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

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Pages (from-to)373-378
Number of pages6
JournalJapanese Journal of Neurosurgery
Volume14
Issue number6
Publication statusPublished - 2005 Jun
Externally publishedYes

Fingerprint

Cell Cycle
Carcinogenesis
Cell Cycle Checkpoints
Neoplasms
M Phase Cell Cycle Checkpoints
G2 Phase
Phase Transition
Therapeutics
Mitosis
Antineoplastic Agents
Cell Death
Radiotherapy
Chromosomes
Drug Therapy
Mutation
Genes

Keywords

  • Checkpoint
  • Mitosis
  • Mitotic catastrophe
  • p53

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Molecular mechanism of tumorigenesis by cell cycle regulation and new therapeutical approaches. / Saya, Hideyuki.

In: Japanese Journal of Neurosurgery, Vol. 14, No. 6, 06.2005, p. 373-378.

Research output: Contribution to journalArticle

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