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Introduction: Cancer is a very important disease especially in older dogs and cats, affecting all breeds with high levels of mortality. In addition, the study of cancer in domestic animals allows progress in the knowledge of human cancer, because they have similarities in several aspects. The most important are related to the clinical part, drug resistance and risk factors for its development. This will expand knowledge in cancer biology, improve palliative treatments and improve the effectiveness of healing attempts. To achieve this, those that resemble the phenotype and molecular aspects should be used, but additionally be identical in the growth pattern, location and immune status of the individual. In this sense it is important both the emulation of genetic alterations, clinical characteristics and variations of the disease due to the biological diversity of cancer. Aims: To analyze the participation of the C-MYC oncogene during cancer, and of the genes P53, MDR-1 and Ki-67 as factors for the development of human cancer and its similarities with Canine Transmissible Venereal Tumor (TVTc).Methods: Theoretical review of 52 bibliographic sources of the search engines Pubmed, Scopus and Google scholar was carried out. Results: Mammalian tumors are the result of alterations in cell proliferation and differentiation genes, inhibition of tumor suppressors, repair gene failures, apoptosis and methylation mechanisms. The protooncogen C-MYC, promotes cell growth and immediate early response, but its expression is well controlled by a series of regulatory mechanisms. It is expressed in different tissues, altering cell differentiation and immortalization and expressing itself in those of greater proliferation. In addition, it is the target of estrogenic action in hormonal receptors due to sensitivity to these hormones during the cell cycle. There are molecular aspects of the C-MYC gene that indicate how it acts during Canine Transmissible Venereal Tumor (TVTc). In the DNA of mammals there are the LINEs that are inserted into the C-MYC gene, causing normal cells to become neoplastic. Canine Transmissible Venereal Tumor (TVTc) is a contagious neoplasm of dogs with two forms, genital and extra genital. The susceptible individual differs from the immune one by its inherent ability to resist contagion, so it is necessary to understand how the immune system is acting and its impact on the final outcome of patients with TVTc. In order for a tumor to become transmissible, cells must undergo adaptive processes to colonize the host. Inactivity of the p16 tumor suppressor gene is associated with human cancers and is a step for tumorigenesis and disruption of the regulation of this gene leads to a malignant transformation. Resistances may be inherent in the tumor strain itself and may appear during illness. When prolonged application of a drug induces overexpression of Pglycoprotein, cross-resistance with other unrelated drugs often appears, making the cell multidrug. The Ki-67 protein is present during all active phases of the cell cycle, but is absent in stationary cells, therefore, its role as a proliferation antigen is virtually restricted. Increased tissue expression and the correlation between the C-MYC, P53, P21 and P27 proteins indicate reduction and / or loss of their functionality in the micro-environment of the TVTc, whereby apoptotic suppression, maintenance of cell growth and progression is generated of the neoplasm. The gene sequencing technique has allowed us to discover the clonal origin of the specific cell lineage of the TVTc and expand the existing knowledge about neoplasms. Conclusions: The ability to determine the presence or absence of genes in the TVTc and its molecular expression, increases both the opportunity to understand the biology of cancer, and to understand from the relationship between the neoplasms of the different species to the common mechanisms between them to develop a competent response from the immune system. This response should be able to control cell proliferation. With this knowledge, better strategies can be proposed to avoid resistance to chemotherapeutics and control the exposure of species to extrinsic factors that influence the presentation of cancer, especially in humans and pets.
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References
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