AI Article Synopsis
- Traditional anticancer treatments mainly targeted tumor cells, but newer approaches focus on immune cells, leading to significant improvements in patient responses.
- DNA repair deficiencies in breast cancer not only affect tumor cells but also change the surrounding microenvironment, particularly through pathways like STING that activate immune responses.
- Breast cancers with DNA repair deficiencies show higher levels of immune checkpoints like PD-L1, suggesting that they could be prime candidates for targeted immunotherapy treatments.
Article Abstract
Historically the development of anticancer treatments has been focused on their effect on tumor cells alone. However, newer treatments have shifted attention to targets on immune cells, resulting in dramatic responses. The effect of DNA repair deficiency on the microenvironment remains an area of key interest. Moreover, established therapies such as DNA damaging treatments such as chemotherapy and PARP inhibitors further modify the tumor microenvironment. Here we describe DNA repair pathways in breast cancer and activation of innate immune pathways in DNA repair deficiency, in particular, the STING (STimulator of INterferon Genes) pathway. Breast tumors with DNA repair deficiency are associated with upregulation of immune checkpoints including PD-L1 (Programmed Death Ligand-1) and may represent a target population for single agent or combination immunotherapy treatment.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6607732 | PMC |
| http://dx.doi.org/10.1155/2019/4325105 | DOI Listing |
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