POSTDOCTORAL FELLOWSHIP IN EPIGENETIC MECHANISMS OF HUMAN DISEASE
Postdoctoral position is available for study of the epigenetics of cancer, metabolism, and behavior, focused on disease mechanisms, model organisms, and the role of epigenetics in gene-environment interaction. All of the studies are interdisciplinary, involving collaborating faculty in experimental design and mentorship at the Johns Hopkins University School of Medicine, preparing fellows for team-based jobs grounded in outstanding scholarship. We are addressing the following scientific questions:
- What are the epigenetic drivers of cancer progression? We are determining how mutations in epigenetic modifier genes alter the epigenetic landscape in normal development and cancer, and increase epigenetic plasticity and tumor cell survival. See Feinberg et al, Nature Rev Genet 2016, 17:284.
- Can epigenetic alterations in cancer be reversed using novel approaches targeted to large blocks of heterochromatin and/or metabolism? See: McDonald et al, Nature Genet 2017, 49:367.
- What are the epigenetic drivers of neuropsychiatric disease and how are they related to brain-region specific developmental epigenetic marks? See: Rizzardi et al, Nature Neurosci, in press.
- What is the relationship between common DNA sequence variants and tissue-specific epigenetic marks in normal development and disease? See: eGTEx Project, Nature Genet 2017, 49:1664.
- How do genome and environment interact to cause disease, and how is this mediated by the epigenome? We are addressing the mechanisms through which environment influences gene function, or “GxE”, focusing on important and contemporary exposures highly relevant to human health: diet, environmental toxicants and their relationship to metabolic disorders and cancer. See: Barrington et al, Genetics 2018, 208:399.
- What is the mathematical foundation of epigenetic information? We are pursuing our novel idea that genetic variants that control phenotypic variance confer a selective advantage in evolution in an environment that changes, and that the same idea may explain phenotypic plasticity in cancer evolution, with the “hallmarks” of cancer being selected for at the expense of the host. We are developing new information theoretic tools to relate DNA methylation, chromatin structure, and gene sequence to stochastic modeling. See: Jenkinson et al, Nature Genet 2017, 49:719.
See our website for details: http://feinberglab.jhu.edu. Interested candidates must have received or expect to have received the PhD or MD/PhD in 2018 or 2019, have a strong graduate school record in genetics and/or biostatistics, and have published or have accepted one or more high-quality peer reviewed publications. To apply, please upload to this website a cover letter, C.V. including bibliography, unofficial graduate school transcript, and contact information for three references, but do not have them send letters at this time. Any questions about the position or application process can be directed to Michael Graziano at firstname.lastname@example.org, but only applications submitted through this website will be considered.
Johns Hopkins is an equal-opportunity employer.
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