Overview
- Editors:
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Wafik S. El-Deiry
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Departments of Medicine, Genetics, and Pharmacology, University of Pennsylvania School of Medicine, Philadelphia
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Table of contents (31 protocols)
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Known Tumor Suppessor Genes and Pathways
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- Marco G. Paggi, Armando Felsani, Antonio Giordano
Pages 3-19
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- Patrice J. Morin, Ashani T. Weeraratna
Pages 21-40
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- Ralph Scully, Nadine Puget
Pages 41-57
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- William M. Grady, Sanford D. Markowitz
Pages 59-83
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- Anthony G. Quinn, Ervin Epstein Jr.
Pages 85-95
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- Arvind K. Virmani, Adi F. Gazdar
Pages 97-115
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- Jun-ichi Okano, Lorraine Snyder, Anil K. Rustgi
Pages 131-145
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- Ramon Parsons, Laura Simpson
Pages 147-166
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- Michael Ohh, William G. Kaelin Jr.
Pages 167-183
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- Kapaettu Satyamoorthy, Meenhard Herlyn
Pages 185-195
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- Teresa Acosta Almeida, Nickolas Papadopoulos
Pages 211-222
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- Margaret E. McLaughlin, Tyler Jacks
Pages 223-237
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- Andrew P. Feinberg, Bryan R. G. Williams
Pages 239-248
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- Theodore L. DeWeese, William G. Nelson
Pages 249-268
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- Paul Dent, Liang Qiao, Donna Gilfor, Michael Birrer, Steven Grant, Paul B. Fisher
Pages 269-292
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Identification of Tumor Suppressor Genes
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Front Matter
Pages 293-293
About this book
It has become clear that tumors arise from excessive cell proliferation and a c- responding reduction in cell death. Tumors result from the successive accumulation of mutations in key regulatory target genes over time. During the 1980s, a number of oncogenes were characterized, whereas from the 1990s to the present, the emphasis shifted to tumor suppressor genes (TSGs). It has become clear that oncogenes and tumor suppressor genes function in the same pathways, providing positive and ne- tive growth regulatory activities. The signaling pathways controlled by these genes involve virtually every process in cell biology, including nuclear events, cell cycle, cell death, cytoskeletal, cell membrane, angiogenesis, and cell adhesion effects. Tumor suppressor genes are mutated in hereditary cancer syndromes, as well as somatically in nonhereditary cancers. In their normal state, TSGs control cancer development and p- gression, as well as contribute to the sensitivity of cancers to a variety of therapeutics. Understanding the classes of TSGs, the biochemical pathways they function in, and how they are regulated provides an essential lesson in cancer biology. We cannot hope to advance our current knowledge and to develop new and more effective therapies without understanding the relevant pathways and how they influence the present approaches to therapy. Moreover, it is important to be able to access the powerful tools now available to discover these genes, as well as their links to cell biology and growth control.
Editors and Affiliations
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Departments of Medicine, Genetics, and Pharmacology, University of Pennsylvania School of Medicine, Philadelphia
Wafik S. El-Deiry
