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For studies of hypothetical until the antioncogenes should carefully study the mechanism of transformation of real prohkorov in as real oncogenes. The first step in this direction was made 20 years ago, when Margaret Vogt and Renato Dulbecco the California Institute of technology received the transformation of normal embryo fibroblasts hamster in malignant cells under the influence of the virus polyami. If from the culture of cancer cells artificially eliminate viral elements, the cells were returning to normal.
In the early 70-ies was allocated viral oncogene rous sarcoma chickens, so named sarcasim viral genome-srv. But soon it was found that the gene srv not a virus, as it is almost a complete copy of the normal gene; the virus only indistinguishable included in the chromosome of the host and transferred further during cellular division. And non-viral genes, being introduced into the DNA of animal cells, transforming them into cancer. Under the action of carcinogenic cells can undergo mutations that also contribute to the activation of proto-oncogene. Division of viral oncogenes and somatic was conditional. Just viruses introduce new genetic information, and carcinogens change the existing ones.
Specific ways activated oncogene to still not clear. In the result of a restructuring of protooncogen can be transported from its normal site (the site) to another chromosome. This process is called translocation help him with some amplifiers. It is illustrated by the example of some of the genes of the immune system, among which the exchange of segments is a normal process. To B-lymphocytes was functioning properly, gene expression, heads of synthesis of a variety of antibodies, must often change. When rebuilding of chromosomes in B-lymphocytes some parts of the DNA will be close to oncogene, will be enhanced and the expression of the latter. In such cases, the possible malignant transformation of B-cells, after which razbiraetsa leukemia.
Translocation between the 14th chromosome that encodes a synthesis of heavy chains of immunoglobulins, and 11-th and 18-th chromosomes frequently observed in chronic B-cell leukemia, and multiple myeloma. When Burkitt's lymphoma oncogene is moved from the 8th chromosome to 14, where it stimulates amplifiers synthesis of immunoglobulins. Translocation segment of the 9th chromosome 22-th often accompanies myeloid leukemia person. It follows that malignant transformation of cells of the immune system particularly often called mobile genetic elements (they are also called "wandering genes", "jumping" and so on). But this process may be relevant and to immune surveillance of cancer development. It is also possible similarity of mobile genetic elements with endogenous proviruses. The big merit in exploring mobile genes belongs to the team, led by laureates of the State prize of the USSR G. P. Georgiev and C. A. Gvozdev.
Some oncogenes not find in primary tumors, but find metasteziruuschem nodes. Hence arose the assumption that at different stages of carcinogenesis activate oncogenes. Changing the genes responsible for proteolytic enzymes may increase proteolysis and the ability of cancer cells to invade normal tissue. Identification and activation of oncogenes the person has just begun.