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Breast Cancer Therapy and Potential Method for Enhancing Radiation Sensitivity via Inhibition of ß1 Integrin IB-1965

Most current research on cancer initiation and progression focuses on the genetics and the clonal expansion and acquisition of abnormal signaling pathways that characterize the tumor. What has been relatively overlooked is the microenvironment – specifically cell-extracellular matrix (ECM) interactions – and the role that these interactions play in tumor progression and development of resistance to treatment. Integrins are an important class of molecules that mediate crucial signals between cells and the ECM. There is a growing body of evidence, including clinical trials against specific integrins, showing that interfering with these signals by inhibiting integrin activity can profoundly affect tumor development. Research has shown that ß1 integrin specifically modifies response to chemotherapy in lung, leukemia, and colon cancers. It has also been shown to play a critical role in expression of the breast cancer phenotype (Weaver et al., 1997). Berkeley Lab Scientist Mina Bissell and University of California at San Francisco Radiation Oncologist Catherine Park, M.D. have now demonstrated that disrupting abnormal cell-ECM interactions by inhibiting ß1 integrin is an effective mechanism for advancing breast cancer therapy and shows promise as a means of enhancing the therapeutic efficacy of ionizing radiation (IR).
In vivo studies have demonstrated the effectiveness of ß1 integrin antibody for anti-tumor therapy - In vitro studies show enhancement of radiation sensitivity - The tissue environment responds to cancer in a consistent manner, providing a reliable mechanism for treatment (compared to the variable routes taken by cells to become cancerous) - ß1 integrin inhibitory antibody had little negative effect on a non-malignant cell line - 3-D cell cultures can be used to distinguish tumors that are susceptible to the Berkeley Lab treatment
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Patent Status: 
Published Patent Application # 12/575,411 available at www.uspto.gov. Available for licensing or collaborative research
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