Daniel R. Premkumar, PhD

  • Research Assistant Professor

Prior to joining the faculty of the Department of Neurological Surgery at the University of Pittsburgh in 2008, Daniel R. Premkumar, PhD, was a senior scientist at a biotechnology company. He graduated from Madurai Kamaraj University in India where he earned his masters and doctorate degrees. Dr. Premkumar then completed his post-doctoral training at Case Western Reserve University in Cleveland.

Dr. Premkumar has published more than 50 papers in refereed journals and has been awarded patents to characterize protein-protein interaction biosensors for cellular systems biology profiling. He is currently examining the efficacy of promising various receptor inhibitors, for inhibiting glioma proliferation in vitro, using genotypically diverse panel of malignant glioma cell lines to identify potential genotype-response associations.

Dr. Premkumar's publications can be reviewed through the National Library of Medicine's publication database.

Specialized Areas of Interest

Major research emphasis is directed towards understanding the molecular mechanisms of receptor tyrosine kinase inhibition and signaling in malignant human glioma cell lines.

Professional Organization Membership

American Association for Cancer Research
American Society of Pharmacology and Experimental Therapeutics

Education & Training

  • BS, Biology, Madura College, 1982
  • MS, Animal Sciences, Madurai Kamaraji University, 1984
  • PhD, Entomology, Madurai Kamaraji University, 1990

Research Activities

Glioblastomas are highly invasive primary tumors with poor prognosis despite current therapies. Individual targeted therapies have failed to offer long-term survival benefits, although combinations of rationally selected inhibitors may have significant therapeutic applicability for these tumors. Studies by Dr. Prekumar’s group and others have also shown aberrant, constitutive activation of NF-κB and Akt as common features of malignant gliomas, supporting their functional role in contributing to apoptosis resistance and refractory growth despite cytotoxic chemotherapy, irradiation, and molecularly targeted therapies. This activation may in part reflect deletions of NF-κB inhibitor-α, a common alteration in malignant gliomas, dysregulated stimulation by cell surface tyrosine kinases, such as EGFR and PDGFRα, which are amplified in molecular subsets of malignant gliomas, and mutations in PTEN and other molecular targets that drive Akt and NF-κB activation. Thus, new therapeutic approaches are urgently needed. Dr. Premkumar’s group has demonstrated that inhibition of important “survival nodes” may constitute a promising strategy to enhance the efficacy of conventional therapies, such as irradiation and cytotoxic chemotherapy, and potentiate the activity of agents targeted against growth signaling mediators.