Data from The DNA Damage Response and Inflammation in Cancer

Abstract

<div>Abstract<p>Genomic stability in normal cells is crucial to avoid oncogenesis. Accordingly, multiple components of the DNA damage response (DDR) operate as bona fide tumor suppressor proteins by preserving genomic stability, eliciting the demise of cells with unrepairable DNA lesions, and engaging cell-extrinsic oncosuppression via immunosurveillance. That said, DDR sig­naling can also favor tumor progression and resistance to therapy. Indeed, DDR signaling in cancer cells has been consistently linked to the inhibition of tumor-targeting immune responses. Here, we discuss the complex interactions between the DDR and inflammation in the context of oncogenesis, tumor progression, and response to therapy.</p>Significance:<p>Accumulating preclinical and clinical evidence indicates that DDR is intimately connected to the emission of immunomodulatory signals by normal and malignant cells, as part of a cell-extrinsic program to preserve organismal homeostasis. DDR-driven inflammation, however, can have diametrically opposed effects on tumor-targeting immunity. Understanding the links between the DDR and inflammation in normal and malignant cells may unlock novel immunotherapeutic paradigms to treat cancer.</p></div>

Tumor-associated macrophages affect the treatment of lung cancer

“…The DNA damage response plays a pivotal role in recruiting and activating immune cells by upregulating the expression of immunostimulatory signals. While the DNA damage response contributes to maintaining the microenvironment and organismal homeostasis, it has been suggested that it might also play a role in tumorigenesis and progression [ 163 ]. Recent studies have shown that DHA triggers cellular iron death, resulting in the production of reactive oxygen species, which in turn induces endoplasmic reticulum stress and DNA damage.…”