Aptamer Selection Against Fibroblast Growth Factor 8 Isoform b for Therapeutic Uses Against Prostate Cancer

Aptamer Selection Against Fibroblast Growth Factor 8 Isoform b for Therapeutic Uses Against Prostate Cancer

Luke Hollifield
September 2, 2013

In the medical world, cancer has been a life threatening force that has evaded eradication. Cancer is the rapid and unregulated growth of cells in an area, which can cause malignant tumors and eventually death. Among the two most common and deadliest kinds of cancer are breast cancer, affecting mostly women, and prostate cancer, affecting mostly men (U.S. Cancer Statistics Working Group, 2013). While great advances have been made in the medical field to combat cancer, it is the second deadliest killer in the United States and is responsible for every one in four deaths (U.S. Cancer Statistics Working Group, 2013). Researchers and doctors continue to search for ways to fight this partially understood disease, and many new and creative methods of treatment are being developed to stop the growth of these harmful cells.

It has been shown that Fibroblast Growth Factor 8b (FGF8b) is naturally over expressed in later stages of prostate cancer, the most common and deadliest cancer among men (Song, Powell, Kasahara, et al., 2000). The FGF8b gene is crucial to embryonic growth and development, but it can reactivate later in life to cause many problems, like cancer (Rudra-Ganguly1, Zheng1, Hoang, Roy-Burman, 1998). By finding an aptamer against FGF8b, the levels of FGF8b would decrease and the speed of the cancer growth would lessen. 
Specific Aim 1: Find an aptamer that binds to FGF8b to keep it from binding to FGFR, a receptor in the prostate. By inhibiting this binding, the protein would lose the affect it has when uninhibited on cancerous and surrounding cells.

Figure 1
Figure one shows the effect of FGF8b in epithelial-stromal cocultures from different places in the body. (A) and (C) both represent the stromal cells from the prostate and seminal vesicles respectively. (A) shows a fast growing amount of cells in the 15 day period, thus supporting the theory of FGF8b affecting cell growth in the prostate (Song, Powell, Kasahara, et al., 2000).

FGF-8b is currently available in lab, purified by Shawn Piasecki.

First Target Proposal
First Progress Report
Second Progress Report
Final Progress Report


Rudra-Ganguly N., J. Zheng, A. T. Hoang, and P. Roy-Burman. (1998) "Downregulation of human      FGF8 activity by antisense constructs in murine Æbroblastic and human prostatic carcinoma cell systems." Oncogene 16: 1487- 1492.
Song, Z., W. C. Powell, N. Kasahara, et al. (2000) "The Effect of Fibroblast Growth Factor 8, Isoform      b, on the Biology of Prostate Carcinoma Cells and Their Interaction with Stromal Cells." CANCER RESEARCH 60: 6730- 6736.
U.S. Cancer Statistics Working Group. United States Cancer Statistics: 1999–2009 Incidence and      Mortality Web-based Report. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention and National Cancer Institute; 2013. 

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