2016 Grant Recipient Ethan Abel, PhD

Home Research Research Grants Program Grants Awarded Grants Awarded by Year 2016 Pancreatic Cancer Action Network Research Grants 2016 Grant Recipient Ethan Abel, PhD

GRANTEE: Ethan Abel, PhD

University of Michigan
Research Project: The Role and Regulation of HNF1A in Pancreatic Cancer Cells
Award: 2016 Pancreatic Cancer Action Network – AACR Pathway to Leadership Grant
Award Period: August 1, 2016 – July 31, 2021
Amount: $600,000

Biographical Highlights
Dr. Abel received his BS degree in biology from the State University of New York at Albany in 2004. In 2012, Dr. Abel received his PhD in genetics from Thomas Jefferson University. Dr. Abel’s thesis work focused on the interplay between proteins that promote cancer cell growth and those that control gene expression in melanoma. Since September of 2012, Dr. Abel has trained as a postdoctoral research fellow under the mentorship of Dr. Diane Simeone at the University of Michigan. Dr. Simeone is a two-time Pancreatic Cancer Action Network research grant recipient and the chair-elect of our Scientific and Medical Advisory Board. Dr. Abel’s research continues to focus on proteins that control gene expression and their roles in pancreatic cancer, including cancer stem cells and drug resistance.

Project Overview
Pancreatic cancer stem cells (PCSCs) are one of many types of cells that comprise tumors of the pancreas. PCSCs play a particularly important role, as these are the cells from which the tumor is thought to originate. Moreover, PCSCs are especially resistant to chemotherapy and other treatment options, allowing regeneration and spread of the tumor.

For his funded project, Dr. Abel seeks to focus on a particular protein, called HNF1A, which is highly expressed by PCSCs. HNF1A is a transcription factor, which means that it functions to regulate the expression of other genes. Manipulation of HNF1A affects the properties of PCSCs, including expression of proteins on the surface of the cells that mark PCSCs and the cells’ ability to form three-dimensional spherical structures when grown in the laboratory, which is considered a defining characteristic of cancer stem cells.

Dr. Abel and his research team’s data also suggest that HNF1A expression is amplified even further upon inhibition of the proteins KRAS or MEK1/2, whose activities are directly influenced by KRAS. KRAS is the most frequently mutated protein in pancreatic cancer; it is thought to be mutated in 95 percent of cases of the disease. Dr. Abel’s hypothesizes that, if KRAS or the proteins it activates were inhibited, HNF1A could compensate and allow the tumor to continue growing and progressing. Finally, preliminary data suggest that another cancer-promoting protein, MYC, may be directly responsible for HNF1A expression.

Based on his compelling data, Dr. Abel has proposed three specific aims that will analyze the biological functions of HNF1A in PCSCs, the role that HNF1A plays upon manipulation of KRAS signaling and the relationship between HNF1A and MYC. Dr. Abel believes that the completion of the above studies will greatly improve understanding of pancreatic cancer biology and uncover novel therapeutic targets as they pertain to HNF1A and the genes and proteins it influences.

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