is cancer a virus or bacteria ?
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Donny S. Alexander
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The term malignant transformation refers to changes in the growth properties, shape, and other features of the tumor Cell. Malignant transformation can be induced by tumor viruses not only in animals but also in cultured cells. In culture, the following changes occur when cells become malignantly transformed.
Altered Morphology
Malignant cells lose their characteristic differentiated shape and appear rounded and more refractile when seen in a microscope. The rounding is due to the disaggregation of actin filaments, and the reduced adherence of the cell to the surface of the culture dish is the result of changes in the surface charge of the cell.
Altered Growth Control
Malignant cells grow in a disorganized, piled-up pattern in contrast to normal cells, which have an organized, flat appearance. The term applied to this change in growth pattern in malignant cells is loss of contact inhibition. Contact inhibition is a property of normal cells that refers to their ability to stop their growth and movement upon contact with another cell. Malignant cells have lost this ability and consequently move on top of one another, continue to grow to large numbers, and form a random array of cells.
Malignant cells are able to grow in vitro at a much lower concentration of serum than are normal cells.
Malignant cells grow well in suspension, whereas normal cells grow well only when they are attached to a Surface (e.g., a culture dish).
Malignant cells are easily cloned (i.e., they can grow into a colony of cells starting with a single cell), whereas normal cells cannot do this effectively.
Infection of a cell by a tumor virus “immortalizes” that cell by enabling it to continue growing long past the time when its normal counterpart would have died. Normal cells in culture have a lifetime of about 50 generations, but malignantly transformed cells grow indefinitely.
Altered Cellular Properties
DNA synthesis is induced. If cells resting in the G1 phase are infected with a tumor virus, they will promptly enter the S phase (i.e., synthesize DNA and go on to divide). The karyotype becomes altered (i.e., there are changes in the number and shape of the chromosomes as a result of deletions, duplications, and translocations).
Antigens different from those in normal cells appear. These new antigens can be either virus-encoded proteins, preexisting cellular proteins that have been modified, or previously repressed cellular proteins that are now being synthesized. Some new antigens are on the cell surface and elicit either circulating antibodies or a cell-mediated response that can kill the tumor cell. These new antigens are the recognition sites for immune surveillance against tumor cells.
Agglutination by lectins is enhanced. Lectins are plant glycoproteins that bind specifically to certain sugars on the cell membrane surface (e.g., wheat germ agglutinin).
The increased agglutination of malignant cells may be due to the clustering of existing receptor sites rather than to the synthesis of new ones.
Altered Biochemical Properties
Levels of cyclic adenosine monophosphate (AMP) are reduced in malignant cells. Addition of cyclic AMP will cause malignant cells to revert to the appearance and growth properties of normal cells.
Malignant cells secrete more plasminogen activator than do normal cells. This activator is a protease that converts plasminogen to plasmin, the enzyme that dissolves the fibrin clot.
Increased anaerobic glycolysis leads to increased lactic acid production (Warburg effect). The mechanism for this change is unknown.
There is a loss of high-molecular-weight glycoprotein called fibronectin. The effect of this loss is unknown.
There are changes in the sugar components of glycoproteins and glycolipids in the membranes of malignant cells.
ROLE OF TUMOR VIRUSES IN MALIGNANT TRANSFORMATION
Malignant transformation is a permanent change in the behavior of the cell. Must the viral genetic material be present and functioning at all times, or can it alter some cell component and not be required subsequently? The answer to this question was obtained by using a temperature-sensitive mutant of Rous sarcoma virus. This mutant has an altered transforming gene that is functional at the low, permissive temperature (35°C) but not at the high, restrictive temperature (39°C). When chicken cells were infected at 35°C they transformed as expected, but when incubated at 39°C, they regained their normal morphology and behavior within a few hours. Days or weeks later, when these cells were returned to 35°C, they recovered their transformed phenotype. Thus continued production of some functional virus-encoded protein is required for the maintenance of the transformed state. Although malignant transformation is a permanent change, revertants to normality do appear, albeit rarely.
PROVIRUSES & ONCOGENES
The two major concepts of the way viral tumorigenesis occurs are expressed in the terms provirus and oncogene. These contrasting ideas address the fundamental question of the source of the genes for malignancy.
In the provirus model, the genes enter the cell at the time of infection carried by the tumor virus.
In the oncogene model, the genes for malignancy are already present in all cells of the body by virtue of being present in the initial sperm and egg. These oncogenes encode proteins that encourage cell growth (e.g., fibroblast Growth factor). In the oncogene model, carcinogens such as chemicals, radiation, and tumor viruses activate cellular oncogenes to overproduce these growth factors. This initiates inappropriate cell growth and malignant transformation.
Both proviruses and oncogenes may play a role in malignant transformation. Evidence for the provirus mode consists of finding copies of viral DNA integrated into cell DNA only in cells that have been infected with the tumor virus. The corresponding uninfected cells have no copies of the viral DNA.