Is Cell Death a Critical End Point for Anticancer Therapies or Is Cytostasis Sufficient?
Open Access
- 15 December 2007
- journal article
- review article
- Published by American Association for Cancer Research (AACR) in Clinical Cancer Research
- Vol. 13 (24), 7280-7287
- https://doi.org/10.1158/1078-0432.ccr-07-2141
Abstract
Since the discovery of conventional chemotherapy and the development of new target-based agents, the importance of cytostasis in anticancer activity has been debated. This review examines the relative importance of both cytostasis and cytotoxicity based on both preclinical data and clinical reports. Several limitations of our basic and clinical methods to evaluate cytostasis and cytotoxicity will be highlighted. Molecular mechanisms of cytostasis will be analyzed, including interference with the cell cycle as well as putative links with necrosis and autophagy. Finally, we will cite evidence that most older and newer compounds are both cytostatic and cytotoxic. The relative role of cytostasis and cytotoxicity on future drug screening and clinical development will be explored.Keywords
This publication has 49 references indexed in Scilit:
- A mathematical model separates quantitatively the cytostatic and cytotoxic effects of a HER2 tyrosine kinase inhibitorTheoretical Biology and Medical Modelling, 2007
- Sorafenib in Renal Cell CarcinomaClinical Cancer Research, 2007
- Sorafenib in Advanced Clear-Cell Renal-Cell CarcinomaNew England Journal of Medicine, 2007
- Epidermal Growth Factor Receptor Activation: How Exon 19 and 21 Mutations Changed Our Understanding of the PathwayClinical Cancer Research, 2006
- Flavopiridol administered using a pharmacologically derived schedule is associated with marked clinical efficacy in refractory, genetically high-risk chronic lymphocytic leukemiaBlood, 2006
- EGF–ERBB signalling: towards the systems levelNature Reviews Molecular Cell Biology, 2006
- Phase I Pharmacokinetic and Pharmacodynamic Study of 17-Allylamino, 17-Demethoxygeldanamycin in Patients With Advanced MalignanciesJournal of Clinical Oncology, 2005
- The Cyclin-dependent Kinase Inhibitor CYC202 ( R -Roscovitine) Inhibits Retinoblastoma Protein Phosphorylation, Causes Loss of Cyclin D1, and Activates the Mitogen-activated Protein Kinase PathwayCancer Research, 2004
- Oxaliplatin, tetraplatin, cisplatin, and carboplatin: Spectrum of activity in drug-resistant cell lines and in the cell lines of the national cancer institute's anticancer drug screen panelBiochemical Pharmacology, 1996
- Taxol in combination with doxorubicin or etoposide possible antagonism in vitroCancer, 1993