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– the malignant process is developed by the haematogenous and lymphogenous spread in the host body while forming the secondary foci – metastases;

– the malignant process impacts haemopoiesis, homeostasis, immunity etc.

Thus, the contemporary notions:

1. The difference between haemoblastosis (leucosis and lymphoma) on the one hand and solid tumours on the other, is in the mechanism of the “birth” of a malignant stem cell;

– in the case of haemoblastosis, following the carcinogenic impact the genotype and epigenetic changes of a pluripotent or unipotent stem cell of myelo- or lymphopoiesis, a block of differentiation and its transformation into a malignant stem cell take place;

– it is supposed that in the case of solid tumours, following the carcinogenic impact genotype and epigenetic changes of a normal proliferating somatic cell take place, which are a launching mechanism for its transformation into a malignant stem cell.

2. The difference between leucosis on the one hand and lymphoma and solid tumours on the other, is in the manifestation of the malignant process:

– in the case of leucosis, the disease manifests itself by the affection of the red marrow, but the primary malignant focus is not formed. The “birth” of a malignant stem cell requires 2-4 genotype alterations of the nuclear DNA of a pluripotent or unipotent stem cell of myelo- or lymphopoiesis. Epigenetic alterations are of secondary importance, that is why changes in the living conditions and microenvironment of the precursor are not a prerequisite;

– in the case of lymphoma and solid tumours, the disease manifests itself by necessary forming of the primary malignant focus. The “birth” of a malignant stem cell requires 7-8 genotype alterations of the nuclear DNA of the precursor of the malignant stem cell. The genotype and epigenetic alterations are of equal importance, that is why changes in the living conditions and microenvironment of the precursor are a prerequisite. The large number of genotype alterations of nuclear DNA and the equally important genotype and epigenetic alterations determine the length of pre-clinical evolution of the disease.