[Frontiers in Bioscience, 3, d250-268, February 15, 1998]

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Bruno Amati, Konstantinos Alevizopoulos and Jaromir Vlach

Swiss Institute for Experimental Cancer Research (ISREC), CH-1066 Epalinges, Switzerland

Received 1/28/98 Accepted 2/11/98


1. Abstract

2. Introduction
2.1. The Myc protein
2.2. G1-S control in mammalian cells: an outline
3. Myc positively regulates CDK function through several pathways
3.1. Myc antagonizes the function of p27Kip1
3.1.1. Constitutive expression of Myc prevents p27-induced growth arrest
3.1.2. Activation of Myc induces cell cycle entry by suppressing p27 function
3.2. Myc up-regulates cyclin E expression, but what is the mechanism?
3.3. Myc target genes and cell cycle control: cdc25A may be one, others are still missing
3.4. The effects of decreasing or increasing Myc activity in growing cells
4. Myc and the p16-pRb pathway
4.1. Cyclin E, the spy who came in from the cold
4.2. Cellular context may determine the ability of Myc to promote cell cycle progression
4.3. Relationship between Myc and cyclin D1 in mitogenic signalling
5. Myc as a downstream target of pocket proteins and E2F
6. Lessons from a Myc knock-out cell line: independent effects on cell cycle and cell growth
7. Cellular transformation and Oncogene cooperation: the example of Myc and Ras
7.1. Myc and Ras: interplay in cell cycle control
7.2. Interplay between tumor suppressor and oncogenic pathways
7.3. Do p21, p27 or p57 function as tumor suppressors?
8. Perspectives
9. Acknowledgments
10. References
11. Entire manuscript

Key words: Cell cycle, Oncogenes, Tumor suppressor genes, Myc, Ras, Cyclins, CDKs, CKIs, p27Kip1,p16INK4a

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