10Īctive immunotherapies, such as cancer vaccines, aim to reprogram the patient’s immune system to recognize and eliminate its own cancer cells via recognition of TAAs.

8 9 Because of the potential to damage the tumor-associated endothelium and induce ICD, combination treatment of RT together with immunotherapy and/or anti-angiogenic agents can often result in improved therapeutic efficacy. 6 7 Tumor-associated endothelium is significantly altered in response to a single large dose of radiation (<10 Gy), which in turn makes the tumor microenvironment (TME) hypoxic, acidic, and nutritionally deprived, thereby indirectly inducing tumor cell death. 3–5 Another important antitumor cell-extrinsic effect induced by RT is radiation-induced damage of the tumor vasculature. Radiation-induced immunogenic cell death (ICD) results in stimulation of dendritic cells (DC), 1 that efficiently engulf tumors and cross-presents tumor-associated antigens (TAAs) to T cells, eliciting an antitumor response 2 capable of recognizing distant non-irradiated tumors, known as the abscopal effect. However, recent antitumor strategies have been increasingly focused on tumor cell-extrinsic factors such as induction of systemic antitumor immunity. Radiation therapy (RT) and chemotherapy have traditionally focused on a cell-intrinsic mode of action such as genetic alteration of tumor cells (ie, DNA double-stranded breaks, DNA cross-linking, mitotic catastrophe, and other chromosome abnormalities) leading to cell cycle arrest and cell death.

Remixlive response delayed