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| Education |
| 2010 |
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Postdoctoral Fellowship |
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Molecular Pharmacology |
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St.Jude Children’s Research Hospital, Memphis, TN |
| 2006 |
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PhD |
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Molecular Tumorbiology |
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Rudolf-Virchow-Center for Experimental Biomedicine, University of Wuerzburg, Wuerzburg, Germany |
| 2002 |
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Masters of Science |
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Biology |
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Max Delbrück Center for Molecular Medicine Humboldt University, Berlin, Germany |
| 1996 |
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BS |
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Biology |
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Cukurova University, Adana, Turkey |
| Professional Experience |
| 2010- PRES |
Principal Investigator, Center for Childhood Cancer, The Research Institute at Nationwide Children's Hospital, Columbus, OH |
Research Interests
-p53 family members
-mTOR signaling
P53
Cancer is a genetic disorder caused by mutations in genes critically involved in the control of cell proliferation. Long-lived organisms, such as humans, have evolved strategies to restrict the development of potentially malignant cells. The p53 family of tumor suppressor genes (Fig. 2) provides important defense against cancer.
Activated in response to DNA damage and to oncogenic signaling the three proteins of this family - p53, p63 and p73 - cooperate to induce apoptosis and thus restrict tumor formation by eliminating potentially malignant cells. Importantly, alteration of this coordination often causes cancer.
Taken together, despite the striking similarities among the p53 family members, however, their roles in tumorigenesis appear to be quite different.
My research focuses on a comparative analysis of the three genes using genetic approaches in both cell culture and animal models to understand:
- How do p53 and its family members suppress tumorigenesis?
- How do the p53 family inhibitors δNp73 and δNp63 enhance tumor formation?
- How do the p53 family members regulate gene expression?
- How do the p53 family members interact with other signaling networks?
- What is the function of the p53 family members in normal development?
mTOR
Mammalian TOR (mTOR) is an evolutionarily conserved serine/threonine kinase that integrates signals from growth factors, nutrients, and stresses to regulate multiple processes, including mRNA translation, cell-cycle progression, autophagy, and cell survival. Several lines of evidence suggest that increased signaling of the mTOR pathway is involved in tumor formation
By using genetic approaches in both cell culture and animal models, my research goals are to understand and identify:
- What are new components or targets of mTOR signaling network?
- What are the functions of the components in the mTOR signaling network?
- How do these functions might be altered or involved in metabolic diseases and cancer?
- How do cells manage the regulation of mTOR pathway under certain conditions?
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| Selected Publications |
| Cam H, Houghton PJ. mTOR: a critical regulator of p53 during a variety of stresses. Cellscience. 2008 Jan; Vol. 4 No 3 ISSN 1742-8130 |
| Cam H, Griesmann H, Beitzinger M, Hofmann L, Beinoraviciute-Kellner R, Sauer M,Hüttinger-Kirchhof N, Oswald C, Friedl P, Gattenlöhner S, Burek C, Rosenwald A, Stiewe T. p53 family members in muscle differentiation and rhabdomyosarcoma development. Cancer Cell. 2006 Oct;10(4):281-93. PubMed ID: 17045206 |
| Huttinger-Kirchhof N, Cam H, Griesmann H, Hofmann L, Beitzinger M, Stiewe T.The p53 family inhibitor δNp73 interferes with multiple developmental
programs. Cell Death Differ. 2006 Jan;13(1):174-7. PubMed ID: 16341031 |
| Engels B, Cam H, Schuler T, Indraccolo S, Gladow M, Baum C, Blankenstein T, Uckert W.Retroviral vectors for high-level transgene expression in T lymphocytes. Human Gene Ther. 2003 Aug 10;14(12):1155-68. PubMed ID: 12908967 |
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