Boyko Atanassov, PhD

Assistant Professor of Oncology
Department of Pharmacology and Therapeutics
Roswell Park Comprehensive Cancer Center

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Areas of Expertise: 
Deubiquitinating enzymes
Chromatin modifying enzymes
Regulation of gene expression
Special Interests: 
Molecular mechanism of cancer metastasis
Cell signaling
Cancer drug discovery


I graduated with a Ph.D. in Molecular Biology from the Bulgarian Academy of Sciences in 2007. During my doctoral studies, I focused on elucidating the DNA repair mechanisms that cancer cells employ to counter the effects of the genotoxic agents used in chemotherapy. I spent half of my doctoral studies as a participant in the Graduate Partnership Program at NIH, where I was working with Barbara Davis and J. Carl Barrett to study the role of the breast cancer-associated BRCA2 in homologous recombination and DNA repair. In 2007, I joined the laboratory of Dr. Sharon Dent at MD Anderson Cancer Center, as a postdoctoral fellow. Dr. Dent is one of the world’s leading scientists in the field of chromatin biology, and I consider my training in her group as a rare chance and an outstanding experience. My postdoctoral studies were focused on understanding the roles that a multi-subunit chromatin modifying complex called SAGA (SPT-GCN5-ADA) has in development and diseases. Because of my achievements as a postdoctoral fellow, in 2012, I was promoted to an Instructor in the Department of Epicegenitcs and Molecular Carcinogenesis at MD Anderson Cancer Center, and in 2016 to an Assistant Professor in the same department. Not only have the results from my work described several “firsts” in the field that were published in high impact journals, but they also provided a ground to build further research strategies and address some of the most pressing questions in cancer biology today. In February 2017, I joined the outstanding environment of Roswell Park Comprehensive Cancer Center where I will continue to work with world-class scientists and clinicians to connect the molecular findings in my laboratory to cancer.

Research Overview

Research in my laboratory is focused on elucidating the molecular mechanisms by which chromatin modifying enzymes and the complexes they form potentiate tumor formation, growth and metastasis. Although genetic changes in cancer are well recognized, epigenetic changes that alter gene expression patterns have also been found to play a major role during development of this disease in recent years. These changes, affecting post-translational modifications of histones and DNA methylation, are mediated by various chromatin modifying enzymes. Our work has revealed that these enzymes often have functions independent of their canonical roles in transcriptional regulation that are critically important for normal cell growth, survival and response to the environment. We are particularly interested in Ubiquitin Specific Proteases (USPs) that are capable of removing ubiquitin moieties from histones, thus altering the expression patterns of target genes. In recent years many USPs have been directly linked to different stages of cancer progression. For example, USP22 is a member of an 11 gene “death-from-cancer” signature that serves as a predictor for treatment resistance, tumor aggressiveness and metastatic probability in cancer patients. Additionally, ablation of USP44 leads to spontaneous lung cancer in mice whereas its function is required for invasion of breast cancer cells in vitro. Further, in our recent studies we identified two uncharacterized USPs, USP27X and USP51, which are remarkably similar to the cancer-associated USP22, to which their ablation severely impacts tumor growth. Thus, using a variety of biochemical and genetic approaches (e.g. tissue culture and mouse models) our lab aims to 1) define the molecular mechanisms by which USP27X, USP51, and other USPs impact tumor growth, and 2) define the in vivo functions of these USPs during normal development and carcinogenesis.

Misregulation of ubiquitin-proteasome pathways is implicated in the pathogenesis of many human diseases, particularly cancer, and proteasome inhibitors are studied as possible treatments for these diseases. Hence, inhibitors of USPs are particularly attractive for therapeutic intervention; specific inhibition of their function would operate upstream of the proteasome and possibly generate specific and less toxic antitumor therapies. Therefore, it is our long-term goal to connect the mechanistic and molecular findings in our laboratory to cancer.


Education and Training: 
2006 - PhD - Molecular Biology, Bulgarian Academy of Sciences
2007-2012 - Postdoctoral fellow, UT MD Anderson Cancer Center, Sharon Dent Lab