Event Title

Levels of Transforming Growth Factor Beta and Programmed Cell Death 1 in Normal and Cancerous Pancreatic Cells

Session Number

P10

Advisor(s)

Paul Grippo, University of Illinois at Chicago

Location

B-108

Start Date

28-4-2016 2:00 PM

End Date

28-4-2016 2:25 PM

Disciplines

Medicine and Health Sciences

Abstract

Pancreatic cancer is the fourth deadliest cancer in America and it continues to take more lives every year. However, there are not many viable options to treat this pernicious cancer. We tested for levels of Transforming Growth Factor Beta (TGFB) and Programmed Cell Death 1 (PD-1) using Western blots. TGFB is used to suppress T cells which are responsible for targeting and destroying cancerous cells, so if we suppress TGFB there should be increased T cell activity. Furthermore, PD-1 also regulates T-cells, and inhibition of PD-1 should lead to specific targeting of the cancerous tumor. Therefore before clinical trials proceed, the levels of these two proteins in cancer cells need to be determined. Results showed that levels of TGFB did not increase significantly in cancerous cells and PD-1 was only expressed in the cancerous cells. Based on these results, we have concluded that TGFB is not necessarily an anticancerous agent and that PD-1 supports the growth of pancreatic cancer. Thus, further studies will need to be completed to analyze the relationship between TGFB and pancreatic cancer’s progression.


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Apr 28th, 2:00 PM Apr 28th, 2:25 PM

Levels of Transforming Growth Factor Beta and Programmed Cell Death 1 in Normal and Cancerous Pancreatic Cells

B-108

Pancreatic cancer is the fourth deadliest cancer in America and it continues to take more lives every year. However, there are not many viable options to treat this pernicious cancer. We tested for levels of Transforming Growth Factor Beta (TGFB) and Programmed Cell Death 1 (PD-1) using Western blots. TGFB is used to suppress T cells which are responsible for targeting and destroying cancerous cells, so if we suppress TGFB there should be increased T cell activity. Furthermore, PD-1 also regulates T-cells, and inhibition of PD-1 should lead to specific targeting of the cancerous tumor. Therefore before clinical trials proceed, the levels of these two proteins in cancer cells need to be determined. Results showed that levels of TGFB did not increase significantly in cancerous cells and PD-1 was only expressed in the cancerous cells. Based on these results, we have concluded that TGFB is not necessarily an anticancerous agent and that PD-1 supports the growth of pancreatic cancer. Thus, further studies will need to be completed to analyze the relationship between TGFB and pancreatic cancer’s progression.