Wednesday, June 6, 2018 - 11:00am - 11:30am
Jasmine Foo (University of Minnesota, Twin Cities)
It has been observed experimentally that epigenetic phenomena can induce temporary or reversible drug-resistant phenotypes in cancer cell populations. For example, changes in methylation status of DNA repair genes may impact the responsiveness of cells to chemotherapies. Although these phenomena may be transient, they can have lasting impact on the genetic evolution of a tumor. Short-term epigenetic adaptations may serve as temporary lifelines for a population until more permanent genetic resistance mechanisms can be established.
Thursday, September 14, 2017 - 10:00am - 10:30am
Christina Leslie (Memorial Sloan-Kettering Cancer Center)
Dysregulated epigenetic developmental programs are a feature of many cancers, and the diverse differentiation states of immune cells as well as their dysfunctional states in tumors are in part epigenetically encoded. We developed an integrative computational strategy to exploit genome-wide data on chromatin accessibility (DNase-seq or ATAC-seq), histone modifications (ChIP-seq), and transcription (RNA-seq) in order to study enhancer landscape and gene expression dynamics in cellular differentiation, with a focus on the hematopoietic system.
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