Defects in G1‐S cell cycle control in head and neck cancer: A review
- 23 May 2002
- journal article
- review article
- Published by Wiley in Head & Neck
- Vol. 24 (7) , 694-704
- https://doi.org/10.1002/hed.10109
Abstract
Tumors gradually develop as a result of a multistep acquisition of genetic alterations and ultimately emerge as selflsh, intruding and metastatic cells. The genetic defects associated with the process of tumor progression affect control of proliferation, programmed cell death, cell aging, angiogenesis, escape from immune control and metastasis. Fundamental cancer research over the last thirty years has revealed a multitude of genetic alterations which specify more or less separate steps in tumor development and which are collectively responsible for the process of tumor progression. The genes affected play in normal cells a crucial role in control over cell duplication and the interaction between cells, and between cells and their direct surrounding. This is illustrated on control during the G1/S phase of the cell cycle by its ultimate regulators: cyclins and cyclin dependent kinases. These proteins not only control the transition through the G1/S phase of the cell cycle, but also serve as mediators of the interaction between cells, and between cells and their surrounding. Defaults in the regulation of these proteins are associated with tumor progression, and, therefore, serve as targets for therapy. Defaults in those genes are found in various tumor types, although some of those prevail in particular tumor types. In this review emphasis is given to the defaults that occur in head and neck cancer.Keywords
This publication has 81 references indexed in Scilit:
- Anoikis mechanismsCurrent Opinion in Cell Biology, 2001
- Reconstitution of Cyclin D1-Associated Kinase Activity Drives Terminally Differentiated Cells into the Cell CycleMolecular and Cellular Biology, 2001
- The ins and outs of signallingNature, 2001
- ONYX-015 selectivity and the p14ARF pathwayOncogene, 2000
- Chemoprevention of Head and Neck CancerOtolaryngology -- Head and Neck Surgery, 2000
- Synergistic induction of centrosome hyperamplification by loss of p53 and cyclin E overexpressionOncogene, 2000
- The Ki-67 protein: From the known and the unknownJournal of Cellular Physiology, 2000
- The Hallmarks of CancerCell, 2000
- Pharmacological Rescue of Mutant p53 Conformation and FunctionScience, 1999
- Disruption of p53 in human cancer cells alters the responses to therapeutic agentsJournal of Clinical Investigation, 1999