Role of Caveolin-1 in Prostate Cancer Angiogenesis; Annual rept. 15 Nov 2006-14 Nov 2007

摘要

My laboratory relocated to M. D. Anderson Cancer Center on October 1, 2008. The move and transition was handled in a very efficient manner and we did not compromise our progress toward the goals of this project in any way. With only slight modifications Tasks 1-3 are on schedule and we are progressing toward our stated goals. Notable achievements for the past year of funding include comprehensive documentation that prostate cancer cell derived, secreted caveolin-1 is taken up by cancer cells and tumor associated endothelial cells (Tahir et al., Cancer Res 68: 731-739, 2008). This autocrine/paracrine activity of secreted caveolin-1 promotes malignant progression and provides an accessible therapeutic target. In pursuit of a clinical therapy based on this mechanism we have also shown that systemic delivery of caveolin-1 antiserum suppresses primary tumor growth and increases survival in an immunocompetent mouse model of prostate cancer (see Fig 5-7). In our view these results represent a paradigm shift in prostate cancer translational research.