Phosphatidylserine’s Exposure on Tumor Cells Determines a Tumor’s Microenvironment and Checkpoint Molecule Exposure, a Hypothesis
Author(s): James Randall Kennedy
One constant in all malignant tumors is their continuous growth and there appear to be only two kinds of cell mutations that can cause this. One causes continuous mitotic cell division at a rate that exceeds the one required for their replacement when they physiologically die by programed cell death (PCD). In the other PCD is eliminated and the cells continuously divide at their normal rate until they finally die a senescent death. Phosphatidylserine (PS) is present on the inner leaflets of cell membranes but it moves to their surface when they are stressed and damaged and when they die by PCD. The hypothesis proposed is that when mutations delete PCD in a cell the PS will move to the surface of the damaged senescent cells where it will produce a tumor with an inflammatory and procoagulant microenvironment where checkpoint (CPMs) are generated by an innate immune response that prevents the immunologic removal of the tumor cells.