Apr 16 2007
Members from the laboratory of Stephen Ethier, Ph.D., deputy center director and director of basic science for the Barbara Ann Karmanos Cancer Institute, will present research findings on breast cancer-causing genes and how they operate at the American Association of Cancer Research Annual Meeting, April 13-18, in Los Angeles, CA.
"We know there are genetic drivers of this disease," said Dr. Ethier, principal investigator of a breast cancer research lab at Karmanos Cancer Institute. "My lab wants to prove what genes are causing (breast) cancer, and we're coming up with some novel research that we believe will prove which genes cause this disease."
Dr. Ethier's laboratory is also researching how these cancer-causing genes, often referred to as oncogenes, function so effective therapies can be targeted toward them.
Two members from his lab, Katie L. Streicher, Ph.D., and Nicole E. Willmarth, are studying a subset of breast cancers with epidermal growth factor receptor (EGFR) overexpression, which correlates with a poor prognosis. They recently discovered that to effectively target EGFR, the ligand amphiregulin (AR) and the cytokine IL-1 must be targeted, or "turned off."
"Members of my lab are conducting exciting, novel research," Dr. Ethier commented. "They are some of the best researchers in the field and perform vitally important work that could benefit generations to come. This smart and talented team remains focused on our ultimate goal of eradicating breast cancer."
Schedule of Presentations
1 - 5 p.m., Sunday, April 15, 2007 -- Zeng-Quan Yang, Stephen P. Ethier. Methylation-associated silencing of SFRP1 in breast cancers with 8p11-12 amplified region.
8 a.m. - 12 p.m., Monday, April 16, 2007 -- Katie L. Streicher, Nicole E. Willmarth, Stephen P. Ethier. Up-regulation of IL-1 by amphiregulin alters EGFR activation by modifying a tyrosine phosphatase.
8 a.m. - 12 p.m., Tuesday, April 17, 2007 -- Nicole E. Willmarth, Stephen P. Ethier. EGFR overexpression as a result of receptor stabilization in breast cancer cells with an amphiregulin/EGFR autocrine loop.
1 - 5 p.m., Tuesday, April 17, 2007 -- Mona Mostafa Mohamed, Dora Cavallo- Medved, Julie Dosescu, Deborah Rudy, Mary Olive, Kamiar Moin, Stephen P. Ethier, Bonnie F. Sloane. Interactions between human monocytic cells and human inflammatory breast cancer cells modulate expression of E-cadherin, caveolin-1 and a caveolai-associated protease, cathepsin B. 11:25 - 11:40 a.m., Wednesday, April 18, 2007 -- Gang Liu, Zeng-Quan Yang, Katie L. Streicher, Stephen P. Ethier. WHSC1L1, a new candidate oncogene within the 8p11-12 amplicon induces a proliferative advantage in breast cancer.
The AACR was founded in 1907 by a group of eleven physicians and scientists interested in research, "to further the investigation and spread the knowledge of cancer." Today, AACR accelerates progress toward the prevention and cure of cancer by promoting research, education, communication, and advocacy.
Based in midtown Detroit, the Barbara Ann Karmanos Cancer Institute is committed to a future free of cancer. The Institute is one of 39 National Cancer Institute-designated comprehensive cancer centers in the United States. Caring for more than 6,000 new patients annually on a budget of $216 million, conducting more than 700 cancer-specific scientific investigation programs and clinical trials, the Karmanos Cancer Institute is among the nation's best cancer centers. Through the commitment of 1,000 staff, including nearly 300 faculty members, and supported by thousands of volunteer and financial donors, the Institute strives to prevent, detect and eradicate all forms of cancer. John C. Ruckdeschel, M.D. is the Institute's president and CEO.
http://www.karmanos.org/