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 neoplasms in domestic animals allows progress in the knowledge of human cancer, since they have similarities in various aspects. The most important ones are related to the clinical part, drug resistance and risk factors for its development. By using these factors, we seek to expand our knowledge of cancer biology, improve palliative treatments, and increase the effectiveness of cure attempts. To achieve this, factors that resemble the phenotype and molecular aspects must be used, but additionally, they must 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 in the disease due to the biological diversity of the cancer. Objectives: To analyze the participation of the C-MYC oncogene during cancer, and of the P53, MDR-1 and Ki-67 genes as factors for the development of human cancer and their similarities with Canine Transmissible Venereal Tumor (TVTc). Methodology: A theoretical review of 52 bibliographic sources of the Pubmed, Scopus and Google scholar search engines was carried out. Results: Mammalian tumors are the result of alterations in cell proliferation and differentiation genes, inhibition of tumor suppressors, failure of repair genes, apoptosis and methylation mechanisms. The C-MYC proto-oncogene 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 with the highest proliferation. In addition, it is a target of estrogenic action at 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 works during Canine Transmissible Venereal Tumor (TVTc). In mammalian DNA there are LINEs that insert 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, the genital and the extra genital. The susceptible individual differs from the immune by its inherent ability to resist contagion, so it is necessary to understand how the action of the immune system is 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 in tumorigenesis and disruption of regulation of this gene leads to malignant transformation. Resistances may be inherent in the tumor line itself and may appear during illness. When prolonged application of a drug induces overexpression of P-glycoprotein, cross-resistance with other unrelated drugs frequently appears, making the cell multidrug-resistant. The Ki67 protein is present during all the active phases of the cell cycle, but it is absent in stationary cells, therefore, its role as a proliferation antigen is virtually restricted. The 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 TVTc microenvironment, thus generating apoptotic suppression, maintenance of cell growth and progression. of the neoplasm. The gene sequencing technique has allowed us to discover the clonal origin of the specific TVTc cell lineage and to 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 among them. to develop a competent response by the immune system. This response should be able to control cell proliferation. With this knowledge, better strategies can be proposed to avoid resistance to chemotherapy and control the exposure of the species to the extrinsic factors that influence the presentation of cancer, especially in humans and pets.