As further novel genes and markers are identified in human prostate carcinogenesis, it is essential that we base new murine models on these findings.
Understanding the function and interactions of the family as a whole, in both cell growth control and carcinogenesis, will be important.
The passage of time is a ubiquitous carcinogen to which we are all exposed but age itself is not the mechanism of carcinogenesis.
Low folate status has been implicated in carcinogenesis, possibly as a result of a higher rate of genetic damage.
Interactions of alcohol with host and environmental factors, alcohol-related various procarcinogens, inherited susceptibility, and methylation have also been involved in the breast carcinogenesis.
Several studies have revealed variations in its cell differentiation and carcinogenesis functions.
Carcinogenesis can result either from the expression of a mutant version or from an altered gene product.
Thus, the search for and identification of these checkpoint mediators naturally led to the recognition of their potential roles in mediating carcinogenesis.
