Professor

Contact Information:
Email: jcarde@lsuhsc.edu
Office Phone: 318-675-5756
Laboratory Phone: 318-675-5769
Office Fax: 318-675-5764

Education/Training:
Postdoctoral Study, University of Wisconsin
Ph.D., 1977, University of Wisconsin, Molecular Biology
B.S, 1973, University of Illinois, Biochemistry and Molecular Biology

Major Research Interests:  Regulation of the invasion and metastasis of cancer cells, and development of novel therapeutics to block or reverse metastatic disease

The major project in my laboratory involves defining the molecular signaling pathways that regulate the invasion and metastasis of cancer cells. Our current primary focus is breast, gastric and prostate cancer. Invasion and metastasis and complicated processes that are poorly understood and they are the primary reasons patients with cancer end up dying, and a better understanding of this process will lead to the development of more effective therapies. Our approach ranges from 1) basic science to define the role of growth factor receptor signaling in regulating changes in cell motility, survival, invasion and metastasis, 2) preclinical testing of novel compounds to block these changes, 3) clinical trials to determine if these compounds actually work in patients with cancer and 4) commercialization of successful compounds.

Representative Publications:

Roop, M., Bellaire, B., Valderas, M. and Cardelli, J. (2004). Adaption of Brucellae to their intracellular niche. Molecular Microbiology. 52: 621-630.

Bellaire, B., Roop, M., and Cardelli, J. (2005). Opsonized Virulent Brucella abortus, but not Attenuated hfq or bacA, Replicate within Non-acidic, ER-negative, LAMP-1-Positive Phagosomes in Human Monocytes. Infect. and Immun. 73: 3702-3713.

Reed, B., Cefalu, C., Bellaire, B., Cardelli, J., Louis, T., Salamon, J., Bloecher, M., and Bunn, R. (2005). GLUTICBP(TIP2/GIPC1) Interacts with Glut1 and Myosin VI: Evidence Supporting an Adaptor Function for GLUT1CBP. Molec. Cell Biol. 16:4183-4201.

Bigelow, B. and Cardelli, J. (2006). The Green Tea Catechins, Epigallocatechin-3 gallate (EGCG) and Epicatechin-3 Gallate (ECG) Inhibit HGF/Met Signaling in Breast Epithelial and Tumor Cells. Oncogene 25: 1922-1930.

Liu, L., Li, F., Cardelli, J., Martin, K.A., Blenis, J. and Huang, S. (2006) Rapamycin Inhibits Cell Motility by Suppression of mTOR-mediated S6K1 and 4EBP1 Pathways. Oncogene 25: 7029-7040.

Duhon, D., Yu, C. and Cardelli, J. (2007). Green Tea Polyphenols Block the Activation of c-Met in  Prostate Tumor Cells; a Process Dependent on Lipid Rafts.  (manuscript submitted).

Rupper, A. and Cardelli, J (2007) Induction of Guanylate Binding Protein 5 by Interferon gamma Increases Susceptibility to Salmonella Induced Cytotoxicity in Raw 264.7 Cells.  Infect. And Immun. (submitted for publication).

Snider, J., Bellaire, B. and Cardelli, J. (2007) Both CagA-dependent Sustained activation of c-Met and Cag independent Activation of MKK7/JNK are Required for Hp-Induced Gastric Cancer Cell Motility. (manuscript submitted).

Bigelow, R., McLarty, J., Elmajian, D., Ankem, M., Smith, M. and Cardelli, J. (2007). Prostate Cancer Patients Administered Green Tea Polyphenols Demonstrate a Reduction in Serum Levels of PSA, HGF and VEGF. (manuscript submitted).