Biomaterial Database

Liver tumor promoters and other mouse liver carcinogens. 1990

J M Ward, and B A Diwan, and R A Lubet, and J R Henneman, and D E Devor

Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD.

Mouse liver tumors are important end points for safety assessment of chemicals in rodent carcinogenicity assays. The mechanisms of induction of these tumors, whether by chemicals with significant genotoxic activities or by chemicals without such activities, remain unknown. If test mice have spontaneous tumors of high or low background incidence, the promotion of these tumors or of spontaneously initiated or susceptible cells may provide a basis for carcinogenesis induced by these compounds. Likewise, chronic toxicity and its associated target cell hyperplasia may also lead to promotion of these tumors. Experimental systems have been developed to study the mechanisms of tumor promotion in mouse liver. These models should significantly advance research into mechanisms of hepatocarcinogenesis and tumor promotion in mouse liver and may subsequently be used for human risk assessment.

UI	MeSH Term	Description	Entries
D006965	Hyperplasia	An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.	Hyperplasias
D008099	Liver	A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.	Livers
D008114	Liver Neoplasms, Experimental	Experimentally induced tumors of the LIVER.	Hepatoma, Experimental,Hepatoma, Morris,Hepatoma, Novikoff,Experimental Hepatoma,Experimental Hepatomas,Experimental Liver Neoplasms,Hepatomas, Experimental,Neoplasms, Experimental Liver,Experimental Liver Neoplasm,Liver Neoplasm, Experimental,Morris Hepatoma,Novikoff Hepatoma
D008297	Male		Males
D002273	Carcinogens	Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.	Carcinogen,Oncogen,Oncogens,Tumor Initiator,Tumor Initiators,Tumor Promoter,Tumor Promoters,Initiator, Tumor,Initiators, Tumor,Promoter, Tumor,Promoters, Tumor
D003043	Cocarcinogenesis	The combination of two or more different factors in the production of cancer.	Cocarcinogeneses
D004249	DNA Damage	Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.	DNA Injury,DNA Lesion,DNA Lesions,Genotoxic Stress,Stress, Genotoxic,Injury, DNA,DNA Injuries
D005260	Female		Females
D006498	Hepatectomy	Excision of all or part of the liver. (Dorland, 28th ed)	Hepatectomies
D000367	Age Factors	Age as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or the effect of a circumstance. It is used with human or animal concepts but should be differentiated from AGING, a physiological process, and TIME FACTORS which refers only to the passage of time.	Age Reporting,Age Factor,Factor, Age,Factors, Age