Tumor is a difficult disease to deal with because our immune system cannot recognize it, plus it is a cell that divides forever. Because telomerase is necessary for the immortalization of tumor cells, telomerase can be a good target for anti-tumor drugs. If there are drugs that can turn off telomerase in tumor cells, the length of telomeres will gradually shorten as the tumor cells divide, mutations will occur, and the cells will become unstable. Experimental drug treatments have been performed in mice, and some drugs are in early clinical trials. In normal human cells, telomeres are programmed to shorten, limiting the cell’s ability to grow, and the re-expression of telomerase plays an important role in the immortalization of cells and in the process of carcinogenesis. Therefore, it has been suggested that cells with normal expression of telomerase activity are more susceptible to carcinogenesis. When measuring telomerase activity, it was found that more than 90% of normal tissue cells were negative for telomerase, thus linking this enzyme to cell immortalization and tumorigenesis. Due to such conditions, telomerase activation, diagnosis and inhibition are of great clinical value. Tumorigenesis The 30 trillion normal cells are a complex and interdependent macroenvironment that co-manages and regulates each other. A cell proliferates only when it receives growth-stimulating signals from other nearby cells, and stops growing when it receives inhibitory signals. This interaction allows each type of tissue to maintain a certain size and shape to suit the needs of the body. Cancer cells, in contrast, ignore the normal signals that control proliferation and only follow their own intrinsic proliferation criteria. They can even move and invade adjacent tissues. Since tumors composed of such malignant cells invade more and more tissues, they lead to the death of the body when they interfere with the organs and tissues needed for the body’s survival. How do cancer cells arise? Many proto-oncogenes function normally by transmitting signals from external growth stimuli into the cell. When a proto-oncogene is mutated to affect an important growth stimulus signal, it activates a gene that should be silent. Some proto-oncogenes are mutated to interfere with parts of the signaling cascade pathway in the cell, such as the Ras protein, so that genes are activated in vivo in the absence of an external growth stimulus signal. External inhibitory signals also fail to enter the cell due to the disruption of signaling cascade pathways. In addition, the cell cycle of cancer cells is also disturbed. p 53 genes are absent or loss of function in 1/2 of the tumor cells, depriving the p 21 protein of its ability to inhibit the cell cycle proteins, CDK5, and the complexes of both, and thus the cell cycle is unrestricted. Tissues generally have two ways of controlling proliferation and avoiding cancer: one leads to apoptosis when important intracellular components are impaired or the control system is dysregulated; the other system is the restriction of cell proliferation ploidy. How does a cell control its own proliferation ploidy? Telomeres at the ends of chromosomes act as counters and start to initiate senescence and crisis at certain periods. Telomeres become slightly shorter as they enter S-phase after each proliferation, and when their length falls below a certain threshold they initiate cellular senescence. If the cell still does not undergo senescence, further shortening will eventually lead to a crisis, where excessively short telomeres cause chromosomes in the cell to fuse or break, dealing a fatal blow to the cell and thus limiting its ability to proliferate. Telomerase, which is virtually absent in normal cells and present in almost all cancer cells, encodes telomeres that replace telomeric segments that are shortened during each cell cycle, thus maintaining telomere length to be free from proliferation limitation.
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