The long-term goal of this research program is to gain knowledge concerning the mechanisms involved in the response of mammalian cells to ionizing radiation, with particular reference to its carcinogenic and mutagenic effects. The approach is a multifaceted one, and the endpoints under investigation include mutagenesis, malignant transformation, cell survival and the induction of chromosomal abnormalities. The program has the overall purpose of further defining the risks of low-level radiation exposure by gaining a better understanding of the cellular and molecular mechanisms for its effects.
Current research is focused in three general areas.
Extensive evidence suggests that carcinogenesis is a multi-stage process that requires multiple genetic and epigenetic alterations. These studies are designed to enhance our understanding of the genetic control of the sensitivity to radiation exposure. Intercellular communication is involved in the bystander regulation of gene expression in human cells exposed to very low fluences of alpha particles. J.B. Loss of Normal G1 checkpoint control is an early step in carcinogenesis, independent of p53 status. Little, J.B. Induction of genetic instability by ionizing radiation.