Avid Bioservices Inc (CDMO)

[entdoc]

jmeyer, good question:you wrote, "Reading through Thorpe's work, it appears that exposed PS mimics [is a normal event in] apoptosis, and Bavi exploits that mechanism [no, Bavi does not exploit that mechanism. Cancer exploits that mechanism. How? because "flipping" cell membrane -PS inside out is a part of normal cellular senescence and death, so -PS on the outside of cancer cells "masks" the underlying cancer, making the body immune system think the cancer is just normal dying cells.
You asked, "when PS gets exposed and the cancer cell mimics apoptosis, it can avoid T-cell's attack (despite the tumor anti-gen), but how does it[the cancer] avoid the clean up system such as macrophage/phagocyte unlike the cell which goes through normal apoptosis?" Answer: routine macrophage garbage collectors are not equal to the task. Its a war. Too little, too late. Too much -PS, too many cancer cells. The -PS on the surface prevents lymphocyte recognition of abnormal cellular DNA. Bavi binds to the flipped -PS, thereby unmasking underlying immunogenic cancer cells to the immune police who photocopy the foreign material and develop a clone of cells that remembers it as foreign, continuing the attack.