Tumor formation Cell division

The body s cells are normally subject to strict social control. They only divide until they come into contact with neighboring cells cell division then ceases due to contact inhibition. Exceptions to this rule include embryonic cells, cells of the intestinal epithelium (where the cells are constantly being replaced), cells in the bone marrow (where formation of blood cells takes place), and tumor cells. Uncontrolled cell proliferation is an important indicator of the presence of a tumor. While normal cells in cell culture only divide 20-60 times, tumor cells are potentially immortal and are not subject to contact inhibition. 

The pRb protein has the characteristics of a tumor suppressor protein. Loss of its function is associated with deregulation of cell division and favors tumor formation (see Chapter 14). 

Furthermore, each cell division round has the potential danger of rearrangement of chromosome sections during mitosis and thus chromosome aberrations. A thorough theoretical and experimental analysis of the dose-effect relation of various canceroge-nic substances has shown that an increased cell division activity is an important risk factor for the creation of tumors (Cohen and Ellwein, 1990). All processes that lead to an increase in the rate of cell division will increase the probability of tumor formation, according to these investigations. 

Cell Division Activity, Errors in Function of Signal Proteins and Tumor Formation... 

Tumor suppressor genes are genes that, by their inactivation due to mutations or deletion, promote tumor formation. The proteins for which they code are known as tumor suppressor proteins. Many of the known tumor suppressor proteins have a suppressing and negatively regulating effect on processes that are either directly associated with regulation of cell division or influence this in an indirect way. Other, equally important functions of tumor suppressor proteins are in the areas of DNA repair and cell adhesion. Inactivation of tumor suppressor genes can have various consequences ... 

Tumor suppressor genes encode proteins that normally restrain cell division. Mutation in one or more of these genes can lead to tumor formation. 

Tumor suppressor genes encode regulatory proteins that normally inhibit cell division mutations in these genes are genetically recessive but can lead to tumor formation. 

Paclitaxel acts by enhancing microtubule assembly and stabilizing microtubules (1,2). Microtubules consist of polymers of tubulin in dynamic equilibrium with tubulin heterodimers. Their principal function is the formation of the mitotic spindle during cell division, but they are also active in many interphase functions, such as cellular motility, intracellular transport, and signal transmission. Paclitaxel inhibits the depolymerization of tubulin, and the microtubules formed in the presence of paclitaxel are extremely stable and dysfunctional. This stabilization impairs the essential assembly and disassembly required for dynamic cellular processes, and death of the cell results through disruption of the normal microtubular dynamics required for interphase processes and cell division. In tumor cells, cytotoxicity is represented by the appearance of abnormal microtubular bundles, which accumulate during G2 and mitosis, blocking the cell cycle (3). 

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