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Vincent L. Cryns, MD
Professor, Department of Medicine
Marian A. and Rodney P. Burgenske Chair,
Endocrinology, Diabetes & Metabolism
University of Wisconsin
Goal: To improve outcomes in breast cancer by identifying aberrant cell processes that lead to tumor formation and progression.
Impact: Drs. Cryns and Gradishar are studying a cell stress protein called alphaβ-crystallin, which contributes to the aggressive behavior of basal-like/triple-negative breast cancer (TNBC). They have shown that it interacts with a mutant form of p53, the most commonly mutated gene in cancer, and links p53 to Akt, a growth-promoting protein that is often upregulated in cancer. Their work may lead to the identification of new approaches to target oncogenes in a broad spectrum of breast tumors.
What’s next: The team will identify the specific role of alphaβ-crystallin in promoting tumor growth by common cancer-causing genes.
Basal-like tumors, which include those classified as triple negative, are aggressive and lack targeted therapies. Drs. Cryns and Gradishar have shown that a protein called alphaβ-crystallin contributes to the aggressive behavior of these tumors and regulates the spread of breast cancer to organs such as the brain. Recently, they discovered that alphaβ-crystallin binds to mutant p53 protein, promoting tumor growth. They have also discovered that this pathway links p53 and with a growth-promoting factor called Akt. The team will now study alphaβ-crystallin’s role in regulating these pathways.
Full Research Summary
Research goal: Developing new approaches to treat aggressive breast cancers.
Impact: Basal-like triple negative breast cancers are aggressive and lack targeted therapies because they don’t depend on the estrogen or progesterone hormones or HER2 for growth, thus the term “triple-negative.” Drs. Cryns and Gradishar are investigating a cell stress protein called alphaβ-crystallin that contributes to the aggressive behavior of basal-like/triple-negative breast cancer (TNBC) by interacting with cancer-promoting proteins. Their findings may inform new targeted therapies that would prevent this protein from promoting metastasis.
Current investigation: The team is screening libraries of chemical compounds to identify drugs that block the interaction between alphaβ-crystallin and p53, the most commonly mutated gene in cancer. Alphaβ-crystallin binds directly to mutant p53 and keeps it active, thereby promoting tumor growth. Drugs that block the interaction between alphaβ-crystallin and p53 are predicted to cause tumor cell death.
What they’ve learned so far: Drs. Cryns and Gradishar showed that blocking alphaβ-crystallin binding to p53 prevents p53 from promoting tumor formation. They also discovered that this pathway directly links p53 and Akt, a potent growth factor.
What’s next: During the next year, the team will identify the specific role of alphaβ-crystallin in keeping p53 and Akt active and in promoting tumor growth by these genes.
Vincent Cryns, MD, is the Marian A. and Rodney P. Burgenske Chair in Diabetes Research and Chief, Division of Endocrinology, Diabetes & Metabolism at the University of Wisconsin School of Medicine and Public Health. He received his bachelor’s and medical degrees from Harvard and did subspecialty training in endocrinology at Massachusetts General Hospital. Before coming to Madison, Dr. Cryns was a Professor of Medicine at Northwestern University’s Feinberg School of Medicine.
Dr. Cryns leads a multidisciplinary team who focus on understanding how cells die. His group is especially interested in elucidating how abnormalities in cell death contribute to diseases such as cancer and obesity and in translating these insights into improved therapies. Dr. Cryns’ research is funded by the NIH, the Breast Cancer Research Foundation and other agencies. His work has been featured on National Public Radio’s "All Things Considered" and highlighted in Nature and Nature Reviews Cancer. Dr. Cryns has been the recipient of several awards, including an Outstanding Junior Faculty Award from the Avon Foundation, and he is an elected member of the American Society for Clinical Investigation.