- Most proto-oncogenes and tumor suppressor genes that have been identified, function in signal transduction to mimic the effects of persistent mitogenic stimulation, thereby uncoupling cells from normal external controls.
- These signaling pathways converge on the machinery that controls passage of the cell through the G1-phase and prevent cell cycle exit.
- In addition, other genes, many of which are targeted by cancer-specific chromosomal translocations, lead to aberrant lineage-specific differentiation and developmental decisions that would normally induce apoptosis. The two tumor suppressor proteins, p53 and Rb, which have key roles in determining cell cycle progression and apoptosis, and the genes coding for these proteins are most frequently disrupted in cancer cells.
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| page 597 |  | | page 598 |
Test your new knowledge:
- How is progression through the cell cycle regulated?
- What roles do caspases and Bcl-2 family members play in the regulation of apoptosis?
- How do mutations in the Rb or p53 genes contribute to tumor progression?
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| O'Connor L, Huang DCS, O'Reilly LA, Strasser A. Apoptosis and cell division. Curr Op Cell Biol 2000;12:257-263.
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Zhu L, Skoultchu AI. Coordinating cell proliferation and differentiation. Curr Op Genet Dev 2001;11:91-97.
Full article
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| Harbour JW, Dean DC. Rb function in cell cycle regulation and apoptosis. Nature Cell Biol 2000;2:E65-67.
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| Hengartner MO. The biochemistry of apoptosis. Nature 2000;407:770-776.
Full article
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| Vogelstein B, Lane D, Levine AJ. Surfing the p53 network. Nature 2000;408:307-310.
Full article
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| The WWW Virtual Library of Cell Biology (cell cycle, apoptosis etc.)
Full article
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| Nature's Encyclopedia of Life Sciences
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| The Genetics of Cancer Resource Center
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| www.intouchlive.com/cancergenetics
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