2.The first human oncovirus was discovered in 1964. Today, a \"tumor virus\" or\
ID: 213793 • Letter: 2
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2.The first human oncovirus was discovered in 1964. Today, a "tumor virus" or"cancer virus" is any virus with a DNA or RNA genome that can cause cancer. Hence, they are classified as either "DNA oncovirus" or "RNA oncovirus". Research them, then choose one. Using no more than two paragraphs (1/2 page max, single-spaced), briefly explain the basic mechanisms of action by which the virus you chose causes cancer (you may refer to lecture slides at the end of L15, but make sure that your search goes beyond that). Cite your source of information at the end of your answerExplanation / Answer
DNA tumor viruses have two life-styles. In permissive cells, all parts of the viral genome are expressed. This leads to viral replication, cell lysis and cell death. In cells that are non-permissive for replication, viral DNA is usually, but not always, integrated into the cell chromosomes at random sites. Only part of the viral genome is expressed. These are the early control functions of the virus. Viral structural proteins are not made, and no progeny virus is released.
DNA tumor virus oncogenes encode viral proteins necessary for viral replication. Oncogenic viruses promote cell transformation, prompt uncontrollable cell generation, and lead to the development of malignant tumors. All malignant tumors are called cancer. Oncogenic abnormalities are seen in pediatric leukemias, lymphomas, and various solid tumors. Virus-promoted malignant transformations in cells are the first step in the complex oncogenesis process. The genes in the viral genome that change host cell proliferation control, lead to the synthesis of new proteins, and are responsible for transformation characteristics are called viral oncogenes (v-onc genes). Protooncogenes (c-onc genes) are the cellular counterparts of v-onc genes. Their functions are cellular growth and development. The activation of c-onc genes with mutation leads to uncontrolled cell growth. C-onc genes are transformed into oncogenic form by amplification, point mutation, deletion, or chromosomal translocation. C-onc genes can be classified into different groups in terms of their protein products, such as protein kinases, growth factors, growth factor receptors, and DNA binding proteins. There are also genes that prevent malignant transformation. They are called antioncogenes (tumor suppressor genes). When these genes lose their suppressive effects, unpreventable growth occurs. Oncogenes are constantly struggling with tumor suppressor genes, which protect DNA and control cell activities. There are many studies that indicate that tumor suppressor genes lose this struggle or that oncogenes win this struggle, which leads to cancer
Mechanism of Oncogenesis
The activation of oncogenes requires genetic changes in cellular protooncogenes. Oncogenes are activated by 3 genetic mechanisms:
a) Mutation
b) Gene amplification
c) Chromosome rearrangements
These mechanisms result in either an increase in protooncogene expression or a change in protooncogene structure. Neoplasia is a multistep process; therefore, more than one of these mechanisms contribute to the formation of tumors. Expression of the neoplastic phenotype includes the capacity for metastasis and usually requires a combination of protooncogene activation and tumor suppressor gene loss or inactivation.
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