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.
Table of ContentsSection I: Overview of Knowledge by Assessments from the System of Morris “Minimal Deviation” Hepatomas.- Historical Development of Transplantable Hepatomas.- Contribution of the Morris Hepatomas to the Biochemistry of Cancer- Establishment of the Phenotypic Heterogeneity of Neoplasms InVivo.- The Morris Hepatomas as Models for Studies of Gene Expression in Neoplasia.- Hormonal Induction of Enzyme Functions, Cyclic AMP Levels and AIB Transport in Morris Hepatomas and in Normal Liver Systems.- The Molecular Correlation Concept of Neoplasia: Recent Advances and New Challenges.- Expression Mechanisms of Abnormality of Ornithine Aminotransferase Level in Morris Hepatoma.- Section II: Nuclear Composition.- Controls of Nucleolar Function in Cancer Cells.- Nuclear Macromolecular Changes in Hepatomas.- Enzymatic Modification of Nuclear Proteins During Neoplastic Growth.- Section III: Regulations of Nuclear Functioning.- Regualtion of DNA Synthesis in Isolated Morris Hepatoma Nuclei.- DNA-Dependent RNA Polymerases from Morris Hepatomas 3924A and 7800 and from Liver Treated with Thioacetamide.- Regulation of Macromolecular Syntheis in Morris Hepatomas.- Control of Specific Messenger RNA Species in Liver and Hepatoma.- Section IV: Intracellular Organelles and Membranes.- Alterations in Peroxisomes of Hepatomas.- Hexokinase: The Direct Link Between Mitochondrial and Glycolytic Reactions in Rapidly Growing Cancer Cells.- The Composition and Metabolism of Microsomal and Mitochondrial Membrane Lipids in the Morris 7777 Hepatoma.- Terminal Sugars in Glycoconjugates: Metabolism of Free and Protein Bound L-Fucose, N-Acetylneuraminic Acid, and D-Galactose in Liver and Morris Hepatomas.- Surface Membranes and Biological Regulation in Differentiated Hepatoma Cells InVitro.- Section V: Regulation of Cytoplasmic Functioning.- Regualtion of Cyclic AMP and Cyclic GMP in Morris Hepatomas and Liver.- Cyclic Nucleotide Metabolism in Solid Tumor Tissues.- Transfer RNA in Hepatomas.- The Synthesis and Secretion of Serum Albumin in Morris Hepatomas 5123tc and 9121.- Loss of Regulation of Lipid Metabolism in Morris Hepatomas: A Potential Role for Cytoplasmic Binding Proteins.- Section VI: Vitamins, Minerals, and Diet.- Vitamin B6 Effect on the Growth of Morris Hepatomas and the Development of Enzymatic Activity.- Iron and Copper Metabolism in Cancer, as Exemplified by Changes in Ferritin and Ceruloplasmin in Rats with Transplantable Tumors.- Abnormal Dietary Regulation of Glutamine Synthetase in Morris Hepatomas.- Section VII: Experimental Therapy.- Solid Tumor Models for the Assessment of Different Treatment Modalities: Perturbations in the Kinetics of Tumor and Host Organ Cellular Regulation Demonstrated by Single and Combined Experimental Therapy.- Special Bibliography of Hepatoma Cell Lines.