Cells malignant transformation

Wang, Z., Zhao, Y., Smith, E., GoodaU, G. L, Drew, P. A., Brabletz,T. and Yang, C., Reversal and prevention of arsenic-induced human bronchial epithelial cell malignant transformation by microRNA-200b Toxicol Sci., 2011 May, 121 (1), 110-122. 

In apoptotic cell death, several factors such as growth factors, NO, the tumor suppressor gene p53, and the protein encoded by this gene contribute to the process that leads to cell death. One of the functions of p53 protein is the activation of apoptosis if a cell is transformed to a malignant cell. Apoptosis typically leads to the formation of smaller membrane-encapsulated particles within the cell. Apoptotic cell death begins in the nucleus and proceeds to other parts of the cell. The death process may be quite advanced before it can... 

Nucleic acids in the DNA contain a high number of nucleophilic sites that can be attacked by electrophilic intermediates (metabolites) of chemical compounds. DNA adducts formed may cause alterations in the expression of a critical gene in the cell and thus lead to cell death. For example, modification of p53 tumor suppressor gene may inactivate the functions of the p53 protein and render cells sensitive to malignant transformation. Also, formation of RNA adducts may inhibit key cellular events because RNA is essential for protein synthesis. 

Some established cell lines were derived from malignant tissue. Many of these cell lines can form tumors when injected into susceptible animals. Other established cell lines are not Uunorigenic. However, exposure to carcinogens, and irradiation can cause these cells to form tumors in susceptible animals. In addition, transformation can be caused by spontaneous mutations, by growth factors, and by viral (or oncogenic) transformation (Table 6). Malignant transformation is defined as consisting of the series of events that cause normal cells to develop the capacity to form tumors. 

Virally induced antigens result from a malignant transformation occurring in the cell, due to an oncogenic vims. These evoke powerful immune responses in experimental animals. 

Current lung dosimetry models are based on the assumption that basal cells of the bronchial epithelium are the critical target cells for malignant transformation and that the alpha dose to these cells is the relevant radiation dose. 

Numerous studies demonstrated that lipid peroxidation significantly decreased in cancer cells and tissues (Ref. [176] and references therein). It has been proposed that this can be a consequence of a decrease in the content of highly unsaturated fatty acids, the concentration of cytochrome p-450, and the contents of NADPH, SOD, and catalase in tumors. Cheeseman et al. [176] suggested that the reduction of lipid peroxidation in tumors may depend on both the expression of malignant transformation and cell division. It should be mentioned that Boyd and McGuire [177] demonstrated that there is a correlation between lipid peroxidation and breast cancer risk in premenopausal women. 

The origin of a malignant tumor is a random genetic mutation leading to the loss of mitotic control by the cells. Normal cells experience mutations regularly, and they are necessary mechanisms of adaptation that are strictly controlled. Malignant transformation, however, means a loss of control and a chaotic, uncontrolled growth. 

Yogeeswaran, G. (1983). Cell surface glycolipids and glycoproteins in malignant transformation. Adv. Cancer Res. 38,289-350. 

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