As immunotherapy has gained increasing interest as a new foundation for cancer therapy, some atypical response patterns, such as pseudoprogression and hyperprogression, have garnered the attention of physicians. Pseudoprogression is a phenomenon in which an initial increase in tumor size is observed or new lesions appear, followed by a decrease in tumor burden; this phenomenon can benefit patients receiving immunotherapy but often leads to premature discontinuation of treatment owing to the false judgment of progression. Accurately recognizing pseudoprogression is also a challenge for physicians. Because of the extensive attention on pseudoprogression, significant progress has been made. Some new criteria for immunotherapy, such as irRC, iRECIST and imRECIST, were proposed to accurately evaluate the response to immunotherapy. Many new detection indexes, such as ctDNA and IL-8, have also been used to identify pseudoprogression. In this review, the definition, evaluation criteria, mechanism, monitoring, management and prognosis of pseudoprogression are summarized, and diagnostic and treatment processes for patients with progression but with a suspicion of pseudoprogression are proposed; these processes could be helpful for physicians in clinical practice and enhances the understanding of pseudoprogression.

Immune checkpoint inhibitors (ICIs) are new and promising therapeutic agents for non-small cell lung cancer (NSCLC). However, along with demonstrating remarkable efficacy, ICIs can also trigger immune-related adverse events. Checkpoint inhibitor pneumonitis (CIP) has been reported to have a morbidity rate of 3% to 5% and a mortality rate of 10% to 17%. Moreover, the incidence of CIP in NSCLC is higher than that in other tumor types, reaching 7% to 13%. With the increased use of ICIs in NSCLC, CIP has drawn extensive attention from oncologists and cancer researchers. Identifying high risk factors for CIP and the potential mechanism of CIP are key points in preventing and monitoring serious adverse events. In this review, the results of our analysis and summary of previous studies suggested that the risk factors for CIP may include previous lung disease, prior thoracic irradiation, and combinations with other drugs. Our review also explored potential mechanisms closely related to CIP, including increased T cell activity against associated antigens in tumor and normal tissues, preexisting autoantibodies, and inflammatory cytokines.