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Apoptosis

Molecular Regulation of Cell Death and Hematologic Malignancies

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Hematologic Malignancies

Part of the book series: Methods in Molecular Medicine™ ((MIMM,volume 55))

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Abstract

Apoptosis, or programmed cell death, represents in cell biology a functional program as important as cell growth or differentiation. Programmed cell death is of basic importance for the development of multicellular organisms and its basic mechanisms are conserved during the evolution of metazoa. Mammalian cells exhibit several different apoptotic pathways that converge to a common endpoint. Each pathway is triggered by a different stimulus: growth factor default, irradiation, induction of the p53 oncosuppressor protein, glucocorticoid hormones (in lymphocytes), ligand binding to Fas/APO (CD95), or tumor necrosis factor receptor (TNF-R), perforin secreted by cytotoxic T cells (reviewed by Hale et al. [1]). As opposed to necrosis, apoptosis is a “clean” process: as the cell shrinks, the cell membrane turns into the “apoptotic shell,” the nucleus is condensed and reduced in volume, and eventually the cell disappears from the tissue, due to phagocytosis by neighboring cells or professional phagocytes, such as macrophages.

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© 2001 Humana Press Inc.

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Chiarugi, V., Cinelli, M., Magnelli, L., Dello Sbarba, P. (2001). Apoptosis. In: Faguet, G.B. (eds) Hematologic Malignancies. Methods in Molecular Medicine™, vol 55. Humana Press. https://doi.org/10.1385/1-59259-074-8:323

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  • DOI: https://doi.org/10.1385/1-59259-074-8:323

  • Publisher Name: Humana Press

  • Print ISBN: 978-0-89603-543-0

  • Online ISBN: 978-1-59259-074-2

  • eBook Packages: Springer Protocols

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