In a normal cell with each cell division a part of the telomere is lost; telomere is the protective end of the chromosome. When it reaches a certain length, the chromosome cannot duplicate and it sends signals to destroy the cell. However, in cancer cells the enzyme telomerase is activated and it elongates the telomere and cell division continues. A recent study suggests that shortening of telomere may destabilize the chromosome causing chromosome fusions, translocations and other rearrangements leading to initiation of precancerous stage in those cells that survive. At a critical time, in certain cells the telomerase is activated and the chromosome ends are stabilized, thus allowing these cells to resume division. This mechanism of carcinogenesis may be prevalent in tumors that develop in aged humans.
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