Session 2F: Expression of Focal Adhesion Proteins in IBD-Associated Neoplasia
Session Number
Session 2F: 4th Presentation
Advisor(s)
Joel Pekow, University of Chicago
Location
Room A115
Start Date
28-4-2017 10:00 AM
End Date
28-4-2017 11:15 AM
Abstract
Colorectal neoplasia is the abnormal growth of tissue in the colon, encompassing dysplasia as well as colorectal cancer cancer. Patients with inflammatory bowel disease have chronic inflammation in their colon. It is thought that the chronic inflammation places them at increased risk for colorectal neoplasia, whereby the colonic lining changes from at risk mucosa with chronic inflammation to dysplasia and ultimately cancer. In previous studies, several genes involved in focal adhesion were demonstrated to be increased in normal appearing non-neoplastic colonic mucosa of patients who had colorectal neoplasia elsewhere in their colon. This experiment was performed to confirm the expression of focal adhesion proteins in inflammatory bowel disease associated neoplasia. We evaluated proteins thrombospondin 2, caveolin 1, and collagen 1A2 in IBD-associated neoplasia by immunohistochemistry. We used different tissue samples such as ulcerative colitis cancer, normal, sporadic colon cancer, and active UC from patients to stain for all three focal adhesion proteins. In this study we demonstrated that all three proteins were differently expressed in IBD-associated neoplasia. In this subsequent investigation we retested this conclusion and also proved that STK-31 was upregulated, as continuation to investigate mechanisms of up-regulation of these proteins in chronic inflammation and cancer in later studies.
Session 2F: Expression of Focal Adhesion Proteins in IBD-Associated Neoplasia
Room A115
Colorectal neoplasia is the abnormal growth of tissue in the colon, encompassing dysplasia as well as colorectal cancer cancer. Patients with inflammatory bowel disease have chronic inflammation in their colon. It is thought that the chronic inflammation places them at increased risk for colorectal neoplasia, whereby the colonic lining changes from at risk mucosa with chronic inflammation to dysplasia and ultimately cancer. In previous studies, several genes involved in focal adhesion were demonstrated to be increased in normal appearing non-neoplastic colonic mucosa of patients who had colorectal neoplasia elsewhere in their colon. This experiment was performed to confirm the expression of focal adhesion proteins in inflammatory bowel disease associated neoplasia. We evaluated proteins thrombospondin 2, caveolin 1, and collagen 1A2 in IBD-associated neoplasia by immunohistochemistry. We used different tissue samples such as ulcerative colitis cancer, normal, sporadic colon cancer, and active UC from patients to stain for all three focal adhesion proteins. In this study we demonstrated that all three proteins were differently expressed in IBD-associated neoplasia. In this subsequent investigation we retested this conclusion and also proved that STK-31 was upregulated, as continuation to investigate mechanisms of up-regulation of these proteins in chronic inflammation and cancer in later studies.