This is the central mechanistic theme of the review: radiotherapy generates ROS that cause oxidative stress in tumors. The review frames this oxidative stress as a regulator of tumor cell death and antitumor immunity.
First-pass extracted concept
radiotherapy-induced oxidative stress
Aliases
radiation-induced oxidative stress, RT-induced OS
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Oxidative stress caused by radiotherapy-induced reactive oxygen species is linked to apoptosis, autophagy, and ferroptosis.
OS not only causes apoptosis, autophagy and ferroptosis, but also affects tumor immune response.
Radiotherapy-induced reactive oxygen species can promote release of tumor-associated antigens, alter immune-cell infiltration and differentiation, manipulate immune checkpoint expression, and remodel the tumor immune microenvironment.
Specifically, RT-induced ROS can promote the release of tumor-associated antigens (TAAs), regulate the infiltration and differentiation of immune cells, manipulate the expression of immune checkpoints, and change the tumor immune microenvironment (TME).
Radiotherapy induces reactive oxygen species and oxidative stress that contribute to tumor cell death.
Radiotherapy (RT) is an effective treatment option for cancer patients, which induces the production of reactive oxygen species (ROS) and causes oxidative stress (OS), leading to the death of tumor cells.
The review emphasizes the interrelationship between radiotherapy-induced oxidative stress and antitumor immunity, with particular focus on ferroptosis and immunogenic death.
we briefly summarize several ways in which IR induces tumor cell death and discuss the interrelationship between RT-induced OS and antitumor immunity, with a focus on the interaction of ferroptosis with immunogenic death.
Regulating oxidative stress may improve radiotherapy in combination with immunotherapy and may be beneficial for clinical treatment.
we conclude the therapeutic opportunity improving radiotherapy in combination with immunotherapy by regulating OS, which may be beneficial for clinical treatment.