Inhibition of vasculogenesis, but not angiogenesis, prevents the recurrence of glioblastoma after irradiation in mice.
By M. Kioi, H. Vogel, G. Schultz, R. Hoffman, G. Harsh, J. Brown. Journal of Clinical Investigation, 2010
776 citations recorded by the source corpus.
Subfields: Cancer Research, Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/21a62cf075f6344e1cd405186169830b3602ca10
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Citations in the corpus
- Strategies to improve radiotherapy with targeted drugs (2011, background): “In addition, the vasculature and other host factors, such as tumour infiltration of inflammatory cells and other bone marrow- derived cells (BMDCs), have been shown to play a par”
- Hypoxia-induced angiogenesis: good and evil. (2011, background): “In fact, Sdf-1 is a transcriptional target of HIF-1α, and pharmacological inhibition of SDF-1/ CXCR4 signaling decreased vascular regrowth after glioblastoma tumor irradiation.(88,89) Intriguingly, inhibition of HIF-1α yielded a similar effect, collectively suggesting that hypoxia plays an important”
- Targeting the ANG2/TIE2 axis inhibits tumor growth and metastasis by impairing angiogenesis and disabling rebounds of proangiogenic myeloid cells. (2011, background): “Because tumor-infiltrating TEMs promote vascular regrowth following therapy-induced vascular damage (Kioi et al., 2010; Kozin et al., 2010), targeting these cells might increase the efficacy of antiangiogenic treatments by counteracting myeloid cell-mediated angiogenesis and resistance to therapy (B”
- Tumor-associated macrophages: from basic research to clinical application (2017, background): “The HIF-1 pathway is stimulated by radiation-induced tumor hypoxia, and the HIF-1 inhibitor can result in decreased infiltration of myeloid cells into tumors [82].”