Glioma Research Group

	Axel H. Schönthal, PhD

Dr. Schönthal’s lab investigates how certain novel anticancer drugs cause tumor growth inhibition and tumor death (apoptosis/necrosis). This includes, for instance, the analysis of cell cycle regulation, signal transduction pathways, and cell death execution at the molecular and cellular level. Towards this goal, various in vitro approaches (tumor cell culture, gene transfection, protein purification, etc.) are combined with in vivo studies in experimental animals.

RESEARCHERS
Primary Investigator: Axel H. Schönthal, PhD
Adel Kardosh : Curriculum Vitae
Nathaniel Soriano: Curriculum Vitae
Yen-Tin ("Tim") Liu: Curriculum Vitae (not available at this time)

RECENT PUBLICATIONS
T.C. Chen, P. Wadsten, S. Su, N. Rawlinson, F.M. Hofman, C. Hill, A.H. Schönthal. 2002. The type IV phosphodiesterase inhibitor rolipram induces expression of the cell cycle inhibitors p21Cip1 and p27Kip1, resulting in growth inhibition, increased differentiation, and subsequent apoptosis of malignant A-172 glioma cells. Cancer Biol. Therapy 1, 268-276.

A. Kardosh, M. Blumenthal, W. J. Wang, T.C. Chen, A.H. Schönthal. 2004. Differential effects of selective COX-2 inhibitors on cell cycle regulation and proliferation of glioblastoma cell lines. Cancer Biol.Therapy 3, 5-12.

A. Kardosh, W. Wang, J. Uddin, N.A. Petasis, F.M. Hofman, T.C. Chen, A.H. Schönthal. 2005. Dimethyl-celecoxib (DMC), a derivative of celecoxib that lacks cyclooxygenase-2-inhibitory function, potently mimics the anti-tumor effects of celecoxib on Burkitt’s lymphoma in vitro and in vivo. Cancer Biol. Ther. 4, 571-582.

A. Kardosh, N. Soriano, J. Uddin, N.A. Petasis, F.M. Hofman, T.C. Chen, A.H. Schönthal. 2005. Inhibition of drug-resistant multiple myeloma cell lines by dimethyl-celecoxib (DMC), a non-COX-2-inhibitory derivative of celecoxib, via multiple signaling pathways. Blood, in press.