Over the summer of June-August 2014 and 2015, I had the opportunity to serve a paid internship before I start my first year of college. I worked at Bradley University in my hometown of, Peoria, IL. 
Above: my awesome possum coworkers and me :)

What did I work on? STEM CELLS! Yes, I was pleasantly floored when I was told that I'd be working in Dr. Craig Cady's neurophysiology and stem cell research laboratory handling real, live, (non-embryonic) stem cells. Like WHAT?! I knew immediately that I was in for the best summer ever, and I was right. I had such a positive experience the first time around that I applied again for a second summer. Dr. Cady was more gracious, welcoming, and kind than I could ever have hoped, and I will always be grateful for the time he took to teach me.

There were 8 other people working full-time in the lab in addition to myself, so there were a LOT of projects going on--including nanofiber scaffolding; plating cells onto nanofibers & tracking them with quantum dots; culturing neurons, various types of adult stem cells, and cancer cells; electrophysiology; immunocytochemistry; differentiating adipose tissue...I was able to see all of these amazing and exciting research advances up close and even help out! For my own project, I focused on cancer research.

My project was titled: Enhancing Potential Stem Cell Therapies for Cancer: The Role of Neoplastic Factors. In short, I worked on improving the efficiency of a proposed stem-cell based cancer treatment by improving the rate of , migration, or movement of stem cells, towards cancer. Stem cells have many unique properties, one being that they are regenerative: they have the ability to move towards areas of inflammation or stress and repair those sites. This includes cancerous tumors. The lab had proposed a model (that has the potential to be, but is not yet in, clinical use) in which injected stem cells, genetically engineered with a CD enzyme, migrate towards a tumor to change a pro-drug, 5-FC (fluorocytocine) into 5-FU (fluorouracil), a cytotoxic chemotherapy agent. Since 5-FU has the ability to stop DNA replication in rapidly dividing cells (i.e., cancer cells), the cells die. However, since stem cells also rapidly divide, those cells die as well--causing them to be dubbed "suicide cells." (Dr. Cady is interviewed about the model here)


I focused not on the pro-drug conversion, but the migration of the stem cells to the site itself. I wanted to increase the rate of migrated stem cells to ensure maximum efficacy. The outline of my project was to expose the stem cells (I used human Wharton's Jelly mesenchymal stem cells) to various cancer-expressed factors and also to ovarian cancer cell conditioned media. I showed that pre-exposing the cells to VEG-F165, in addition to migrating towards ovarian cancer, yielded the highest migration of cells.


At the end of the summer, I also presented my data to other interns, labs, professors, and the general public. It was quite nerve-racking, but I'm glad I did it. 


My abstract can be found below. Any questions/comments are welcome!


Enhancing Potential Stem Cell Therapies for Cancer: The Role of Neoplastic Factors

Abstract:

In 2015, approximately 21,290 women will be diagnosed with ovarian cancer in the United States. Late stage ovarian cancer can be extremely lethal; early detection is rare and the survival rate of metastasized ovarian cancer is only 20%. In our previous studies, human Wharton’s Jelly umbilical cord mesenchymal stem cells (hWJMSCs) migrated towards pancreatic and breast cancer cells, suggesting a potential role as a drug carrier for localized cell-based chemotherapy. This project focuses on enhancing the migration rate of hWJMSCs toward ovarian cancer (HEY) cell conditioned media. We hypothesize that both pre-treating hWJMSCs with the cancer produced factor, vascular endothelial growth factor 165 (VEGF-165), and exposing the cells to various cancer-expressed proteins or HEY cell conditioned media, will affect the migration rate of hWJMSCs towards cancer. To enhance migration, hWJMSCs were either pre-exposed to 750 ng/ml of VEGF-165 or not pre-exposed to a known cancer factor. Both non-exposed and pre-exposed cells were assessed at how readily they migrated towards: 1% LifeFactor, 4% LifeFactor, 500 ng/ml VEGF-165, 450 ng/ml WNT-1 and HEY cell conditioned media for 24 hrs at 5% CO2 and 9% O2 by using microporous inserts. Migrated cells were counted by staining the underside of the migration membrane with an H&E stain.  Cells pre-treated with VEGF-165 and exposed to HEY cell conditioned media and 4% LifeFactor (positive control) showed statistically significant increases in migration based on migrated cell numbers relative to the non-pretreated cells.  Our laboratory has genetically engineered hWJMSCs to overexpress the enzyme cytosine deaminase (CD) that will convert a pro-drug into an active chemotherapy drug at the site of the tumor following successful migration.  Although ongoing experiments are being conducted to verify hWJMSC overexpression of CD these data demonstrate that pretreatment of hWJMSCs will increase the migration rate towards ovarian cancer for the delivery of CD to the tumor potentially increasing the effectiveness of this cell based treatment.

 




 


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