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Alteration of cell division cycle regulation in human cancers: The role of CDKN2A gene

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Cell Growth and Oncogenesis

Abstract

Cancer might be thought of as a disease characterized by a deregulated cellular growth. Thus, it is not surprising that some of the molecular components of cell division cycle machinery are altered in human tumors. The cell cycle of all post-embryonic eukaryotic cells (including malignant cells) is divided into four phases, namely: G1 phase (period prior to DNA synthesis), S phase (period of DNA synthesis), G2 phase (period between DNA synthesis and mitosis) and M phase (mitosis). Collectively, G1, S and G2 are called interphase, the cell cycle period distinct from division of the nucleus (mitosis) and cytoplasm (cytokinesis) (Pardee, 1989; Desai et al., 1992). The length of the S, G2 and M phases is remarkably similar in many different cells, while the greatest variation is seen in the length of G1. At some point late in G1, called restriction or R point, a cell becomes committed to traverse the remainder of the cell cycle. Thus, variations in cell cycle time are mostly due to variations in the length of G1 up to the R point (Pardee, 1989; Desai et al., 1992).

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Della Ragione, F. et al. (1998). Alteration of cell division cycle regulation in human cancers: The role of CDKN2A gene. In: Bannasch, P., Kanduc, D., Papa, S., Tager, J.M. (eds) Cell Growth and Oncogenesis. Molecular and Cell Biology Updates. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8950-6_10

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  • DOI: https://doi.org/10.1007/978-3-0348-8950-6_10

  • Publisher Name: Birkhäuser, Basel

  • Print ISBN: 978-3-0348-9841-6

  • Online ISBN: 978-3-0348-8950-6

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