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Employment Type:
Part time
Job Category:
Post Doc Fellow - Cancer Biology
(This job is no longer available)
University of Cincinnati | Cincinnati, OH
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Job Description

Post Doc Fellow

College of Medicine

Department of Cancer Biology



The University of Cincinnati is a premier, public, urban research university; ranked as one of America’s top 26 public research universities by the National Science Foundation. U.S. News has ranked UC in the Top Tier of America’s Best Colleges. The Chronicle of Higher Education calls UC a “research heavyweight”. Forbes, Delta Sky and Travel + Leisure magazines have named UC one of the most beautiful campuses. #HottestCollegeInAmerica


UC is one of the largest employers in the Cincinnati region, employing over 15,000 full time and part time faculty, staff and student workers. The College of Medicine, Department of Cancer Biology is looking for a Post Doc Fellow. This position will support the University’s mission and commitment to excellence and diversity in our students, faculty, staff and all our activities.


Job Summary/Duties:   The laboratory of Dr. Maria Czyzyk-Krzeska, M.D., Ph.D. invites applicants for a postdoctoral position available immediately in the Department of Cancer Biology at the University of Cincinnati ( http://cancerbiology.uc.edu/).  Candidates must have a PhD, MD, or equivalent degree, and show productivity reflected in quality publications. Preference will be given to candidates looking for the first postdoctoral training after graduation. The C-K lab conducts mechanistic studies of signaling pathways and molecular mechanisms by which autophagy regulates cancer cell survival and tumor growth in renal cancer. In particular, we have focused our interests on the von Hippel-Lindau tumor suppressor (VHL), lost in majority of renal cancers, and autophagy. Renal cancer accounts for 2-3% of adult malignancies in the USA with clear cell renal carcinoma (ccRCC) as the main histological type. Current treatments include anti-angiogenic agents based on the understanding that the loss of VHL results in activation of HIF and VEGF. However, these treatments have a limited impact on survival. Thus, it is critical to identify novel pathways as specific targets for the development of new therapies. Autophagy is a tightly regulated homeostatic process which allows cells to eliminate defective structures and to recycle nutrients. In several cancers, including ccRCC, basic autophagy is elevated and necessary for tumor growth. Autophagy is also induced by inhibitors of angiogenesis, mTOR pathway or proteasome, leading to resistance to treatments. We established that in ccRCC, a specific LC3B-mediated autophagic program is activated by the loss of VHL, and LC3B activity contributes to tumor growth. Another autophagic program, mediated by LC3B paralog, LC3C, is stimulated by VHL and has tumor suppressing activity. LC3B and LC3C form separate autophagosomes. Most recently we identified that two products of TRPM3 gene, microRNA 204 (miR-204) and transient receptor potential channel, TRPM3, have opposite roles in ccRCC. Mir-204 is induced by VHL and acts as a tumor suppressor inhibiting oncogenic autophagy, while TRPM3 acts as an oncogene and promotes oncogenic autophagy. We are currently conducting experiments to establish connections between different autopahgic programs and oncogenic metabolic pathways. Candidates with an interest in cancer metabolism are particularly encouraged to apply.


Relevant publications:

  1. Mikhaylova, O, Stratton Y, Hall D , Kellner E, Ehmer B,  Drew AF, Gallo CA, Plas  DR, Biesiada J, Meller J,  Czyzyk-Krzeska MF (2012) VHL-regulated miR-204 Suppresses Tumor Growth through Inhibition of LC3B-mediated Autophagy in Renal Clear Cell Carcinoma. Cancer Cell. 21:532-546.
  2. Czyzyk-Krzeska MF, Meller J, Plas DR (2012) Not all autophagy equal. Autophagy. 8:1-2. Hall DP,  Cost NG, Hegde S, Kellner E, Mikhaylova O, Stratton Y, Ehmer B, Abplanalp WA, Pandey R, Biesiada J, Harteneck C,  Plas DR, Meller J, Czyzyk-Krzeska MF (2014) TRPM3 and miR-204 establish a regulatory circuit that controls oncogenic autophagy in clear cell renal cell carcinoma. Cancer Cell. 26, 738-753.

Commentary: Cecconi F and Jaattela M (2014) Trageting Ions-induced autophagy in cancer. Cancer Cell, 26, 599-600.


Interested individuals should contact Dr. M. Czyzyk-Krzeska at maria.czyzykkrzeska@uc.eduand apply online under requisition # 9947.


Minimum Qualifications: Ph.D., M.D., or M.D./Ph.D., or comparable degree.



The University of Cincinnati is an Affirmative Action / Equal Opportunity Employer / M / F / Vet / Disabled.

REQ ID: 9947