Almost done!

I am excited to be wrapping up my summer research at Dana Farber next week. My results thus far have thoroughly helped to answer the question that I began the summer interested in.  I have extensively been studying the TNFa receptor that mediates extrinsic apoptosis (cell death) and have found that when blocking the receptor in breast cancer cells, apoptosis is prevented, but when you solely add the receptor to a negative control, apoptosis is not induced, indicating that TNFa is necessary for cell death to occur, but is not sufficient.  I will continue studying the receptor throughout my last week here as well as begin looking into other proteins and post translational modifications that when coupled with TNFa will induce apoptosis.

On another note, I will be presenting all of my research to the lab members and director that I’ve been working with on this coming Wednesday.  I am supposed to speak for an hour which I am slightly nervous about because I’ve never given a presentation remotely near that long.  Nonetheless it will be a good preparation for the Charles Center presentation that we give back at school in the fall.


  1. castephens says:

    Very interesting work! I’m actually building a model for prion disease which involves the misregulated production of cytokines and pro-inflammatory/pro-apoptotic agents like TNFalpha! Much of the research I have read similarly concludes that TNFalpha alone cannot induce apoptosis, but has been linked to exciting production TNFalpha in other cells. Has your research looked into other pro-apoptotic agents like HSPs? Or the upregulation of cell survival signals?