Hypotheses Cohnheim, Rotter and Rippert explain the age-specific incidence of cancer.

Consider three old hypotheses about the causes of cancer:
1. Cohnheim (1875) hypothesized that cancers arise from putative embryonal cells present in mature tissues (embryonal rest theory).
2. Rotter (1921) assumed that germinal cells wander through the tissue of the developing embryo and can accidentally lodge anywhere and could serve as the origin of tumors.
3. Rippert (1911) suggested that the critical factor is the isolation of these potential cancer cells (embryonal cell rests) from their normal environment.
Now let us assume that these hypotheses are true. Given recent data on the normal stem and cancer stem cells can draw the following conclusions and assumptions:
1. From the hypothesis of Cohnheim the following conclusion: in the absence of other causes of death in all people will develop cancer.
It is unlikely, that at the early development of embryo there are a few needless embryonal cells, since each embryonal cell contains a program for constructing some part of the fetus. Therefore, I assume the existence of only one extra embryonal cell. It is possible that at the stage of early embryogenesis nature cannot continue further development of the embryo without the formation of the one extra embryonal cell. I called this cell as embryonal cell of Cohnheim (ECC). This ECC subsequently serves as the origin of tumor. From the standpoint of reliability theory, embryonal or stem cell represents potentially vast supply of cells (redundant) for constructing and continuous renewal of the tissues. Therefore, these cells must not respond to a signal to apoptosis.
2. Under the assumption of Rotter, ECC accidentally migrates to any site in the fetus and serves as the origin of tumor. Moreover, this assumption explains the differences in cancer morbidity among populations. The difference ought to be associated with the difference in the probabilities of migration of ECC in tissue sites. For example, in Japan are often diseases of stomach cancer, but rarely get cancer of the prostate and breast (female). In the U.S., conversely, disseminated prostate and breast (female) cancer, diseases of gastric cancer are rare (Cancer Incidence in Five Continents, Vol. VIII /Parkin D.M., Whelan S.L., Ferlay J., Teppo L., Thomas D.B. eds. IARC Scientific Publications No. 155. Lyon: IARC, 2002).
3. Under the assumption of Rippert, being isolated from the organism, ECC begins to divide uncontrollably, leading to the development of caricatures of organ or tumor. (…that carcinomas are caricatures of tissue renewal, in that they are composed of a mixture of malignant stem cells, which have a marked capacity for proliferation and a limited capacity for differentiation under normal homeostatic conditions, and of the differentiated, possibly benign, progeny of these malignant cells. Pierce G.B., Speers W.C.- Cancer Research. 1988. V. 48. P. 1996-2004.). Being isolated from the organism, ECC at the same time deprived of nutrient. Further, up to the stage of vascularization, growth tumor occurs only due to diffusion of nutrients ( and, may be, signal proteins). This implies that the increase in the number cells of tumor is very slow random process.
In fact, ECC can be considered as single-celled organism genetically identical cells of an organism, which gave it birth. Because ECC genetically identical cells of the organism immune system does not "see" ECC. Then the single-celled organism is developing a multicellular organism - a cancerous tumor. Due to the lack of nutrients, the development of a multicellular organism occurs in a constant struggle for existence. Because of a tumor consists of the most aggressive cancer stem cells. This, perhaps, explains the ability of cancer stem cells to resist drug treatment and irradiation.
Physical model of tumor growth from ECC.
As mentioned above, the increase in the number cells of tumor is very slow random process. This process will describe the following equation
dn/dt=V+r(t)
where n is the number of tumor cells, V - average velocity of growth of cell number, s(t) - the random component of the rate of growth of cell number (birth and death of non-malignant tumor cells), t - time.