Donaldson Translational Fellow
Harvard University, 2017
email@example.com | (516) 367-4128
Are you really what you eat? Our goal is to uncover the precise mechanisms that link nutrition to organismal health and disease states at the cellular and molecular level. A particular focus in our lab is to understand how dietary perturbations affect the immune system and contribute to the risk of diseases that are associated with immune dysfunction such as cancer.
Cells respond and adapt to the signals that they receive from their environment. Environmental factors such as nutrients affect cellular states by altering cell state-specific gene expression or metabolic programs. My research group investigates the causal cellular and molecular mechanisms that link nutrition to organismal health and disease. For example, diets that lead to obesity, such as high fat diets are significant environmental risk factors that influence cancer incidence and progression in several tissues. Although the interactions between tumor cells and the immune system play a significant role in tumorigenesis, little is known about how dietary perturbations impact immunity against cancer. Our studies interrogate the functional consequences of diets on immune recognition and response pathways that play critical role in cancer immunity. By identifying the altered gene expression and metabolic programs in the immune system in response to dietary perturbations, our goal is to uncover mechanistic links that can be therapeutically exploited for the treatment of diseases associated with immune dysfunction such as cancer.
The Janeway Award, New England Immunology Conference
Trainee Award, American Association of Immunologists
Outstanding Poster Award, International Society for Stem Cell Research
Zhongmei Chen Yong Travel Award for Scientific Excellence, International Society for Stem Cell Research
Merit Award, International Society for Stem Cell Research
Thermo-Fisher Trainee Achievement Award, American Association of Immunologists
Public Lecture – DIET & DISEASE: Exploring the relationship between nutrition and cancer
May 2, 2019
Please join us for a free public lecture… DIET & DISEASE Exploring the relationship between nutrition and cancer Speakers: SEMIR BEYAZ, Ph.D. CSHL Fellow Donaldson Translational Fellow Cold Spring Harbor Laboratory JAMIE KANE, M.D. Director, Center for Weight Management, Northwell Health Assistant Professor, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell Coffee reception to follow...
CSHL Fellow Semir Beyaz wins three awards
July 11, 2018
The CSHL Fellows Program is known for bringing in some of the best and brightest young minds in science, and cancer researcher Semir Beyaz is no exception. Arriving at CSHL in December 2017, Beyaz has been received three different honors for his research, which looks at how dietary choices impact the body’s immunity against cancer....
New CSHL Fellow studies nexus of diet, metabolism, and cancer
March 1, 2018
Of the many factors that contribute to the formation and growth of tumors, diet is one that is often casually mentioned but has not yet been subjected to rigorous scientific investigation. For Semir Beyaz, the newest CSHL Fellow, what we eat is an important part of understanding environmental risk factors that affect the incidence of...
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Das, P. P. and Hendrix, D. A. and Apostolou, E. and Buchner, A. H. and Canver, M. C. and Beyaz, S. and Ljuboja, D. and Kuintzle, R. and Kim, W. and Karnik, R. and Shao, Z. and Xie, H. and Xu, J. and De Los Angeles, A. and Zhang, Y. and Choe, J. and Jun, D. L. and Shen, X. and Gregory, R. I. and Daley, G. Q. and Meissner, A. and Kellis, M. and Hochedlinger, K. and Kim, J. and Orkin, S. H. (2015) PRC2 Is Required to Maintain Expression of the Maternal Gtl2-Rian-Mirg Locus by Preventing De Novo DNA Methylation in Mouse Embryonic Stem Cells. Cell Rep, 12(9) pp. 1456-70.
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Lucas, C. L. and Workman, C. J. and Beyaz, S. and LoCascio, S. and Zhao, G. and Vignali, D. A. and Sykes, M. (2011) LAG-3, TGF-beta, and cell-intrinsic PD-1 inhibitory pathways contribute to CD8 but not CD4 T-cell tolerance induced by allogeneic BMT with anti-CD40L. Blood, 117(20) pp. 5532-40.Additional materials of the author at
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