Hematogenous metastasis of lung cancer.

Blood vessel metastasis of lung cancer characterizes an importantbiological feature of its malignant growth. Complex processes occurring in the outer cell membrane of cells and intercellular contacts of the primary tumor are characterized by their loss of adhesion. Then the cells separated from the tumor enter the bloodstream.

The transfer of individual cancer cells or their complexes through the blood vessels leads to the formation of new foci of tumor growth outside the lung and chest cavity.

To date, a large number of observations have been accumulated and generalized, allowing us to outline the complex relationships arising from hematogenous metastasis between the patient’s body and various manifestations of a growing malignant tumor in the lung.

The formation and development of hematogenous metastases is accompanied by numerous changes in the body of a patient with lung cancer. Some of them are well studied and clarify the features of the pathogenesis of hematogenous metastasis.

Reliably established increased tendency to blood coagulation and thrombus formation with a decrease in antithrombogenic activity of the blood vessel wall. At the same time, tumor cells circulating in the vascular bed adhere platelets on their surface, become covered with fibrin and form an oncogenous thrombogenic embolus. A decrease in the antithrombogenic properties of the vascular wall contributes to the delay of the embolus in the vessels, most often in the zone of the microvasculature. Subsequently, with the growth of metastasis, the destruction of the vascular wall and the exit of the tumor into the surrounding tissue with their progressive lesion occur.

It is known that metastases develop especially intensively when the suppression of the T-system of immunity and decrease in androgen hormones, increase in cortisol levels, and violation of the ratio between individual fractions of steroids are regularly observed in patients with lung cancer.

Tissue hypoxia observed in cancer patients also reduces the antitumor resistance of their body. Tissue hypoxia is one of the leading factors contributing to the engraftment and development of metastatic cancer cells. It is likely that it is realized to varying degrees in different organs and anatomical structures of the body with lung cancer, and this determines the well-known “tropism”, the selectivity of its hematogenous metastasis. It is known that, first of all, lung cancer metastases affect organs that normally have rich blood supply and a well-developed microcirculatory bed: the liver, kidneys, adrenal glands, brain, bones and the lungs themselves. These structures become a kind of “biological trap” for metastases due to the peculiarities of the structure and functioning in the circulatory system, like lymph nodes in the lymphatic channel.

Thus, the spread of cancer cells in the vascular system occurs by the lymphogenous and hematogenous pathways. For lung cancer, the lymphogenous or mixed lymphohematogenous pathway of metastasis is more characteristic and is realized earlier . The peculiarity of the relationship of the lymphatic and circulatory systems in the lung and beyond determines the frequency during the course of the disease. Usually, hematogenous dissemination of lung cancer is preceded by damage to regional lymphatic collectors. Nevertheless, extensive lymphogenous metastasis of lung cancer can often be observed in the absence of hematogenous metastases or only local, single lesion of one of the organs by them.

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