Emily Bernstein, PhD
- PROFESSOR | Oncological Sciences
- PROFESSOR | Dermatology
Research Topics:Cancer, Chromatin, Epigenetics, Gene Regulation, Molecular Biology, Stem Cells
Emily Bernstein, PhD, Professor of Oncological Sciences and Dermatology, is Co-leader of the Cancer Mechanisms Research Program at The Tisch Cancer Institute. As such, Dr. Bernstein facilitates basic research on genetic, epigenetic, biochemical, and developmental pathways that drive cancer initiation and progression, and fosters intra- and inter-program collaborations that accelerate the development of novel, targeted therapies for cancer.
Dr. Bernstein studies epigenetic regulation of gene expression in cancer and development, with the long-term goal of understanding the chromatin changes that take place at the molecular level during the transformation process of normal cells to cancer cells. Her team studies melanoma, breast cancer, and neuroblastoma.
Dr. Bernstein regularly teaches courses on cancer biology and serves on numerous PhD thesis committees at the Icahn School of Medicine at Mount Sinai. She is permanent member of the Cancer Genetics Study Section of the NIH Center for Scientific Review and serves as a reviewer for additional grant foundations.
Multi-Disciplinary Training AreasCancer Biology [CAB], Development, Regeneration, and Stem Cells [DRS]
PhD, SUNY Stony Brook/Cold Spring Harbor Laboratory
The Rockefeller University
Established Investigator Award
Sohn Prize for Young Investigators in Cancer Research
Irma T. Hirschl Charitable Trust Research Award
Young Cancer Scientist Research Award
Innovative Research Grant Finalist
Tisch Cancer Institute Developmental Fund Award
New Scholar Award
Research Scholar Award
National Science Foundation Postdoctoral Fellowship
The Dr. Harold and Golden Lamport Research Award
Specific Clinical/Research Interest: Our focus is on epigenetic regulation of gene expression in multiple biological pathways including cancer (melanoma and breast cancer), cellular senescence and stem cell biology. This includes various mechanisms that alter the chromatin template, including histone modifications, histone variants and their dedicated chaperones, and non-coding RNAs.
Summary of Current Research
Chromatin is the complex of DNA and its intimately associated proteins -with histones constituting the major component. This template is an attractive candidate for shaping the features of a cell's epigenetic landscape. Disruption of a cell's epigenetic balance can perturb chromatin structure and gene regulation, contributing to disease states.
Our work focuses on the study of histone variant proteins. When incorporated into chromatin, histone variants participate in diverse nuclear functions including centromeric regulation, DNA damage responses, transcriptional activation and repression, and play a role in epigenetic inheritance of chromatin states. Histone variants alter the structure and stability of the nucleosome, and provide the cell with the potential to change its post-translational modification (PTM) profile due to amino acid sequence differences from their conventional histone counterparts. We are interested in variant-specific PTMs and their binding proteins, as well as the chaperones that escort these proteins in and out of the chromatin template. We have uncovered a critical suppressive role for the histone variant macroH2A in the progression of malignant melanoma. In addition to acting as a barrier to melanoma growth and metastasis, we reported that macroH2A also acts as a barrier to induced pluripotency by repressing a set of genes required for the early stages of reprogramming.
The Polycomb Group (PcG) proteins are also focus of the lab. In mammals, there are five homologs of the single Drosophila Pc protein and it has been a longstanding goal to understand the consequences of such expansion and diversification of this protein family in both development and disease. We have previously demonstrated that each individual Pc protein is unique not only in its histone binding-specificity, but also in its association with heterochromatin (in particular, the inactive X chromosome in female mammals). Recently, we identified Cbx7 as the primary Polycomb protein expressed in ESCs, which is important for maintaining pluripotency. We have also identified novel PTMs of Cbx family members.
Our long-term goal is to understand the chromatin changes that take place at the molecular level during the transformation process of 'normal cells' to 'cancer cells' and during the reprogramming of somatic cells to stem cells. We currently have studies underway (targeted and unbiased) to identify new players in the epigenetic regulation of melanoma progression and drug resistance to targeted therapies, as these processes remain poorly understood. We are also investigating the role of histone chaperone mutations in the context of pediatric tumor biology.
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