(NKFI FK-138593) Támogató: Hungarian National Research, Development and Innovation
Office
(NKFI K-119283) Támogató: Hungarian National Research, Development and Innovation
Office
(NKFI ANN-128524) Támogató: Hungarian National Research, Development and Innovation
Office
Similarly to our healthy organs, the tumor tissue also constitutes an ecosystem. This
implies that stromal cells acquire an altered phenotype in tandem with tumor cells,
thereby promoting tumor survival. Cancer cells are fueled by abnormal blood vessels,
allowing them to develop and proliferate. Tumor-associated fibroblasts adapt their
cytokine and chemokine production to the needs of tumor cells and alter the peritumoral
stroma by generating more collagen, thereby stiffening the matrix; these processes
promote epithelial-mesenchymal transition and tumor cell invasion. Chronic inflammation
and the mobilization of pro-tumorigenic inflammatory cells further facilitate tumor
expansion. All of these events can impede the effective administration of tumor treatment;
so, the successful inhibition of tumorous matrix remodeling could further enhance
the success of antitumor therapy. Over the last decade, significant progress has been
made with the introduction of novel immunotherapy that targets the inhibitory mechanisms
of T cell activation. However, extensive research is also being conducted on the stromal
components and other cell types of the tumor microenvironment (TME) that may serve
as potential therapeutic targets.