Molecular mechanism of tumorigenesis by cell cycle regulation and new therapeutical approaches

研究成果: Article

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Cell cycle checkpoints prevent transition from one phase of the cell cycle to the next until all processes of the present phase are completed. Defects in the checkpoint functions result in gene mutations and chromosome damages, which contribute to the development and progression of tumors. However, loss of checkpoint function in some cancer cells is considered to be associated with their sensitivity to antineoplastic treatments such as chemotherapy and radiation therapy. Most cancer therapies target cell cycle checkpoints by activating checkpoint-mediated cell death or by enhancing chemical sensitivity due to loss of checkpoint function. By treatment with genotoxic agents, cancer cells, which generally have impairment of checkpoint functions, initially arrest in the G2 phase of the cell cycle but are unable to maintain cell-cycle arrest. Those cells eventually die as they entered mitosis. This process is called 'mitotic catastrophe'. This review discusses the critical relationship between mitotic checkpoint function and sensitivity of cancer cells to anti-tumor therapies.

元の言語English
ページ(範囲)373-378
ページ数6
ジャーナルJapanese Journal of Neurosurgery
14
発行部数6
DOI
出版物ステータスPublished - 2005 6
外部発表Yes

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ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology

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