Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. ====== Neovascularization ====== The degree of neovascularization is critical in assessing tumor grade and malignancy. [[Glioblastoma]] (GBM) is the most lethal primary adult brain tumor and its pathology is hallmarked by distorted neovascularization, diffuse tumor-associated [[macrophage]] infiltration, and potent [[immunosuppression]]. ---- Neovascularization is a key therapeutic target for [[cancer treatment]]. However, [[Anti-angiogenic therapy]] have shown modest success, as tumors develop rapid resistance to treatment owing to activation of redundant pathways that aid [[vascularization]]. Shenoy et al. hypothesized that simultaneously targeting different pathways of neovascularization will circumvent the current issue of drug resistance and offer enhanced therapeutic benefits. To test this hypothesis, they used of two distinct models of tumor-neovascularization, which exhibit equally dense [[microvasculature]] but show disparate sensitivity to anti-SDF-1 treatment. Lewis lung carcinoma (LLC) is primarily a vasculogenic-tumor that is associated with [[Hematopoietic stem cell]]s functioning as a hemangioblast to generate circulating Endothelial Progenitor Cells contributing to formation of new blood vessels, and responds to anti-SDF-1 treatment. B16F0 melanoma is an angiogenic-tumor that derives new blood vessels from existing vasculature and is resistant to anti-SDF-1 therapy. In this study, we observed increased expression of the angiogenic-factor, Robo1 predominantly expressed on the blood vessels of B16F0 tumor. Blockade of Robo1 by the decoy receptor, RoboN, resulted in reduced microvascular-density and tumor-growth. However, this was associated with mobilization of BM-cells into the B16F0 tumor, thus switching the mode of neovascularization from angiogenic to vasculogenic. The use of a combinatorial treatment of RoboN and the monoclonal anti-SDF-1 antibody effectively attenuated tumor-growth and inhibited both angiogenic and BM-derived microvessels ((Shenoy AK, Pi L, Ligocki AP, Hosaka K, Cogle CR, Scott EW. Targeting Redundant [[ROBO1]] and SDF-1 Pathways Prevents Adult Hemangioblast Derived-EPC and CEC Activity Effectively Blocking Tumor Neovascularization. Stem Cell Rev Rep. 2023 Jan 18. doi: 10.1007/s12015-022-10498-7. Epub ahead of print. PMID: 36652143.)) neovascularization.txt Last modified: 2024/06/07 02:59by 127.0.0.1