CAITLIN KENT RESEARCH

Regulation of epithelial–mesenchymal transition in endometrial cancer

kent-caitlin-research.jpgCaitlin Kent ’15 led by faculty member Irene Reed, Ph.D. investigated the role of specific genes in the development and progression of endometrial cancer.  Their work focused on the role of a process called epithelial-mesenchymal transition in the metastasis of cancer, which is the spread of the disease from the primary site to other organs.  Metastasis is responsible for the majority (90%) of cancer-related deaths, therefore understanding the genetic cues that activate this process may lead to novel biomarkers or therapeutics for cancer.

Learn more about Caitlin’s research and read her published review article:

Title: Regulation of epithelial–mesenchymal transition in endometrial cancer: connecting PI3K, estrogen signaling, and microRNAs

Citation: Kent, C.N. & Guttilla Reed, I.K. Clin Transl Oncol (2016). doi:10.1007/s12094-016-1492-2

 

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Award Winning Research Presentation at the 2015 Beta Beta Beta NE-1 Regional Conference

Caitlin won the 1st place Frank G. Brooks Award for her oral presentation entitled: “Development of Spheroid Culture to Induce EMT and Further Classify Invasive Potential in Endometrial Cancer”

In the United States alone there are 40,000 new cases of endometrial cancer diagnosed and over 7,000 deaths related to endometrial cancer per year.  Endometrial cancer prognosis is dependent on many factors: time of diagnosis, histologic type, degree of myometrial invasion and lymphovascular invasion. Endometrial cancer is separated into two categories by clinicopathological features.  Type I endometrial cancer has been related to estrogen stimulation and was termed estrogen-dependent endometrial cancer (EDEC), while Type II estrogen independent endometrial cancer (EIEC) does not. It is well established that EIEC displays a much more aggressive phenotype, and is therefore tied to a poorer prognosis. Recent work suggests that despite the epithelial nature of the tumor, EDECs will undergo a true epithelial-mesenchymal transition (EMT), which has the potential to cause myometrial invasion. However, said phenomenon has not been observed in a laboratory setting. Currently preliminary data and literature support that an EDEC cell line, Ishikawa cells, tend to transform into undifferentiated cells and lose expression of their estrogen receptor after long term passage.  In breast cancer, loss of the estrogen receptor is associated with a process called epithelial-mesenchymal transition (EMT).  EMT is hypothesized to be the main driver of metastasis, or the spreading of a cancer from the primary organ site to another organ site.  Metastasis is responsible for the majority of cancer-related deaths, and therefore understanding the genes that control this process is important to understanding the progression of endometrial cancer, and potentially develop novel treatment options.  With no method of classifying or studying epithelial-mesenchymal transition (EMT) specifically in endometrial cancer, this work aims to develop an in vitro model system to study EMT in endometrial cancer.

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