Overview of perinatal and multigeneration carcinogenesis

Abstract

One of the characteristics of recent decades, which have seen a formidable expansion of cancer research, has been the co-existence of the generally agreed hypothesis that most cancers are multifactorial in origin, with the attitude of concentrating nevertheless on single carcinogenic agents and on attempting to quantify cancer risks as if they were due to single factors. It is not possible at present to quantitatively estimate the role of prenatal exposures to carcinogens/mutagens in determining or modulating the risk of cancer in humans. It is not unreasonable to assume, however, that the consequences of prenatal exposures and of prenatal events are among the factors that are often ignored. Prenatal events can contribute to the occurrence of cancer as the consequence of either: (1) the direct exposure of embryonal or fetal cells to a carcinogenic agent; (2) a prezygotic exposure of the germ cells of one or both parents to a carcinogen/mutagen before mating; (3) a genetic instability and/or a genetic rearrangement resulting from selective breeding which may favour a deregulation of cellular growth and differentiation. By offering the possibility of investigating the role played by events involving both germ and somatic cells, studies on prenatal carcinogenesis may become essential for a more accurate estimation of risks attributable to environmental agents, and may at the same time contribute to the understanding of some of the mechanisms underlying the genetic predisposition to cancer.