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Editorial

Antiangiogenesis: biology and utility in the treatment of gliomas

Pages 1419-1423 | Published online: 09 Jan 2014

References

  • Lakka SS, Rao JS. Anti-angiogenic therapy in brain tumors. Expert Rev. Neurother.8(10), 1457–1473 (2008).
  • Bergers G, Benjamin L. Tumorigenesis and the angiogenic switch. Nat. Rev. Cancer3(6), 401–410 (2003).
  • Hanahan D, Folkman J. Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis. Cell86(3), 353–364 (1996).
  • Kerbel RS. Tumor angiogenesis. N. Engl. J. Med.358(19), 2039–2044 (2008).
  • Semenza GL. A new weapon for attaching tumor blood vessels. N. Engl. J. Med.358(19), 2066–2067 (2008).
  • Gao D, Nolan DJ, Mellick AS, Bambino K, McDonnell K, Mittal V. Endothelial progenitor cells control the angiogenic switch in mouse lung metastasis. Science319, 195–198 (2008).
  • Nolan DJ, Ciarrocchi A, Mellick AS et al. Bone marrow-derived endothelial progenitor cells are a major determinant of nascent tumor neovascularization. Genes Dev.21, 1546–1558 (2007).
  • Peters BA, Diaz LA, Polyak K et al. Contribution of bone marrow-derived endothelial cells to human tumor vasculature. Nat. Med.11, 261–262 (2005).
  • Rajantie I, Ilmonen M, Alminaite A et al. Adult bone marrow-derived cells recruited during angiogenesis comprise precursors for periendothelial vascular mural cells. Blood104(7), 2084–2086 (2004).
  • Santarelli JG, Udani V, Yung CY et al. Preuss Resident Research Award: bone marrow-derived Flk-1-expressing CD34+ cells contribute to the endothelium of tumor vessels in mouse brain. Clin. Neurosurg.52, 384–388 (2005).
  • Leenders WP, Küsters B, Verrijp K et al. Antiangiogenic therapy of cerebral melanoma metastases results in sustained tumor progression via vessel co-option. Clin. Cancer Res.10, 6222–6230 (2004).
  • Ferrara N, Gerber HP, LeCouter J. The biology of VEGF and its receptors. Nat. Med.9(6), 669–676 (2003).
  • Kowanerz M, Ferrara N. Vascular endothelial growth factor signaling pathways: therapeutic perspective. Clin. Cancer Res.12(17), 5018–5022 (2006).
  • Fischer I, Gagner JP, Law M et al. Angiogenesis in gliomas: biology and molecular pathophysiology. Brain Pathol.15(4), 297–310 (2005).
  • Kargiotis O, Rao JS, Kyritsis AP. Mechanisms of angiogenesis in gliomas. J. Neurooncol.78(3), 281–293 (2006).
  • Lamszus K, Heese O, Westphal M. Angiogenesis-related growth factors in brain tumors. Cancer Treat. Res.117, 169–190 (2004).
  • Plate KH, Risau W. Angiogenesis in malignant gliomas. Glia15(3), 339–347 (1995).
  • Jain RK. Normaliziing tumor vasculature with anti-angiogenic therapy: a new paradigm for combination therapy. Nat. Med.7(9), 987–989 (2001).
  • Jain RK. Normalization of tumor vasculature: an emerging concept in antiangiogenic therapy. Science307(5706), 58–62 (2005).
  • Kaur B, Khwaja FW, Severson EA, Matheny SL, Brat DJ, Van Meir EG. Hypoxia and the hypoxia-inducible-factor pathway in glioma growth and angiogenesis. Neuro-oncology7(2), 134–153 (2005).
  • Kaur B, Tan C, Brat DJ et al. Genetic and hypoxic regulation of angiogenesis in gliomas. J. Neurooncol.70(2), 229–243 (2004).
  • Tong RT, Boucher Y, Kozin SV et al. Vascular normalization by vascular endothelial growth factor receptor 2 blockade induces a pressure gradient across the vasculature and improves drug penetration in tumors. Cancer Res.64(11), 3731–3736 (2004).
  • Weis SM, Cheresh DA. Pathophysiological consequences of VEGF-induced vascular permeability. Nature437, 497–504 (2005).
  • Ferrara N. VEGF as a therapeutic target in cancer. Oncology69(Suppl. 3), 11–16 (2005).
  • Jain RK, Duda DG, Clark JW, Loeffler JS. Lessons from Phase III clinical trials on anti-VEGF therapy for cancer. Nat. Clin. Pract. Oncol.3(1), 24–40 (2006).
  • Kerbel RS. Antiangiogenic therapy: a universal chemosensitization strategy for cancer? Science312(5777), 1171–1175 (2006).
  • Chi A, Norden AD, Wen PY. Inhibition of angiogenesis and invasion in malignant gliomas. Expert Rev. Anticancer Ther.7(11), 1537–1560 (2007).
  • Giese A, Bjerkvig R, Berens ME, Westphal M. Cost of migration: invasion of malignant gliomas and implications for treatment. J. Clin. Oncol.21(8), 1624–1636 (2003).
  • Lamszus K, Kunkel P, Westphal M. Invasion as limitation to anti-angiogenic glioma therapy. Acta Neurochir.88(Suppl.), 169–177 (2003).
  • Rao JS. Molecular mechanisms of glioma invasiveness: the role of proteases. Nat. Rev. Cancer3(7), 489–501 (2003).
  • Salhia B, Tran NL, Symons M, Winkles JA, Jutka JT, Berens ME. Molecular pathways triggering glioma cell invasion. Expert Rev. Mol. Diagn.6(4), 613–626 (2006).
  • Lefranc F, Brotchi J, Kiss R. Possible future issues in the treatment of glioblastomas: special emphasis on cell migration and the resistance of migrating glioblastoma cells to apoptosis. J. Clin. Oncol.23(10), 2411–2422 (2005).
  • Abounader R, Laterra J. Scatter factor/hepatocyte growth factor in brain tumor growth and angiogenesis. Neuro-oncology7(4), 436–451 (2005).
  • Kunkel P, Ulbricht U, Bohlen P et al. Inhibition of glioma angiogenesis and growth in vivo by systemic treatment with monoclonal antibody against vascular endothelial growth factor receptor-2. Cancer Res.61(18), 6624–6628 (2001).
  • Plate KH, Breier G, Millaauer B et al. Up-regulation of vascular endothelial growth factor and its cognate receptors in a rat glioma model of tumor angiogenesis. Cancer Res.53(23), 5822–5827 (1993).
  • Reardon DA, Wen PY, Desjardins A, Batchelor TT, Vredenburgh JJ. Glioblastoma multiforme: an emerging paradigm of anti-VEGF therapy. Expert Opin. Biol. Ther.8(4), 541–553 (2008).
  • Samoto K, Ikezaki K, Ono M et al. Expression of vascular endothelial growth factor and its possible relation with neovascularization in human brain tumors. Cancer Res.55(5), 1189–1193 (1995).
  • Stefanik DF, Fellows WK, Rizkalla LR et al. Monoclonal antibodies to vascular endothelial growth factor (VEGF) and the VEGF receptor, FLT-1, inhibit the growth of C6 glioma in a mouse xenograft. J. Neurooncol.55, 91–100 (2001).
  • Stefanik DF, Rizkalla LR, Soi A et al. Acidic and basic fibroblast growth factors are present in glioblastoma multiforme. Cancer Res.51(20), 5760–5765 (1991).
  • Winkler F, Kozin SV, Tong R et al. Kinetics of vascular normalization by VEGFR2 blockade governs brain tumor response to radiation: role of oxygenation angiopoietin-1 and matrix metalloproteinases. Cancer Cell6, 553–563 (2004).
  • Zagzag D, Zhong H, Scalzitti JM et al. Expression of hypoxia-inducible factor 1α in brain tumors: association with angiogenesis, invasion, and progression. Cancer88(11), 2606–2618 (2000).
  • Zheng PP, Hop WC, Luider TM et al. Increased levels of circulating endothelial progenitor cells and circulating endothelial nitric oxide synthase in patients with gliomas. Ann. Neurol.62, 40–48 (2007).
  • Pope WB, Lai A, Nghiemphu P, Mischel P, Cloughesy TF. MRI in patients with high-grade gliomas treated with bevacizumab and chemotherapy. Neurology66(8), 1258–1260 (2006).
  • Vredenburgh JJ, Desjardins A, Herndon JE et al. Phase II trial of bevacizumab and irinotecan in recurrent malignant glioma. Clin. Cancer Res.13, 1253–1259 (2007).
  • Vredenburgh JJ, Desjardins A, Herndon JE et al. Bevacizumab plus irinotecan in recurrent glioblastoma multiforme. J. Clin. Oncol.25(30), 4722–4729 (2007).
  • Chen C, Silverman DHS, Geist C et al. Predicting treatment response of malignant gliomas to bevacizumab and irinotecan by imaging proliferation with [18F] fluorothymidine positron emission tomography: a pilot study. J. Clin. Oncol.25(30), 4714–4721 (2007).
  • Norden AD, Young GS, Setayesh K et al. Bevacizumab for recurrent malignant glioma: efficacy, toxicity and patterns of recurrence. Neurology70, 779–787 (2008).
  • Cloughsey TF, Prados MD, Mikkelsen T et al. A Phase II randomized non-comparative trial of bevacizumab alone or in combination with irinotecan on 6-month progression free survival in recurrent treatment refractory glioblastoma. J. Clin. Oncol.26(Suppl. 15), 91 (2008).
  • Batchelor TT, Sorensen AG, diTomaso E et al. AZD2171, a pan-VEGF receptor tyrosine kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma patients. Cancer Cell11, 83–95 (2007).
  • Eremina V, Jefferson JA, Kowalewska J et al. VEGF inhibition and renal thrombotic microangiopathy. N. Engl. J. Med.358(11), 1129–1136 (2008).
  • Eskens FA, Verweij J. The clinical toxicity profile of vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor (VEGFR) targeting angiogenesis inhibitors: a review. Eur. J. Cancer42, 3127–3139 (2006).
  • Brandes AA, Scelzi E, Salmistraro G et al. Incidence of risk of thromboembolism during treatment of high-grade gliomas: a prospective study. Eur. J. Cancer33, 1592–1596 (1997).
  • Marras LC, Geerts WH, Perry JR. The risk of venous thromboembolism is increased throughout the course of malignant glioma: an evidence-based review. Cancer89, 640–646 (2000).
  • Semrad TJ, O’Donnell R, Wun T et al. Epidemiology of venous thromboembolism in 9489 patients with malignant glioma. J. Neurosurg.l06(4), 601–608 (2007).
  • Stark-Vance V. Bevacizumab and CPT-11 in the treatment of relapsed malignant glioma. Neuro Oncol.7(3), 369 (2005) (Abstract).

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