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Mark E. Ewen, PhD
Associate Professor of Medicine, Tufts University School of Medicine; Principal Investigator, Molecular Oncology Research Institute
Department + Services
Molecular Oncology Research Institute, Ewen Laboratory
Molecular genetics, cellular biology
|Training + Education
University of Chicago; Harvard Medical School
1. Lamb J, Ramaswamy S, Ford HL, Contreras B, Martinez RV, Kittrell FS, Zahnow CA, Patterson N, Golub TR, Ewen ME. A mechanism of cyclin D1 action encoded in the patterns of gene expression in human cancer. Cell 2003; 114:323-324.
2. Lamb J, Ewen ME. Cyclin D1 and molecular chaperones: implications for tumorigenesis. Cell Cycle 2003; 2:525-527.
3. Ewen ME, Lamb J. The activities of cyclin D1 that drive tumorigenesis. Trends Mol Med 2004; 10:158-162.
4. Takahashi C, Contreras B, Bronson RT, Loda M, Ewen ME. Genetic interaction between Rb and K-ras in the control of differentiation and tumor suppression. Mol Cell Biol 2004; 24:10406-10415.
5. Takahashi C, Contreras B, Iwanaga T, Takegami Y, Bakker A, Bronson RT, Noda M, Loda M, Hunt JT, Ewen ME. Nras loss induces metastatic conversion of Rb1-deficient neuroendocrine thyroid tumor. Nat Genet 2006; 38:118-123.
6. Takahashi C, Ewen ME. Genetic interaction between Rb and N-ras: differentiation control and metastasis. Cancer Res 2006; 66:9345-9348.
7. Fotiadou PP, Takahashi C, Rajabi HN, Ewen ME. Wild-type NRas and KRas perform distinct functions during transformation. Mol Cell Biol 2007; 27:6742-6755.
8. Chen J, Yao Y, Gong C, Yu F, Su S, Chen J, Liu B, Deng H, Wang F, Lin L, Yao H, Su F, Anderson KS, Liu Q, Ewen ME, Yao X, Song E. CCL18 from tumor-associated macrophages promotes breast cancer metastasis via PITPNM3. Cancer Cell 2011; 19:541-555.
9. Liu Q, Boudot A, Ni J, Hennessey T, Beauparlant S, Rajabi HN, Zahnow C, Ewen ME. Cyclin D1 and C/EBPβ LAP1 operate in a common pathway to promote mammary epithelial differentiation. Mol Cell Biol 2014; 34:3168-3179.
10. Rajabi HN, Takahashi C, Ewen ME. Retinoblastoma protein and MyoD function together to effect the repression of Fra-1 and in turn cyclin D1 during terminal cell arrest associated with myogenesis. J Biol Chem 2014; 289:23417-23427.
The focus of our laboratory is to understand the role of cyclin D1 in tumorigenesis. Cyclin D1 is the second most frequently amplified oncogene in human cancer. In our effort to functionally dissect the mechanism of action for cyclin D1 in cancer, we discovered that overexpressed cyclin D1 activates a cdk-independent transcriptional program. Here, the transcription factor C/EBPβ was identified as the effector of cyclin D1. Ongoing efforts are directed toward determining how the cyclin D1-C/EBPβ pathway participates in breast cancer and other epithelial malignancies. Further, guided by the belief that understanding the normal function of cyclin D1 and C/EBPβ will provide insights into their oncogenic action, we are studying the role of cyclin D1’s C/EBPβ-dependent transcriptional function in mammary gland development.
Email: Mark Ewen
Molecular Oncology Research Institute
Tufts Medical Center
800 Washington Street, Box #5609
Boston, MA 02111