Faculty
| FIORENZA IANZINI, Ph.D. Assistant Professor Director, Large Scale Digital Cells Analysis System (LSDCAS) - a Core Facility of the Holden Comprehensive Cancer Center Doctorate in Biology, University of Rome “La Sapienza”, Rome, Italy, 1980 Fellow, Istituto Superiore di Sanita', Rome, Italy, 1981-1987 Visiting Scientist, Charles University, Prague, Czechoslovakia, 1983 Visiting Scientist, Central Research Institute for Chemistry- Hungarian Academy of Sciences, Budapest, Hungary, 1986 Visiting Scientist, Medical Research Council, Didcot, England, 1989 Visiting Scientist, Yale University, School of Medicine, New Haven, Connecticut, USA, 1993 Postdoctoral Fellowship, University of Wisconsin-Madison, 1984-1986 |
Major areas of research in my laboratory focus on:
Alteration of cell-cycle progression induced by ionizing radiation and anti-cancer drug treatments in human cell lines with functional or non-functional p53. The goals of this research are to study the role played by cell cycle deregulation in the molecular mechanisms that promote cancer.
Early and late effects of ionizing radiation on cellular DNA. The studies conducted in this area aim principally at defining mechanism of acquisition of genomic instability and its role in cell transformation.
Application of the Large Scale Digital Cell Analysis System (LSDCAS) to study various cellular and molecular phenomena, such as: characterization of loss of cell cycle regulation following cell perturbation; quantification of cell motility; determination of the fate of cells overproducing pro-oxidants.
Role of high-LET radiation-induced mitotic catastrophe in mutagenesis and its implication in carcinogenesis. These studies are funded by NASA (PI: F. Ianzini) and aim at testing three major hypotheses: iron and proton ions of varying energies induce mutations in exposed human cells via processes occurring in cells that undergo mitotic catastrophe; mitotic catastrophe is an initiating mechanism that contributes to mutagenesis; the yield of mitotic catastrophe can be regarded as a predictor of carcinogenesis in vivo.
Activation of meiotic or pseudo-meiotic pathways during depolyploidization of polyploid tumor cells formed via radiation-induced mitotic catastrophe, and how activation of these pathways may play a role in cancer resistance to treatment and cancer progression.