A pathologist looks at spontaneous regression of cancer

We are all subjected to varying amounts of mutating, potential cancer-inducing events, which are cumulative. In most instances, the accumulations are repaired or are lethal. If a viable clone survives, it must proliferate in order to become manifest and eventually to overpower the host's normal regulatory and defense mechanisms. The proliferation may be incited and sustained by cocarcinogens, hormone excess, chronic infections such as schistosomiasis, and in the case of lymphoid cells, by immune incompetence. On the other side are the protective reparing enzymes, which serve to cut out the damaged segments of DNA and repair them as fast as they can. The normal homeostatic mechanisms tend to keep cell proliferation and activity within the beneficial bounds of need. The controlling forces that cause cells to stop reproducing themselves and differentiate to perform a useful function also tend to slow or even stop the useless proliferation if all the cells can undergo maturation to a postmitotic state. There are also the protective mechanisms of immunity: Sensitized B lymphocytes tag the antigenic sites of tumor cells and activate the T-cell macrophages to destroy the tagged cells.