| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Review |
Medicine Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892 [M. V. B.], and Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115 [A. B. P.]
Chemotherapy of cancer is limited by its toxicity to normal cells. On the basis of discoveries in signal transduction and cell cycle regulation, novel mechanism-based therapeutics are being developed. Although these cell cycle modulators were designed to target cancer cells, some of them can also be applied for a different purpose, i.e., to protect normal cells against the lethality of chemotherapy. Loss of sensitivity of cancer cells to cell cycle inhibitors can be exploited for selective protection of normal cells that retain this response. Indeed, inhibition of redundant or overactivated pathways (e.g., growth factor-activated pathways) or stimulation of absent pathways in cancer cells (e.g., p53, Rb, and p16) may not arrest cycling of cancer cells. But growth arrest of normal cells will then permit selective killing of cancer cells by cycle-dependent chemotherapy.
This article has been cited by other articles:
|
|
 |
|
  A. Zeuner, M. Signore, D. Martinetti, M. Bartucci, C. Peschle, and R. De Maria Chemotherapy-Induced Thrombocytopenia Derives from the Selective Death of Megakaryocyte Progenitors and Can Be Rescued by Stem Cell Factor Cancer Res., May 15, 2007; 67(10): 4767 - 4773. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Filomeni, G. Cerchiaro, A. M. Da Costa Ferreira, A. De Martino, J. Z. Pedersen, G. Rotilio, and M. R. Ciriolo Pro-apoptotic Activity of Novel Isatin-Schiff Base Copper(II) Complexes Depends on Oxidative Stress Induction and Organelle-selective Damage J. Biol. Chem., April 20, 2007; 282(16): 12010 - 12021. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-K. Sha, T. Sato, H. Kobayashi, M. Ishigaki, S. Yamamoto, H. Sato, A. Takada, S. Nakajyo, Y. Mochizuki, J. M. Friedman, et al. Cell cycle phenotype-based optimization of G2-abrogating peptides yields CBP501 with a unique mechanism of action at the G2 checkpoint Mol. Cancer Ther., January 1, 2007; 6(1): 147 - 153. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Kim, I.-Y. Park, J. Lim, Y. Kim, K. T. Han, W. H. Chung, and K. Han Antitumor and Normal Cell Protective Effect of PKC412 in the Athymic Mouse Model of Ovarian Cancer Ann. Clin. Lab. Sci., January 1, 2006; 36(4): 455 - 460. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Choudhuri, S. Pal, T. Das, and G. Sa Curcumin Selectively Induces Apoptosis in Deregulated Cyclin D1-expressed Cells at G2 Phase of Cell Cycle in a p53-dependent Manner J. Biol. Chem., May 20, 2005; 280(20): 20059 - 20068. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Carvajal, C. Tovar, H. Yang, B. T. Vu, D. C. Heimbrook, and L. T. Vassilev Activation of p53 by MDM2 Antagonists Can Protect Proliferating Cells from Mitotic Inhibitors Cancer Res., March 1, 2005; 65(5): 1918 - 1924. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. A. Giuliano, Y.-T. Chen, and D. L. Taylor High-Content Screening with siRNA Optimizes a Cell Biological Approach to Drug Discovery: Defining the Role of P53 Activation in the Cellular Response to Anticancer Drugs J Biomol Screen, October 1, 2004; 9(7): 557 - 568. [Abstract] [PDF]
|
|
|
|
 |
|
 C. Conticello, F. Pedini, A. Zeuner, M. Patti, M. Zerilli, G. Stassi, A. Messina, C. Peschle, and R. De Maria IL-4 Protects Tumor Cells from Anti-CD95 and Chemotherapeutic Agents via Up-Regulation of Antiapoptotic Proteins J. Immunol., May 1, 2004; 172(9): 5467 - 5477. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Mendoza, S. Fong, J. Marsters, H. Koeppen, R. Schwall, and D. Wickramasinghe Selective Cyclin-dependent Kinase 2/Cyclin A Antagonists that Differ from ATP Site Inhibitors Block Tumor Growth Cancer Res., March 1, 2003; 63(5): 1020 - 1024. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. C. Weinberg and M. F. Denning P21WAF1 CONTROL OF EPITHELIAL CELL CYCLE AND CELL FATE Critical Reviews in Oral Biology & Medicine, November 1, 2002; 13(6): 453 - 464. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Zeng Selenite and Selenomethionine Promote HL-60 Cell Cycle Progression J. Nutr., April 1, 2002; 132(4): 674 - 679. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |
