Editorial: Tumor microenvironment, inflammation, and resistance to immunotherapies

The tumor microenvironment (TME) refers to the complex ecosystem surrounding a tumor, including stromal cells, blood vessels, extracellular matrix, and different types of immune cells such as T-cells, B-cells, dendritic cells, neutrophils, natural killer cells, myeloid-derived suppressor cells, and tumor-associated macrophages. Cancer cells exploit the inflammatory mechanisms present in the TME to promote their growth and survival. In turn, immunotherapies, including immune checkpoint inhibition (ICI), adoptive cell transfer (ACT), and genetically-modified T-cell receptor (TCR) and chimeric antigen receptor (CAR-T) based therapies, aim to modulate the immune system to better recognize and eliminate cancer cells. However, the molecular profile of cancer cells affect the TME, hampering the response to these therapies. The causes of immunotherapy resistance remain unclear, but immune dysregulation within the TME, the tumor mutational landscape, inflammation, hypoxia, and epithelial-mesenchymal transition (EMT) have been implicated. Understanding the key immunosuppressive and resistance mechanisms associated with the TME is crucial to develop new therapeutic strategies, limit immune escape, and tailor effective treatments.

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Published in: Frontiers in Oncology
License: https://creativecommons.org/licenses/by/4.0/
See article on publisher's website: https://dx.doi.org/10.3389/fonc.2023.1215332