Prostate cancer is the second leading cause of cancer-related death in American men, resulting in 29,480 fatalities last year. Death from prostate cancer most frequently occurs following the development of resistance to first- or second-line androgen deprivation therapy (ADT). As such, there is a critical need to discover early drivers of ADT resistance to help guide selection of patients for earlier intensification of therapy.
The majority of cancer biomarker research has focused, to date, on protein-coding genes, which are pieces of DNA that are converted to RNA and then converted to protein. Our team instead focuses on investigating long noncoding RNAs (lncRNAs), which are pieces of DNA that are converted to RNA but are not further converted to protein. These lncRNAs, which function as RNAs instead of proteins, represent an underexplored, but crucial, area of cancer biology. Our team recently identified over 45,000 novel lncRNAs, and determined that several lncRNAs, including one named SChLAP1, were better indicators of disease progression than conventional protein-coding genes.
Based on our initial findings, we hypothesize that lncRNAs serve as important mediators of treatment resistance in prostate cancer. The goals of this application are: 1) to investigate the mechanism by which our top candidate lncRNA, SChLAP1, promotes ADT resistance and 2) to determine if SChLAP1 and other lncRNAs can serve as predictive biomarkers to guide therapy selection in patients with aggressive prostate cancer, using tumor samples from a phase III clinical trial.
Funded by the Dick Vitale Gala in memory of Chad Carr
Approximatively 10 percent of deadly brain tumors in children are diffuse intrinsic pontine gliomas (DIPG), an aggressive cancer that impacts the body’s most vital functions such as breathing and heart rate. DIPG originates from a genetic mutation and creates an environment that hides cancer cells from the immune system, preventing it from recognizing and fighting the disease. While the prognosis for DIPG has not significantly improved in 25 years, immunotherapy — an approach that encourages the immune system to protect against malignant tumors — has yielded remarkable results in patients with otherwise incurable cancers.
Support from the V-Foundation will help U-M scientists as we seek to identify which genetic mutations in DIPG can be targeted in each patient to restore the immune function, either alone or in combination with other immunotherapeutic methods.
Pancreatic cancer is a very aggressive disease. The 5-year survival rate is a shockingly low 8%. This statistic has hardly changed in 30 years. This is because effective treatment options for pancreatic cancer do not exist.
A notable feature of pancreatic tumors is a scar-like barrier that protects the cells from anti-cancer drugs. This barrier also restricts oxygen and nutrient access, placing the cancer cells on the brink of starvation. The Lyssiotis lab seeks to figure out how these cancer cells survive and grow with limited nutrient access.
Pancreatic tumors are also known to be made up primarily of non-cancer support cells. My lab recently found that these non-cancer cells provide the cancer cells with nutrients. In this proposal, my laboratory will determine the role of these nutrients on tumor growth. A means to block this pathway would starve the already nutrient deprived cancer cells. This will provide important insights to design new therapies for this dreadful disease.
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