appears comparatively muted in contrast to its influence on other cancer types. This discrepancy stems from the diminished immunogenicity characterizing prostate cancers [32].









