fig3

C-kit expression in cancer cells or hematopoietic cells of the tumoral microenvironment: which is the basis for efficacy of TK inhibitors and immunotherapy in HCC?

Figure 3. The cartoon, drawn on the basis of own data obtained from immunohistological and RNA studies on GIST and melanoma tissue and on published studies, indicates a hypothetical mechanism of how TKIs and anti-checkpoint antibodies may exert anticancer activity in different solid tumors including HCC. Immune cells, which are recruited by the chemokines released from the tumor cells, establish a symbiotic relationship with the tumor cells. Immune cells may be in close contact with tumor cells and continuously release factors necessary for tumor growth and survival. TKI and checkpoint inhibitors may induce tumor cell death by blocking the supply of those factors by means of different mechanisms. The success of the different drugs is dependent on the assembly and the metabolic status of the different cells of the tumor microenvironment which may be similar in different solid tumors such as GIST, HCC, or melanoma. The cartoon represents a modification of that published by Cameron et al.[22] (reprinted with permission). TKIs: Kinase inhibitors; NK: natural killer cell; DC: dendtric cell; TAM: tumor associated macrophages; TC: tumor cell; EC: endothelial cell.

Hepatoma Research
ISSN 2454-2520 (Online) 2394-5079 (Print)

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Portico

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https://www.portico.org/publishers/oae/