APOPTOS1S AS A TARGET fOR CANCER THERAPY
Ahmad Samir Mohamed Raslan;
Abstract
There are two major mechanisms of cell death: necrosis and apoptosis. Necrosis is a passive response to injury in which cells swell and lyse; the release of cellular contents into the intercellular space elicits an inflammatory resp(!nse. In contrast, apoptosis involves the activation of a genetic program during which cells lose viability before they lose membrane integrity, and no inflammatory response is produced.
apoptosis is a genetically encoded cell elimination program, which ensures equilibrium between cell proliferation and cell death. Cells dying of apoptosis detach themselves from their neighbors and generally, there is celi shrinkage with reduced cell volume ending in cell break into membrane bound "apoptotic bodies". A major trigger of apoptosis is cellular injury as anticancer drugs as well as ionizing and UV radiation.
The first of the negative regulators of apoptosis to be identified in mammalian cells was the bcl-2 gene, which can stop apoptosis. On the other hand, P53 induces apoptosis when overexpressed. DNA damage by irradiation or chemotherapy induces p53 to cause apoptosis to delete cells with genotoxic injury or inducing growth arrest followed by DNA repair.
Apoptosis can be measured by differet ways like light and electron microscopy, flowcytometry, gel electrophoresis and others. Since 1990, radiation induced apoptosis has been observed in several animal tumors and in several different cell lines in culture, and many investigators have been identifYing molecular signals that control the induction of apoptosis in cells exposed to radiation.
The application of the ideal anti-cancer drug would result in killing the malignant cells without affecting normal cells. However, as the currently used drugs are not directed against specific features of malignant cells, they usually
apoptosis is a genetically encoded cell elimination program, which ensures equilibrium between cell proliferation and cell death. Cells dying of apoptosis detach themselves from their neighbors and generally, there is celi shrinkage with reduced cell volume ending in cell break into membrane bound "apoptotic bodies". A major trigger of apoptosis is cellular injury as anticancer drugs as well as ionizing and UV radiation.
The first of the negative regulators of apoptosis to be identified in mammalian cells was the bcl-2 gene, which can stop apoptosis. On the other hand, P53 induces apoptosis when overexpressed. DNA damage by irradiation or chemotherapy induces p53 to cause apoptosis to delete cells with genotoxic injury or inducing growth arrest followed by DNA repair.
Apoptosis can be measured by differet ways like light and electron microscopy, flowcytometry, gel electrophoresis and others. Since 1990, radiation induced apoptosis has been observed in several animal tumors and in several different cell lines in culture, and many investigators have been identifYing molecular signals that control the induction of apoptosis in cells exposed to radiation.
The application of the ideal anti-cancer drug would result in killing the malignant cells without affecting normal cells. However, as the currently used drugs are not directed against specific features of malignant cells, they usually
Other data
| Title | APOPTOS1S AS A TARGET fOR CANCER THERAPY | Other Titles | السكته الخلوية كوسيلة لعلاج السرطان | Authors | Ahmad Samir Mohamed Raslan | Issue Date | 2000 |
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