Charles J Gomer, PhD
|Title||Professor of Pediatrics|
|School||Keck School of Medicine of USC|
|Address||CHL Mail Stop 67|
Los Angeles California 90089
|Phone||+1 323 361 2335|
|Title||Vice Chair, Faculty Development (Pediatrics CHLA)|
My research program is involved in the areas of radiation biology, photobiology and laser medicine. A large portion of our work focuses on the examination of photodynamic therapy, in which tumor localizing photosensitizers are exposed to laser generated light for the selective generation of reactive oxygen species. PDT is used in the clinical treatment of solid tumors as well as for the treatment of vascular and dermal proliferative disorders. We are using molecular, biochemical, cellular and in-vivo methodologies to examine the biological consequences of exposure to reactive oxygen species and oxidative stress.
One area of investigation involves the use of the inducible heat shock (hsp) promoter as a molecular switch for the selective activation of heterologous genes. We have shown that photooxidative stress and laser generated hyperthermia are strong transcriptional inducers of the heat shock proteins. We have also shown that photooxidative stress can drive selective and temporal expression of reporter genes ligated to the hsp promoter. Work is now underway to evaluate our hypothesis that targeted gene therapy using recombinant constructs with oxidative stress and heat inducible promoters will provide a novel mechanism for expression of cytotoxins, growth factors, immuno-modulators, suppressor genes and antisense molecules. A second area of investigation involves the analysis of wild type and mutated p53 tumor suppressor gene expression on sensitivity of tumor cells to photooxidative stress. Loss of p53 function has been correlated with decreased sensitivity to chemotherapy and radiation therapy in a variety of human tumors. We are currently evaluating cell photosensitivity, cell cycle perturbations and apoptosis in tumor cell lines exhibiting either wild type p53, mutated p53 or deleted p53 expression. We have also isolated a cell line exhibiting a photooxidative stress resistant phenotype and we are evaluating the molecular determinants responsible for inducing cellular resistant to oxidative stress. A third area of investigation involves the use of photosensitizers and laser generated light for the treatment of the pediatric eye tumor retinoblastoma.
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