Eileen A Friedman, PhD

Eileen A Friedman, PhD
Appointed 01/26/96
2305 Weiskotten Hall
766 Irving Ave.
Syracuse, NY 13210

315 464-4460

Current Appointments

Hospital Campus

  • Downtown

Research Programs and Affiliations

  • Biomedical Sciences Program
  • Cancer Research Institute
  • Research Pillars

Education & Fellowships

  • Fellowship: Albert Einstein School of Medicine, Bronx, NY, 1978, Cell Biology
  • Fellowship: New York University School of Medicine, 1974, Cell Biology
  • Fellowship: Johns Hopkins University, 1973, Molecular Biology
  • PhD: Johns Hopkins University, 1972, Molecular Biology

Research Interests

  • The role of the kinase Mirk/dyrk1B in solid tumors


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Research Abstract

Our lab cloned Mirk/Dyrk1B, a member of the Minibrain/dyrk family of serine/threonine kinases [1] which is amplified in ovarian cancers, pancreatic cancers,  non-small cell lung cancers, and colon cancers.

Mirk/dyrk1B is an unusual kinase in that its expression and abundance varies during the cell cycle, with the highest levels found in quiescent, noncycling cells in G0, and with 10-fold lower levels in S [2], [3]. Furthermore, Mirk helps to maintain cells in the G0 quiescent state by increasing levels of the CDK inhibitor p27kip by phosphorylation of p27 at a site which blocks its degradation [2]. Mirk also prevents cells from entering G1 by destabilizing the cyclin D family of G1 cyclins, by phosphorylation at a conserved ubiquitination site which leads to rapid turnover  [4].

Mirk is expressed in several cancers and has been shown to mediate the clonogenic growth of pancreatic cancer cells, colon carcinoma cells and rhabdomyosarcoma cells [1], [5],[6]. We recently have shown that  Mirk mediates the survival of quiescent pancreatic cancer cells by inducing expression of a group of antioxidant genes which protect cells against oxidative stress generated by reactive oxygen species (ROS). Depletion of Mirk enabled these cells to escape the quiescent G0 state and enter S phase damaged by ROS and thus with reduced viability [7], [8]. Pharmacological inhibition of Mirk kinase will allow some quiescent tumor cells to be killed by their increased levels of ROS and also sensitize noncycling cells to chemotherapeutic drugs by inducing them to enter cycle by increasing their cyclin D levels.


Faculty Profile Shortcut: http://www.upstate.edu/faculty/friedmae

Faculty Honors

Dr. Dennis Stelzner has been elected a Fellow in the American Association of Anatomists. He was presented with a citation and plaque at the annual meeting of the American Association of Anatomists during the FASEB meeting on April 12, 2011 in Washington, DC.

The citation reads:
Spinal cord injury (SCI) has been studied during his entire career using neuroanatomical and ultrastructural methods. He showed that the ability of nerve tracts to regenerate or grow around partial SCI during development is dependent on their maturation at the time of injury.

Differences were also found in the ability of frog optic and tectal efferent axons to regenerate through the same diencephalic injury. The intrinsic cellular response needed for CNS axons to regenerate is the focus of his present work on propriospinal neurons using "molecular neuroanatomy" to determine factors underlying a maximal regenerative response after spinal cord injury.