Titlebook: Apoptosis; Enrico Mihich,Robert T. Schimke Book 1994 Springer Science+Business Media New York 1994 Antigen.DNA.apoptosis.cancer.cell.cell

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Book 1994 to Programmed Cell Death (PCD) or Apoptosis, and the mechanisms involved. With presentations at the cutting edge of progress and stimulating discussions, this Symposium addressed the genetics and molecular mechanisms determining PCD and the role of this suicidal process in cancer and the immune sys

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https://doi.org/10.1007/978-3-662-30606-2 replicate its DNA prior to repairing lesions in the DNA may be more likely to result in daughter cells which have altered genetic information relative to the parental cell. It would be predicted that such altered daughter cells would be more likely to develop the genetic changes which contribute to a transformed phenotype (Figure 1).

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Molecular Controls of Cell Cycle Progression Following DNA Damage: Roles of P53 and Ataxia-Telangie replicate its DNA prior to repairing lesions in the DNA may be more likely to result in daughter cells which have altered genetic information relative to the parental cell. It would be predicted that such altered daughter cells would be more likely to develop the genetic changes which contribute to a transformed phenotype (Figure 1).

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Elemente der Achten Nebengruppe, however, extremely rare as demonstrated by the fact that cancer arises in only one in three individuals during the entire course of their lives. Part of the answer to this paradox appears to reside in the multifunctional nature of the components that mediate cell proliferation. One of these, c-Myc, is the subject of this paper.

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Elemente der Achten Nebengruppe1992), whereas viruses (Rao et al., 1992) and bacterial toxins (Fiorentini et al, 1993) can directly elicit an apoptotic response in target cells. Finally, exposure to ionizing radiation (Zhivotovsky et al., 1981 and 1993b) or chemical toxicants (McConkey et al., 1988; Aw et al., 1990) can accelerate apoptosis in immature T cells.

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