Prize Winner

Science

Streaming Media

Type of Proposal

Oral presentation

Start Date

29-3-2016 4:00 PM

End Date

29-3-2016 5:00 PM

Faculty

Faculty of Science

Faculty Sponsor

Dr. Lisa Porter

Abstract

Primary liver cancer represents one of the fastest rising cancers in Canada. The increasing incidence of this pluralistic and multi-faceted malignancy make having a full understanding of the disease an essential step when considering treatment options. The most common type of liver cancer, hepatocellular carcinoma (HCC), may stem from a variety of lifestyle factors and circumstances. Cirrhosis and advanced fibrosis of the liver are two common causes. These chronic disease states are often associated with alcoholism, but can also arise due to non-alcoholic steatohepatitis (NASH) and fatty liver disease. Hepatitis and fatty liver elicit liver cell injury, inflammation and oxidative damage, which in turn activate the liver’s regenerative processes. Regeneration, especially when continually called upon, represents a proliferative process that may render patients susceptible to HCC. Spy 1 is a cyclin-like protein that promotes cell cycle progression and drives cell growth during select regenerative processes. A serendipitous finding in mice developed to study the role of Spy1 in the mammary gland revealed that the male Spy1 mice had significantly more primary HCC than their littermate controls. To further explore the role of Spy1 in HCC, NASH has been initiated in wild-type mice using a methionine-choline deficient diet. Spy1 levels and inflammatory, proliferative and regenerative responses are being monitored by analyzing gene expression, protein levels, fat accumulation and morphological changes. This data will determine the physiological processes that correlate with elevated Spy1 levels during liver injury and regeneration. The resulting information will aid in establishing a causal link in the progression of HCC. Future work will determine whether this mechanism represents a target for treatment for patients with this aggressive form of cancer.

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Creative Commons Attribution-Noncommercial 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License

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Mar 29th, 4:00 PM Mar 29th, 5:00 PM

Exploring a Link Between Spy1 and Hepatocellular Carcinoma Progression

Primary liver cancer represents one of the fastest rising cancers in Canada. The increasing incidence of this pluralistic and multi-faceted malignancy make having a full understanding of the disease an essential step when considering treatment options. The most common type of liver cancer, hepatocellular carcinoma (HCC), may stem from a variety of lifestyle factors and circumstances. Cirrhosis and advanced fibrosis of the liver are two common causes. These chronic disease states are often associated with alcoholism, but can also arise due to non-alcoholic steatohepatitis (NASH) and fatty liver disease. Hepatitis and fatty liver elicit liver cell injury, inflammation and oxidative damage, which in turn activate the liver’s regenerative processes. Regeneration, especially when continually called upon, represents a proliferative process that may render patients susceptible to HCC. Spy 1 is a cyclin-like protein that promotes cell cycle progression and drives cell growth during select regenerative processes. A serendipitous finding in mice developed to study the role of Spy1 in the mammary gland revealed that the male Spy1 mice had significantly more primary HCC than their littermate controls. To further explore the role of Spy1 in HCC, NASH has been initiated in wild-type mice using a methionine-choline deficient diet. Spy1 levels and inflammatory, proliferative and regenerative responses are being monitored by analyzing gene expression, protein levels, fat accumulation and morphological changes. This data will determine the physiological processes that correlate with elevated Spy1 levels during liver injury and regeneration. The resulting information will aid in establishing a causal link in the progression of HCC. Future work will determine whether this mechanism represents a target for treatment for patients with this aggressive form of cancer.