Keck School Faculty

Charles J Gomer, PhD
Charles J Gomer, PhD
Professor of Pediatrics;Vice Chair, Faculty Development (Pediatrics CHLA);Chair, FAPTC
CHL Mail Stop 67 Off Campus Los Angeles
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.

Rational drug design and synthesis of new a-Santonin derivatives as potential COX-2 inhibitors Bioorg Med Chem Lett. 2018 Apr 01; 28(6):993-996. . View in PubMed

Rational drug design and synthesis of new a-Santonin derivatives as potential COX-2 inhibitors Bioorg Med Chem Lett. 2018 04 01; 28(6):993-996. . View in PubMed

Rabbit model of ocular indirect photodynamic therapy using a retinoblastoma xenograft Graefes Arch Clin Exp Ophthalmol. 2017 Dec; 255(12):2363-2373. . View in PubMed

Targeting Survivin Enhances Chemosensitivity in Retinoblastoma Cells and Orthotopic Tumors PLoS One. 2016; 11(4):e0153011. . View in PubMed

Induction of prosurvival molecules during treatment: rethinking therapy options for photodynamic therapy J Natl Compr Canc Netw. 2012 Oct 01; 10 Suppl 2:S35-9. . View in PubMed

Pro-apoptotic and anti-inflammatory properties of the green tea constituent epigallocatechin gallate increase photodynamic therapy responsiveness Lasers Surg Med. 2011 Sep; 43(7):644-50. . View in PubMed

Enhancement of photodynamic therapy by 2,5-dimethyl celecoxib, a non-cyclooxygenase-2 inhibitor analog of celecoxib Cancer Lett. 2011 May 01; 304(1):33-40. . View in PubMed

Targeting the 90 kDa heat shock protein improves photodynamic therapy Cancer Lett. 2010 Mar 28; 289(2):188-94. . View in PubMed

Targeting the tumor microenvironment using photodynamic therapy combined with inhibitors of cyclooxygenase-2 or vascular endothelial growth factor Methods Mol Biol. 2010; 635:121-32. . View in PubMed

Identification of MAP kinase pathways involved in COX-2 expression following photofrin photodynamic therapy Methods Mol Biol. 2010; 635:47-63. . View in PubMed

Cyclooxygenase-2 expression induced by photofrin photodynamic therapy involves the p38 MAPK pathway Photochem Photobiol. 2008 Mar-Apr; 84(2):509-14. . View in PubMed

Multiple components of photodynamic therapy can phosphorylate Akt Photochem Photobiol. 2007 Sep-Oct; 83(5):1029-33. . View in PubMed

Survivin, a member of the inhibitor of apoptosis family, is induced by photodynamic therapy and is a target for improving treatment response Cancer Res. 2007 May 15; 67(10):4989-95. . View in PubMed

Photodynamic therapy: combined modality approaches targeting the tumor microenvironment Lasers Surg Med. 2006 Jun; 38(5):516-21. . View in PubMed

Avastin enhances photodynamic therapy treatment of Kaposi's sarcoma in a mouse tumor model J Environ Pathol Toxicol Oncol. 2006; 25(1-2):251-9. . View in PubMed

Celecoxib and NS-398 enhance photodynamic therapy by increasing in vitro apoptosis and decreasing in vivo inflammatory and angiogenic factors Cancer Res. 2005 Oct 15; 65(20):9473-8. . View in PubMed

Spontaneous and controllable activation of suicide gene expression driven by the stress-inducible grp78 promoter resulting in eradication of sizable human tumors Hum Gene Ther. 2004 Jun; 15(6):553-61. . View in PubMed

The matrix metalloproteinase inhibitor prinomastat enhances photodynamic therapy responsiveness in a mouse tumor model Cancer Res. 2004 Apr 01; 64(7):2328-32. . View in PubMed

CHOP activation by photodynamic therapy increases treatment induced photosensitization Lasers Surg Med. 2004; 35(5):336-41. . View in PubMed

Cyclooxygenase-2 inhibitor treatment enhances photodynamic therapy-mediated tumor response Cancer Res. 2002 Jul 15; 62(14):3956-61. . View in PubMed

Enhanced photodynamic therapy efficacy with inducible suicide gene therapy controlled by the grp promoter Cancer Res. 2002 Mar 01; 62(5):1458-61. . View in PubMed

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