165 research outputs found
Biological Basis of Differential Susceptibility to Hepatocarcinogenesis among Mouse Strains*
There is a vast amount of literature related to mouse liver tumorigenesis generated over
the past 60 years, not all of which has been captured here. The studies reported in this
literature have generally been state of the art at the time they were carried out. A
PubMed search on the topic βmouse liver tumorsβ covering the past 10 years yields over
7000 scientific papers. This review address several important topics related to the
unresolved controversy regarding the relevance of mouse liver tumor responses observed in
cancer bioassays. The inherent mouse strain differential sensitivities to
hepatocarcinogenesis largely parallel the strain susceptibility to chemically induced
liver neoplasia. The effects of phenobarbital and halogenated hydrocarbons in mouse
hepatocarcinogenesis have been summarized because of recurring interest and numerous
publications on these topics. No single simple paradigm fully explains differential mouse
strain responses, which can vary more than 50-fold among inbred strains. In addition to
inherent genetics, modifying factors including cell cycle balance, enzyme induction, DNA
methylation, oncogenes and suppressor genes, diet, and intercellular communication
influence susceptibility to spontaneous and induced mouse hepatocarcinogenesis. Comments
are offered on the evaluation, interpretation, and relevance of mouse liver tumor
responses in the context of cancer bioassays
- β¦