No abstract

No abstract

With the success of immune checkpoint inhibitors (ICIs), significant progress has been made in the field of cancer immunotherapy. Despite the long-lasting outcomes in responders, the majority of patients with cancer still do not benefit from this revolutionary therapy. Increasing evidence suggests that one of the major barriers limiting the efficacy of immunotherapy seems to coalesce with the hypoxic tumor microenvironment (TME), which is an intrinsic property of all solid tumors. In addition to its impact on shaping tumor invasion and metastasis, the hypoxic TME plays an essential role in inducing immune suppression and resistance though fostering diverse changes in stromal cell biology. Therefore, targeting hypoxia may provide a means to enhance the efficacy of immunotherapy. In this review, the potential impact of hypoxia within the TME, in terms of key immune cell populations, and the contribution to immune suppression are discussed. In addition, we outline how hypoxia can be manipulated to tailor the immune response and provide a promising combinational therapeutic strategy to improve immunotherapy.

With the increasing incidence of thoracic tumors, radiation therapy (RT) has become an important component of comprehensive treatment. RT improves survival in many cancers, but it involves some inevitable complications. Radiation-induced heart disease (RIHD) is one of the most serious complications. RIHD comprises a spectrum of heart disease including cardiomyopathy, pericarditis, coronary artery disease, valvular heart disease and conduction system abnormalities. There are numerous clinical manifestations of RIHD, such as chest pain, palpitation, and dyspnea, even without obvious symptoms. Based on previous studies, the pathogenesis of RIHD is related to the production and effects of various cytokines caused by endothelial injury, inflammatory response, and oxidative stress (OS). Therefore, it is of great importance for clinicians to identify the mechanism and propose interventions for the prevention of RIHD.