Resistance of cancer cells to immune recognition and killing

It is well recognized that, in order for a wound to heal, the fibrin clot must be eliminated by fibrinolytic enzymes. In certain instances, however, fibrin is ineffectively degraded or even not degraded. For example, in pregnancy, the placenta contains a layer of fibrin (Nitabuck's layer) which presents as 'self' to the immune system. Similar situations have been observed in many solid tumors. A hypothesis is presented according to which tumor cells can escape detection and attack by the immune system in most cancer patients. The tumor dons a 'coat' of the host's own protein on its cell surface. The coat is composed of fibrin and of a polymeric form of human serum albumin (HSA) which, by contrast to pure fibrin, is resistant to fibrinolytic degradation. Such a coated tumor appears as 'self' to the immune system, and thus is not detected as a tumor by the immune system (i.e. natural killer cells). When tumors are prepared for in vitro assays against drugs, they are routinely treated with proteolytic enzymes (e.g. pepsin, or chymotrypsin, etc.) which dissolve the protein coat, exposing the tumor cell surface to the drug. Thus, the in vivo existence of a coat on the tumor surface may explain why some drugs have little or no effect in vivo, while the same drugs are active in vitro.