Cellular/molecular pharmacology; signal transduction,
hematopoietic growth factors, and cancer.
Department of Pharmacology 8683, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112-2699. tel 504-988-5444; fax 504-988-5283; e-mail: firstname.lastname@example.org
The primary focus of Dr. Beckman’s laboratory is the identification and increased understanding of signal transduction pathways in hypoxia-regulated gene expression, as well as in chemoresistance of cancer cell model systems. The laboratory has defined a number of kinases that are critical for hypoxia-induced erythropoietin gene regulation in human hepatocellular carcinoma cells and has linked these to specific transcription factors. In addition, Dr. Beckman’s research has described post-transcriptional events in hypoxia-linked gene expression. Identifying new therapeutic targets for solid tumors is the underlying rationale for these studies. Gene array studies have defined candidate genes in MCF-7 breast cancer cells that may be involved in chemoresistance pathways. In addition, the lab identified a marker for laryngeal cancer. The identification of specific molecular determinants for stabilization of messenger RNAs for oxygen sensing genes is another goal of our laboratory in collaboration with Dr. Aline Scandurro, Assistant Professor, in the Department of Microbiology and Immunology. The sphingolipid pathway is one of several major pathways whose dysregulation is involved in chemoresistance in breast cancer. We are currently evaluating sphingosine kinase inhibitors in the MCF-7 breast cancer cell model as well as in a mouse model.
In collaboration with Drs. John McLachlan and Matthew Burow we are investigating a soybean product produced under stressful environmental conditions. This natural product is called glyceollin and has anti-estrogenic effects in breast cancer model systems. We are investigating its mechanism of action. We are also studying a lung epithelial cell model to explore the specific interplay between estrogen and hypoxia. The lung is rich in estrogen receptor beta. When this receptor is not expressed abnormal lung structure and systemic hypoxia prevail. Systemic hypoxia may be a determinant of systemic hypertension and heart hypertrophy in ER beta deficient animals. In collaboration with Dr. Joe Lasky we are exploring the specific cell signaling events between the estrogen receptor and hypoxia-inducible factor (HIF) in the lung.
1430 Tulane Avenue, SL-83, New Orleans, LA 70112 504-988-5444 email@example.com