Massachusetts Institute of Technology, USA
Michael Hemann performed his PhD thesis work in Carol Greider’s Laboratory at the Johns Hopkins School of Medicine working on the consequences of telomere dysfunction mice. As a post-doctoral fellow in Scott Lowe’s laboratory at the Cold Spring Harbor Laboratory he worked on developing tractable mouse models of cancer development and therapeutic response. As an independent scientist for the past 10 years at MIT, his laboratory has continued to focus on mechanisms of cancer drug resistance. They have extensive experience in the use of mice as preclinical systems to examine neoplastic progression and have developed hematopoietic and solid tumor models that can effectively interrogate aspects of acquired and intrinsic chemoresistance. This includes work on understanding how the tumor microenvironment can impact therapeutic response. Their work has pioneered the development of novel screening strategies to characterize the genetic determinants of drug action in relevant physiological settings. These systems are highly tractable, such that one can rapidly progress from candidate gene identification to cell-based and in vivo validation experiments. Thus, they can apply diverse existing systems and technologies to our research objectives. They have also been able to extend this work into the clinic in the context of treatment refractory malignancies. Here, the consistent objective is the development of combination drug regimens that can overcome acquired and intrinsic drug resistance.