Overview
- Editors:
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Harold P. Morris
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Department of Biochemistry and Howard Cancer Research Center, Howard University Medical School, USA
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Wayne E. Criss
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Department of Biochemistry and Howard Cancer Research Center, Howard University Medical School, USA
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Table of contents (27 chapters)
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Overview of Knowledge by Assessments from the System of Morris “Minimal Deviation” Hepatomas
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- Harold P. Morris, Lynnard J. Slaughter
Pages 1-19
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- Henry C. Pitot, James Cardelli
Pages 21-37
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- Jennie B. Shatton, Sidney Weinhouse
Pages 39-58
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- George Weber, Harutoshi Kizaki, Taiichi Shiotani, Diana Tzeng, Jim C. Williams
Pages 89-116
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- Nobuhiko Katunuma, Keiko Kobayashi
Pages 117-123
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Nuclear Composition
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- H. Busch, N. R. Ballal, R. K. Busch, Y. C. Choi, F. Davis, I. L. Goldknopf et al.
Pages 125-180
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- Jen-Fu Chiu, Lubomir S. Hnilica, Luc Belanger, H. P. Morris
Pages 181-203
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- Woon Ki Paik, Samuel Nochumson, Sangduk Kim
Pages 205-232
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Regulations of Nuclear Functioning
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- Peter Ove, Mona L. Coetzee
Pages 233-271
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- Samson T. Jacob, Kathleen M. Rose, Thomas B. Leonard, Barry W. Duceman
Pages 273-288
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- Philip Feigelson, Linda W. DeLap
Pages 307-330
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Intracellular Organelles and Membranes
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- Hideyuki Tsukada, Yohichi Mochizuki, Mikio Gotoh
Pages 331-362
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- Ernesto Bustamante, Harold P. Morris, Peter L. Pedersen
Pages 363-380
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- Richard Morton, Moseley Waite, John W. Hartz, Carol Cunningham, Harold P. Morris
Pages 381-403
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Regulation of Cytoplasmic Functioning
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About this book
In 1960, Dr. Van R. Potter and Dr. Henry Pitot (at McCardle Laboratory in Madison, Wisconsin), Dr. Tetsuo Ono (then at McCardle Laboratory and now at the Japanese Foundation for Cancer Research in Tokyo, Japan) and Dr. Harold P. Morris (then at the National Cancer Institute and now at Howard University, Washington, D. C. ) decided that an experimental cancer model would be an invaluable tool to examine neoplastic changes in cells. Since they were study ing the various highly specific metabolic processes which are unique to liver tissues, they determined that a transplantable liver cancer model would be the ideal system to work with. This system would provide for comparison of normal liver tissue of the non-tumor bear ing animal, the tumor bearing animal's (host) liver and the liver cancer. Dr. Morris undertook a series of rat studies employing several chemicals known to cause liver cancer. Soon the first Morris hepatomas (#3683, 3924A, 5123) were being studied by several labs. During the next 18 years, Dr. Morris developed and transplanted numerous strains of hepatomas of which no two were identical. These tumors ranged from the very slowly-growing, highly differentiated cancer tissues, e. g. , 96l8A which is a diploid tumor containing gly cogen and a "nearly normal" complement of enzymes, to a large group of rapidly-growing, poorly differentiated cancer tissues, e. g.