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- W85250985 abstract "Apoptosis can be distinguished from necrosis, the classical form of cell death, by several morphological and biochemical criteria. Apoptotic cells, but not necrotic cells, show early condensation of chromatin as well as endonuclease activation resulting in cleavage of the nuclear DNA into oligonucleosomal fragments. Both physiological and low level cytotoxic stimuli have been shown to induce apoptosis, which in some cell models can be suppressed by inhibitors of protein and RNA synthesis. The concept of the cell being actively involved in its own death, combined with the demonstration that factors which alter the rate of cell death, such as the proto-oncogene bcl-2, can directly affect the number of cells within a population, has resulted in the identification of cell death alongside proliferation and differentiation as a means for controlling celi population growth. The purpose of this study was to determine if bcl-2 and the Epstein-Barr virus gene BHRF1, which share 25% primary amino acid sequence homology, could suppress apoptosis in response to a variety of anti-cancer treatments. After demonstrating apoptotic cell death on treatment with chemotherapeutic agents in an IL-3 dependent cell line (FDCP-1) and three different EBV genome-positive Burkitt's lymphoma cell lines, the survival of EBV-BL cell lines expressing either exogenous bcl-2 or BHRF1 was examined. Suppression of apoptosis in response to treatment with chemotherapeutic drugs or y radiation was clearly shown in EBVBL cells expressing bcl-2 or BHRF1 when compared to control transfectants. This study has further confirmed that BHRF1 is functionally homologous to bcl-2, suggesting that BHRF1 may act to prevent apoptosis during EBV infection. Suppression of chemotherapeutic drug induced cell death by either bcl-2 or BHRF1 also represents a novel form of drug resistance and may form an alternative mechanism by which multidrug resistance may arise during chemotherapy. The identification and investigation of other genes which produce suppression of apoptosis is also important in order to determine the extent of involvement of apoptotic suppression in the transformation to the malignant state and in the acquisition of multidrug resistance. A protocol to screen for 'apoptosis-suppressed cells' in the FDCP-1 E -3 dependent cell line was developed to identify new genes involved in the pathway(s) of apoptosis." @default.
- W85250985 created "2016-06-24" @default.
- W85250985 creator A5039242992 @default.
- W85250985 date "1994-07-18" @default.
- W85250985 modified "2023-09-23" @default.
- W85250985 title "Apoptosis induced by cancer chemotherapeutic drugs and its genetic suppression" @default.
- W85250985 cites W135475331 @default.
- W85250985 cites W138285015 @default.
- W85250985 cites W140810763 @default.
- W85250985 cites W1485476587 @default.
- W85250985 cites W1495692618 @default.
- W85250985 cites W1501566065 @default.
- W85250985 cites W1507635569 @default.
- W85250985 cites W1510023231 @default.
- W85250985 cites W1514575046 @default.
- W85250985 cites W1520057413 @default.
- W85250985 cites W1522890891 @default.
- W85250985 cites W1528844330 @default.
- W85250985 cites W1532539996 @default.
- W85250985 cites W1533488446 @default.
- W85250985 cites W1535244363 @default.
- W85250985 cites W153582684 @default.
- W85250985 cites W1538279368 @default.
- W85250985 cites W1538805645 @default.
- W85250985 cites W1545715398 @default.
- W85250985 cites W1546320853 @default.
- W85250985 cites W1552857477 @default.
- W85250985 cites W1554380543 @default.
- W85250985 cites W155748415 @default.
- W85250985 cites W1558473055 @default.
- W85250985 cites W1559053841 @default.
- W85250985 cites W1559184092 @default.
- W85250985 cites W1567730870 @default.
- W85250985 cites W15716873 @default.
- W85250985 cites W1572054014 @default.
- W85250985 cites W1572398159 @default.
- W85250985 cites W1575024932 @default.
- W85250985 cites W1578072993 @default.
- W85250985 cites W1582630245 @default.
- W85250985 cites W1588630125 @default.
- W85250985 cites W1589415602 @default.
- W85250985 cites W1591166893 @default.
- W85250985 cites W1592664042 @default.
- W85250985 cites W1594804854 @default.
- W85250985 cites W1598586133 @default.
- W85250985 cites W1606829096 @default.
- W85250985 cites W1648720631 @default.
- W85250985 cites W1660272883 @default.
- W85250985 cites W1667442117 @default.
- W85250985 cites W1706373226 @default.
- W85250985 cites W173175059 @default.
- W85250985 cites W174558702 @default.
- W85250985 cites W1760923416 @default.
- W85250985 cites W1766184558 @default.
- W85250985 cites W1770289754 @default.
- W85250985 cites W1804273004 @default.
- W85250985 cites W1812374189 @default.
- W85250985 cites W1826859465 @default.
- W85250985 cites W1832527043 @default.
- W85250985 cites W1836338391 @default.
- W85250985 cites W1842375597 @default.
- W85250985 cites W1847864430 @default.
- W85250985 cites W1862346079 @default.
- W85250985 cites W1876134060 @default.
- W85250985 cites W1883033938 @default.
- W85250985 cites W1892554314 @default.
- W85250985 cites W1898236813 @default.
- W85250985 cites W1898775203 @default.
- W85250985 cites W1899316739 @default.
- W85250985 cites W1909649638 @default.
- W85250985 cites W1909751364 @default.
- W85250985 cites W1911240597 @default.
- W85250985 cites W1915857360 @default.
- W85250985 cites W1921208916 @default.
- W85250985 cites W1923009678 @default.
- W85250985 cites W1924646174 @default.
- W85250985 cites W1950367760 @default.
- W85250985 cites W1964264035 @default.
- W85250985 cites W1964819620 @default.
- W85250985 cites W1965322366 @default.
- W85250985 cites W1965606263 @default.
- W85250985 cites W1967217459 @default.
- W85250985 cites W1967297582 @default.
- W85250985 cites W1967608740 @default.
- W85250985 cites W1967787805 @default.
- W85250985 cites W1968075576 @default.
- W85250985 cites W1968213454 @default.
- W85250985 cites W1969331809 @default.
- W85250985 cites W1970629830 @default.
- W85250985 cites W1970734978 @default.
- W85250985 cites W1971234510 @default.
- W85250985 cites W1971749209 @default.
- W85250985 cites W1972364920 @default.
- W85250985 cites W1972992388 @default.
- W85250985 cites W1973061854 @default.
- W85250985 cites W1973363947 @default.
- W85250985 cites W1973792489 @default.
- W85250985 cites W1973793798 @default.
- W85250985 cites W1975113868 @default.
- W85250985 cites W1976133790 @default.