Hakan Cam, PhD

View CV »

Gender:

• Male

Languages Spoken:

• English

Research Center:

• Center for Childhood Cancer

Areas of Interest:

• 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?
• 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 dNp73 and dNp63 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?

Undergraduate

• Cukurova University
  Date Completed: 06/30/1996

Graduate School

• Max Delbrück Center for Molecular Medicine Humboldt University
  Date Completed: 06/30/2002

Post Doctoral

• Rudolf-Virchow-Center for Experimental Biomedicine, University of Wuerzburg
  Date Completed: 06/30/2006

Fellowship

• St.Jude Children’s Research Hospital
  Date Completed: 06/30/2010

2010–present

• Principal Investigator, Center for Childhood Cancer, The Research Institute at Nationwide Children's Hospital, Columbus, OH

• Cam H; Easton JB; High A; Houghton PJ. 2010. mTORC1 signaling under hypoxic conditions is controlled by ATM-dependent phosphorylation of HIF-1?.  Molecular Cell. Vol. 40, no. 4. (November 24): 509.
• Cam H, Easton JB, High A, Houghton PJ. mTORC1 signaling under hypoxic conditions is controlled by ATM-dependent phosphorylation of HIF-1α. Mol Cell. 2010 Nov 24;40(4):509-20. PubMed ID: 21095582
• 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, Houghton, PJ. 2008. mTOR: a critical regulator of p53 during a variety of stresses.  Cellscience. Vol. 4, no. 3. (January)
• 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. 2006. p53 family members in myogenic differentiation and rhabdomyosarcoma development.  Cancer Cell. Vol. 10, no. 4. (October 1): 281.
• 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
• Huttinger-Kirchhof N*, Cam H*, Griesmann H, Hofmann L, Beitzinger M, Stiewe T. 2006. The p53 Family Inhibitor Np73 Interferes with Multiple Developmental Programs.  Cell Death Differ. Vol. 13, no. 1. (January): 174-177.
• Engels B; Cam H; Schüler T; Indraccolo S; Gladow M; Baum C; Blankenstein T; Uckert W. 2003. Retroviral vectors for high-level transgene expression in T lymphocytes.  Human Gene Therapy. Vol. 14, no. 12. (August 10): 1155.
• 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
• Hakan Cam, Presenter. 2007. Complex Regulation of mTOR Function by p53 Protein. Presented at American Association for Cancer Research Annual Meeting 2007. Los Angeles, CA, United Stated.
• Hakan Cam, Presenter. 2005. The p53 Family Inhibitor Np73 Interfers with Multiple Differentiation Programs. Presented at Congress: Cell Fate and Decision. 1st International Graduate College of University Wurzburg. Wurzburg, Germany.
• Hakan Cam, Poster Presenter. 2005. p53 Family Members in Muscle Differentiation and Rhabdomyosarcoma Development. Presented at ELSO-Meeting. Dresden, Germany.
• Hakan Cam, Poster Presenter. 2005. p53 Family Members in Muscle Differentiation and Rhabdomyosarcoma Development. Presented at 13th International AEK/AIO Cancer Congress. Wurzburg, Germany.
• Hakan Cam, Poster Presenter. 2008. The Role of p53 Family Members in Regulation of mTOR Function. Presented at American Association for Cancer Research. San Diego, CA, United States. [Peer Reviewed]
• Hakan Cam, Presenter. 2010. Regulation of mTORC1 by Hypoxia. Presented at OSUCCC Pediatric Oncology Program. Roberts Centre. Wilmington, OH, United States.
• Hakan Cam, Poster Presenter. 2004. p53 Family Members in Muscle Differentiation and Rhabdomyosarcoma Development. Presented at 12th p53 Workshop. Dunedin, New Zealand.
• Hakan Cam, Poster Presenter. 2009. mTORC1 Signaling Under Hypoxic Conditions is Controlled by ATM-dependent Phosphorylation of HIF-1a. Presented at American Association for Cancer Research Annual Meeting 2009. Denver, CO, United States.