Breast Cancer Stem Cells/Cancer Biology/Stem Cell Biology/Epigenetics
I earned my BA in Biology in 2011 from Western Connecticut State University (Danbury, CT). My fascination with stem cells led me to the Stein/Lian lab where I began working with human embryonic stem cells and looking at epigenetic regulation in the pluripotent cell cycle. I have since transitioned to breast cancer research, and my thesis work is focused on breast cancer stem cells (BCSCs). I am interested in elucidating epigenetic mechanisms that govern stemness in the BCSC population, and the role that the RUNX proteins play in BCSCs and tumorigenesis. When I am not in the lab I enjoy getting outdoors as much as possible. Hiking, biking, swimming, snowshoeing, and snowboarding are some of the activities I enjoy the most, and the beautiful state of Vermont is an amazing place for all sorts of outdoor adventures! The Burlington, VT area is such a wonderful place to live and work!
Over the course of the last decade there have been significant advances made in the diagnosis and treatment of breast cancer. However, despite these advances, the fact remains that this disease is still virtually incurable once it becomes metastatic. Mortality rates from this disease remain high due in part to the fact that current therapies are unable to target a dangerous sub-population of breast cancer cells with stem cell-like properties. Just as adult tissues and organs are maintained and sustained by stem cell populations, cancers also contain subpopulations of cells that exhibit varying degrees of stemness. There is now strong evidence that these BCSCs mediate metastasis, are highly resistant to radiation and chemotherapy, and contribute to relapse and ultimately death. My research focuses on isolating and investigating BCSCs in order to gain insight into how they differ genetically and epigenetically from the rest of the bulk tumor cells. The primary phenotype that characterizes the BCSC population is an absence of the cell-surface marker CD24 coupled with the presence of the cell-surface marker CD44 (CD24-/CD44+). Using this criteria, it is possible to sort the BCSCs apart from the rest of the tumor cells and therefore compare both cell populations. I am most interested in elucidating the role that certain epigenetic modifications play, namely post-translational histone modifications, in governing stemness in the BCSC population.
Office: E209 E Given
Lab: E209 Given
- 6/30/2015 11:30 AM – 12:00 PM
- 6/30/2015 12:00 PM – 12:30 PM
- 7/7/2015 11:30 AM – 12:00 PM
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