Ethan Dmitovsky, MD, Oral History Interview, July 6, 2015
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Description
Major Topics Covered:
- The Institute for Applied Cancer Science and a new model of research
- The Provost’s Office: support for faculty, leadership training, research support
- Global Academic Programs and international partnerships
Interview Chapters
Chapter 15: The Institute for Applied Cancer Science: The Research Model
Chapter 16: Global Academic Programs: the Advantages of Collaboration Part I
Chapter 17: Global Academic Programs: the Advantages of Collaboration Part II
Identifier
DmitrovskyE_03_20150706
Publication Date
7-6-2015
Publisher
The Making Cancer History® Voices Oral History Collection, The University of Texas MD Anderson Cancer Center
City
Houston, Texas
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.
Topics Covered
University of Texas MD Anderson Cancer Center; UT MD Anderson Cancer Center; University of Texas System. M.D. Anderson Cancer Center; M.D. Anderson Hospital and Tumor Institute at Houston; University of Texas M.D. Anderson Cancer Center; M.D. Anderson Hospital and Tumor Institute
Disciplines
History of Science, Technology, and Medicine | Oncology | Oral History
Recommended Citation
Dmitrovsky, Ethan MD and Rosolowski, Tacey A. PhD, "Ethan Dmitovsky, MD, Oral History Interview, July 6, 2015" (2015). Interview Sessions. 105.
https://openworks.mdanderson.org/mchv_interviewsessions/105
Conditions Governing Access
Open
About the Interview
About the Interview Subject:
Ethan Dmitrovsky, MD came to MD Anderson in 2013 to serve as the institution’s Provost and Executive Vice President. He has a faculty appointment in the Department of Thoracic/Head and Neck Medical Oncology in the Division of Cancer Medicine.
Dr. Dmitrovsky’s translational research areas include: retinoid differentiation-based therapy for acute promyelocytic leukemia (APL); developed the molecular genetic test used to detect the PML/RARalpha transcript from the APL t(15;17) rearrangement; retinoid mechanisms leading to cell cycle arrest and repair of DNA damage in normal/malignant lung epithelial cells; engineered transgenic mouse models that express wild-type or proteasomal degradation-resistant cyclin E species in the lung; derived lung cancer cell lines leading to a new model to assess activity of lung cancer therapy and chemopreventive agents (antineoplastics).