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 Historical Resources Center, Research Medical Library, The University of Texas 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).