You must provide complete citations in APA format (you don’t need to double spac

Question

You must provide complete citations in APA format (you don’t need to double space) for the sources of information you used to support your answers for the questions in Part B. If you include them at the end of the quiz, then include in-text citations. The topic title should be included in citations from the course modules, Boundless Microbiology and other multi-topic sources. No credit for questions without citations.

Question: 9. State the normal function of proto-oncogenes, and describe how some viruses may contribute to the development of tumors by altering proto-oncogenes. Name two oncogenic viruses and the type of cancer they cause.

Explanation / Answer

an oncogene is any gene that encodes a protein able to transform cells in culture or to induce cancer in animals. Of the many known oncogenes, all but a few are derived from normal cellular genes (i.e., proto-oncogenes) whose products participate in cellular growth-controlling pathways. For example, the ras gene discussed previously is a proto-oncogene that encodes an intracellular signal-transduction protein; the mutant rasD gene derived from ras is an oncogene, whose encoded oncoprotein provides an excessive or uncontrolled growth-promoting signal. Because most proto-oncogenes are basic to animal life, they have been highly conserved over eons of evolutionary time.

Conversion, or activation, of a proto-oncogene into an oncogene generally involves a gain-of-function mutation. At least three mechanisms can produce oncogenes from the corresponding proto-oncogenes.

Point mutations in a proto-oncogene that result in a constitutively acting protein product

Localized reduplication (gene amplification) of a DNA segment that includes a proto-oncogene, leading to overexpression of the encoded protein

Chromosomal translocation that brings a growth-regulatory gene under the control of a different promoter and that causes inappropriate expression of the gene

An oncogene formed by the first mechanism encodes an oncoprotein that differs slightly from the normal protein encoded by the corresponding proto-oncogene. In contrast, the latter two mechanisms generate oncogenes whose protein products are identical with the normal proteins; their oncogenic effect is due to their being expressed at higher-than-normal levels or in cells where they normally are not expressed. However they arise, the gain-of-function mutations that convert proto-oncogenes to oncogenes act dominantly; that is, mutation in only one of the two alleles is sufficient for induction of cancer.

At some frequency the integration process leads to rearrangement of the viral genome and the consequent incorporation of a portion of the host genome into the viral genome. This process is termed transduction. Occasionally this transduction process leads to the virus acquiring a gene from the host that is normally involved in cellular growth control. Because of the alteration of the host gene during the transduction process as well as the gene being transcribed at a higher rate due to its association with the retroviral LTRs the transduced gene confers a growth advantage to the infected cell. The end result of this process is unrestricted cellular proliferation leading to tumorigenesis. The transduced genes are termed oncogenes. The normal cellular gene in its unmodified, non-transduced form is termed a proto-oncogene since it has the capacity to transform cells if altered in some way or expressed in an uncontrolled manner. Numerous oncogenes have been discovered in the genomes of transforming retroviruses.

There are two classes of cancer viruses: DNA and RNA viruses. Several viruses have been linked to certain types of cancer in humans. These viruses have varying ways of reproduction and represent several different virus families.

DNA Oncogenic Viruses include the following:

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.

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