Hakan Cam PhD


Hakan Cam PhD
Research Asst ProfessorCollege of MedicineHakan.Cam@nationwidechildrens.org
Research Bldg II 700 Children's Drive Columbus OH 43205
Phone:614-355-1998Fax: 614-355-2927
  • Molecular Biology and Cancer Genetics

General Research Interest

p53 family members, mTOR protein

Research Description

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 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. My lab is interested in: • 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? Moreover, we focus on mTOR protein. 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. Body of evidence suggest that deregulation of mTOR pathway occurs in common diseases; including cancer and diabetes that emphasizes the importance of identifying and understanding mTOR signaling. Therefore, by using genetic approaches in both cell culture and animal models, my research goals are to understand and identify: how disruption of mTOR regulation can lead to pediatric diseases such as cancer.

Transinstitutional Work

Our projects are likely to collaborate with various research areas including (A) pharmacology (for therapeutic drug discovery), (B) pathology (for developing biomarkers), (C) bioinformatics (for studying global genomic architecture) and (D) statistics (for modeling childhood cancer progression).

Current Publications

  • Cam M, Bid HK, Xiao L, Zambetti GP, Houghton PJ, Cam Hp53/TAp63 and AKT regulate mammalian target of rapamycin complex 1 (mTORC1) signaling through two independent parallel pathways in the presence of DNA damage.J Biol Chem 289 4083-94 2/14/2014
  • Bid HK, Roberts RD, Cam M, Audino A, Kurmasheva RT, Lin J, Houghton PJ, Cam HΔNp63 promotes pediatric neuroblastoma and osteosarcoma by regulating tumor angiogenesis.Cancer Res 74 320-9 1/1/2014
  • Shen C, Oswald D, Phelps D, Cam H, Pelloski CE, Pang Q, Houghton PJRegulation of FANCD2 by the mTOR pathway contributes to the resistance of cancer cells to DNA double-strand breaks.Cancer Res 73 3393-401 6/1/2013

The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James) 300 W. 10th Ave. Columbus, OH 43210 Phone: 1-800-293-5066 | Email: jamesline@osumc.edu