Vascular and haematopoietic stem cells: novel targets for anti-angiogenesis therapy?
By Shahin Rafii, D. Lyden, R. Benezra, K. Hattori, B. Heissig. Nature Reviews. Cancer, 2002
716 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/a11431f341b6820a954f05a2bd4216eaf13caaf0
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Citations in the corpus
- Microenvironmental regulation of metastasis (2009, background): “Bone marrow-derived endothelial cell precursors are recruited to metastases by VEGFA signalling through VEGFR2 (Ref”
- Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis. (2004, background): “All of these ment, also contribute to tumor vascular formation (Asahara et studies show the intense research and debate on this subject. al., 1997; Lyden et al., 2001; Rafii et al., 2002).”
- AZD2171, a pan-VEGF receptor tyrosine kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma patients. (2007, background): “Subsets of CPCs (e.g., endothelial and/or hematopoietic progenitors) have been suggested to play an important role in angiogenesis (Rafii et al., 2002; Stoll et al., 2003), and moreover, these cells may represent targets for antiangiogenic therapy (Carmeliet, 2005).”
- Angiogenesis in health and disease (2003, background): “Recent evidence, however, indicates that endothelial progenitors contribute to vessel growth both in the embryo and in ischemic, malignant or inflamed tissues in the adult, and can even be therapeutically used to stimulate vessel growth in ischemic tissues, a process termed 'therapeutic vasculogenes”
- Therapeutic targeting of the tumor microenvironment. (2005, neutral): “The tumor vasculature is derived by angiogenesis, new blood vessel growth from pre-existing ves sels, and vasculogenesis, the recruitment of circulating endothelial progenitor cells (Carmeliet, 2003; Rafii et al., 2002).”
- Tumor microenvironment abnormalities: Causes, consequences, and strategies to normalize (2007, background): “, 1996] and the mobilization and recruitment of bone marrow-derived cells [Rafii et al., 2002].”
- HIF1alpha induces the recruitment of bone marrow-derived vascular modulatory cells to regulate tumor angiogenesis and invasion. (2008, background): “We noticed that most VEGFR1+ hemangiocytes and TEMs express MMP-9, which may explain why inhibition of these cells impairs neovascularization, although these cell types constitute less than 10% of the CD45+ population (De Palma et al., 2005; Jin et al., 2006; Rafii et al., 2002 ).”
- Stem cell plasticity: time for a reappraisal? (2005, neutral): “EPC may persist in the marrow and circulate in the blood during adult life.(72) In fact, recent preclinical and clinical studies have indicated that EPC can restore tissue vascularization and that the growth of some neoplastic diseases may depend on EPC-induced vasculogenesis rather than on angiogen”
- The SDF-1-CXCR4 signaling pathway: a molecular hub modulating neo-angiogenesis. (2007, background): “Recruitment of EPCs and supporting cells contributes to the acceleration of ischemic revascularization and augments neo-angiogenesis in specific tumors, including lymphomas [5,6].”
- Lessons from phase III clinical trials on anti-VEGF therapy for cancer (2006, background): “VEGF can also affect new-vessel formation in tumors by acting as a chemoattractant for bone-marrow-derived progenitor/stem cells”
- Isolation of renal progenitor cells from adult human kidney. (2005, methodology): “Endothelial differentiations were obtained by culturing the cells in EBM medium (Cambrex Bio Science, Baltimore, MD) with vascular endothelial growth factor (10 ng/ml, Sigma) and 10% fetal calf serum on endothelial cell attachment factor (Sigma).(11) CD133 cells were also isolated from the blood of ”