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Aims are to study the nature of the processes of carcinogenesis  of experimental B16/F10 melanoma in uPA gene knockout mice  modified by chronic neurogenic pain and investigate some  electrophysiological mechanisms of melanoma development. Materials and methods. We used 48 C57BL/6-PlautmI. IBug-ThisPlau6FDhu/GFDhu mice of both genders with urokinase gene knockout and 102 C57BL/6 mice of both genders  with the normal genotype. Chronic neurogenic pain (CNP) was  produced due to bilateral ligation of the sciatic nerve. Against  the above background, all animals were transplanted with  B16/F10 melanoma. To study the mechanism of CNP, studies of  the intracellular electrophysiological activity of neurons of the  central nervous system of the snail Helix pomatia in the body in  vivo were carried out. CNP was reproduced by dosed pressing  of four main nerves with Fresnel hairs that with time turned into  increasing pain. Membrane potential (MP), action potential (AP)  and firing rate (FR) parameters of intracellular bio-potentials of  the command neuron RPaG3, continuously recorded using an  ultrathin glass microelectrode for 4-5 days, were analyzed. Results. It was detected that an activation of cancerogenesis  during the modification of the progression of experimental B16/ F10 melanoma in C57BL/6-PlautmI.IBug-ThisPlau6FDhu/GFDhu  mice with uPA gene knockout using CNP is accompanied by a  2-fold acceleration in the time of tumor production, stimulation  of the growth of the primary tumor nodes from 1.05±0.08 cm3 to 9.50±0.98 cm3  (p&lt;0.001) and multiple metastasizing to  the lungs, a reduction in the life span from 34.67±0.67 to  21.33±2.19 days (p&lt;0.001) &lt;0.05) in the genetically modified  mice, by changing some gender-specific characteristics of the  progression of the malignant process. The neuropathic nature of pain resulting from command neuron compression or ligation of the sciatic nerves is essentially identical to the implementation of genetic programs responsible for the control of  life and death, reproducing events in carcinogenesis with the  progression of a malignant tumor.  Conclusion. The initiation and chronization of pain at the local  level of the nervous system can lead to generalization of the  pain syndrome and contribute to the cancellation of genetically  predetermined programs of carcinogenesis.

Mechanisms of cancellation by pain of genetically determined inhibition of a malignant tumor growth in experiment