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.

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Finding the killing trigger

I’m happy to report that I just reached the halfway point of my time at Dana Farber and my research has been moving along quite well.  My cell lines have remained healthy and my media sterile which has greatly helped me avoid any small technical mishaps that might prevent my work from moving forward.  I’ve been busy carrying out a procedure that measures how close a cell is to apoptosis (death) called BH3 profiling. I am doing this by measuring varying peptides that will depolarize as a cell nears death.  I then compare the rates of depolarization amongst cells that have been treated by different conditions each acting either as a control or attempting to push the cell closer to death.  I have noticed that the Bim peptide (involved in the apoptotic pathway) shows the greatest change in pushing the cell closer to death when treated with a conditioned media solution from macrophages with an anti-tumor phenotype.

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Busy in Boston

Last week I began my summer research at Dana Farber Cancer Institute in Boston, MA.  After clearing orientation, lab safety, and animal safety I was finally able to get started in the lab.  My first week primarily consisted of reorienting myself with the lab and practicing standard procedures and protocols that I will be carrying out for the rest of the summer.  Throughout the summer I will be testing varying cancer cell lines to determine how close they are to cell death and how likely they are to respond to chemotherapy.  Additionally, I will be treating these cell lines grown in vitro with a drug produced in the lab designed to push these cancer cells closer to cell death in order for chemotherapy to have a more significant response on the cell lines that it might not otherwise destroy.  We are currently working with a pharmaceutical company to get this drug out to clinical trial patients in the next 12-18 months, but before we do so, we also will be doing running these tests on tumors being grown in mice.

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Determining which cancer patients will benefit from macrophage modulation

My name is Sara Schad and I am a rising junior here at William and Mary. I am a biology major and specifically interested in biomedical research.  This summer I will be conducting research off-campus in a medical oncology laboratory at Dana Farber Cancer Institute in Boston, MA. This lab as a whole analyzes cancer cell lines (breast cancer, lung cancer, prostate cancer ect) to determine which cell lines will best react to chemotherapy.  If it is known that a certain cell line won’t respond well to chemotherapy, as indicated by the cancer cells not dying with radiation exposure, than alternative treatments might be considered to avoid unnecessary radiation.  In addition to determining how close a cell is to cell death, and the likely hood that chemotherapy will have a positive impact in destroying the tumor, this lab also investigates how to push a cancer cell closer to cell death.  This can be done by using macrophages in your immune system. We have two general types of macrophages that either promote or destroy cancer cells (M1 macrophages promote tumor growth while M2 macrophages promote cell death).  If we can chemically alter the genetic make-up of M1 macrophages to inhibit tumor growth and thus promote cell death, than certain cancer patients might be more likely to see positive results with chemotherapy.  My role in this larger process is to use a technique called BH3-profiling which is a method of determining how close a cell is to death.  I aim to test over 20 cell lines and contribute my results to the lab’s previous findings that will eventually be published in a scientific journal and optimally lead to a successful clinical trial drug and treatment.