Resistance of tumor cells to cytolytic T lymphocytes involves Rho-GTPases and focal adhesion kinase activation.

Tumor cells evade adaptive immunity by a variety of mechanisms, including selection of variants that are resistant to specific cytotoxic T lymphocyte (CTL) pressure. Recently, we have reported that the reorganization of the actin cytoskeleton can be used by tumor cells as a strategy to promote their resistance to CTL-mediated lysis. In this study, we further examined the functional features of a CTL-resistant tumor variant and investigated the relationship between cytoskeleton alteration, the acquisition of tumor resistance to CTL-induced cell death, Rho-GTPases, and focal adhesion kinase (FAK) pathways.

[Immune response and cancer].

Cellular transformation is initiated by genetic and epigenetic mutations that activate oncogenes and inactivate tumor suppressor pathways. Cancers thus arise when somatic cells escape intrinsic and extrinsic tumor suppressor mechanisms in the context of their cellular microenvironment. Given the well established importance of the immune system at controlling and shaping developing tumors, pointing the different strategies of tumor escape may provide important insights for the development of effective cancer therapies.