Modes of resistance to anti-angiogenic therapy
Tóm tắt
Từ khóa
Tài liệu tham khảo
Hanahan, D. & Folkman, J. Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis. Cell 86, 353 (1996).
Folkman, J. Angiogenesis: an organizing principle for drug discovery? Nature Rev. Drug Discov. 6, 273–286 (2007).
Ferrara, N., Hillan, K. J. & Novotny, W. Bevacizumab (Avastin), a humanized anti-VEGF monoclonal antibody for cancer therapy. Biochem. Biophys. Res. Commun. 333, 328–335 (2005).
Jain, R. K. Antiangiogenic therapy for cancer: current and emerging concepts. Oncology (Williston Park) 19, 7–16 (2005).
Smith, J. K., Mamoon, N. M. & Duhe, R. J. Emerging roles of targeted small molecule protein-tyrosine kinase inhibitors in cancer therapy. Oncol. Res. 14, 175–225 (2004).
Ferrara, N., Damico, L., Shams, N., Lowman, H. & Kim, R. Development of ranibizumab, an anti-vascular endothelial growth factor antigen binding fragment, as therapy for neovascular age-related macular degeneration. Retina 26, 859–870 (2006).
Gragoudas, E. S., Adamis, A. P., Cunningham, E. T. Jr, Feinsod, M. & Guyer, D. R. Pegaptanib for neovascular age-related macular degeneration. N. Engl. J. Med. 351, 2805–2816 (2004).
Apte, R. S. Pegaptanib sodium for the treatment of age-related macular degeneration. Expert Opin. Pharmacother. 9, 499–508 (2008).
Karaman, M. W. et al. A quantitative analysis of kinase inhibitor selectivity. Nature Biotechnol. 26, 127–132 (2008).
Ellis, L. M. & Hicklin, D. J. VEGF-targeted therapy: mechanisms of anti-tumour activity. Nature Rev. Cancer 8, 579–591 (2008).
Avraamides, C. J., Garmy-Susini, B. & Varner, J. A. Integrins in angiogenesis and lymphangiogenesis. Nature Rev. Cancer 8, 604–617 (2008).
Murdoch, C., Muthana, M., Coffelt, S. B. & Lewis, C. E. The role of myeloid cells in the promotion of tumour angiogenesis. Nature Rev. Cancer 8, 618–631 (2008).
Neufeld, G. & Kessler, O. The semaphorins: versatile regulators of tumour progression and tumour angiogenesis. Nature Rev. Cancer 8, 632–645 (2008).
Yan, M. & Plowman, G. D. Delta-like 4/Notch signaling and its therapeutic implications. Clin. Cancer Res. 13, 7243–7246 (2007).
Thurston, G., Noguera-Troise, I. & Yancopoulos, G. D. The Delta paradox: DLL4 blockade leads to more tumour vessels but less tumour growth. Nature Rev. Cancer 7, 327–331 (2007).
Shojaei, F. et al. Bv8 regulates myeloid-cell-dependent tumour angiogenesis. Nature 450, 825–831 (2007).
Petit, I., Jin, D. & Rafii, S. The SDF-1–CXCR4 signaling pathway: a molecular hub modulating neo-angiogenesis. Trends Immunol. 28, 299–307 (2007).
Bergers, G., Song, S., Meyer-Morse, N., Bergsland, E. & Hanahan, D. Benefits of targeting both pericytes and endothelial cells in the tumor vasculature with kinase inhibitors. J. Clin. Invest. 111, 1287–1295 (2003).
Erber, R. et al. Combined inhibition of VEGF and PDGF signaling enforces tumor vessel regression by interfering with pericyte-mediated endothelial cell survival mechanisms. FASEB J. 18, 338–340 (2004).
Pietras, K., Pahler, J., Bergers, G. & Hanahan, D. Functions of paracrine PDGF signaling in the proangiogenic tumor stroma revealed by pharmacological targeting. PLoS Med. 5, e19 (2008).
Saltz, L. B. et al. Randomized phase II trial of cetuximab, bevacizumab, and irinotecan compared with cetuximab and bevacizumab alone in irinotecan-refractory colorectal cancer: the BOND-2 study. J. Clin. Oncol. 25, 4557–4561 (2007).
Shojaei, F. & Ferrara, N. Antiangiogenic therapy for cancer: an update. Cancer J. 13, 345–348 (2007).
Kindler, H. L. et al. A double-blind, placebo-controlled, randomized phase III trial of gemcitabine (G) plus bevacizumab (B) versus gemcitabine plus placebo (P) in patients (pts) with advanced pancreatic cancer (PC). J. Clin. Oncol. 25, 4508 (2007).
Miller, K. D., Sweeney, C. J. & Sledge, G. W. Jr. Can tumor angiogenesis be inhibited without resistance? EXS 2005, 95–112 (2005).
Gatenby, R. A. & Gillies, R. J. A microenvironmental model of carcinogenesis. Nature Rev. Cancer 8, 56–61 (2008).
Kerbel, R. S. Inhibition of tumor angiogenesis as a strategy to circumvent acquired resistance to anti-cancer therapeutic agents. Bioessays 13, 31–36 (1991).
Kerbel, R. S. et al. Possible mechanisms of acquired resistance to anti-angiogenic drugs: implications for the use of combination therapy approaches. Cancer Metastasis Rev. 20, 79–86 (2001).
Casanovas, O., Hicklin, D. J., Bergers, G. & Hanahan, D. Drug resistance by evasion of antiangiogenic targeting of VEGF signaling in late-stage pancreatic islet tumors. Cancer Cell 8, 299–309 (2005). This study demonstrates the existence of evasive resistance by alternative pro-angiogenic signalling.
Blouw, B. et al. The hypoxic response of tumors is dependent on their microenvironment. Cancer Cell 4, 133–146 (2003).
Kerbel, R. S. Therapeutic implications of intrinsic or induced angiogenic growth factor redundancy in tumors revealed. Cancer Cell 8, 269–271 (2005).
Shojaei, F. et al. Tumor refractoriness to anti-VEGF treatment is mediated by CD11b+Gr1+ myeloid cells. Nature Biotechnol. 25, 911–920 (2007). This study reveals CD11b+Gr1+ monocytes to be mediators of intrinsic resistance to anti-VEGF treatment in murine transplant tumours.
Glade Bender, J., Cooney, E. M., Kandel, J. J. & Yamashiro, D. J. Vascular remodeling and clinical resistance to antiangiogenic cancer therapy. Drug Resist. Updat. 7, 289–300 (2004).
Mizukami, Y. et al. Induction of interleukin-8 preserves the angiogenic response in HIF-1α-deficient colon cancer cells. Nature Med. 11, 992–997 (2005).
Gorre, M. E. & Sawyers, C. L. Molecular mechanisms of resistance to STI571 in chronic myeloid leukemia. Curr. Opin. Hematol. 9, 303–307 (2002).
O'Connor, R., Clynes, M., Dowling, P., O'Donovan, N. & O'Driscoll, L. Drug resistance in cancer — searching for mechanisms, markers and therapeutic agents. Expert Opin. Drug Metab. Toxicol. 3, 805–817 (2007).
Rubenstein, J. L. et al. Anti-VEGF antibody treatment of glioblastoma prolongs survival but results in increased vascular cooption. Neoplasia 2, 306–314 (2000). First study demonstrating vessel co-option of tumour cells in response to anti-VEGF therapy.
Fernando, N. T. et al. Tumor escape from endogenous, extracellular matrix-associated angiogenesis inhibitors by up-regulation of multiple proangiogenic factors. Clin. Cancer Res. 14, 1529–1539 (2008).
Kadenhe-Chiweshe, A. et al. Sustained VEGF blockade results in microenvironmental sequestration of VEGF by tumors and persistent VEGF receptor-2 activation. Mol. Cancer Res. 6, 1–9 (2008).
Batchelor, T. T. et al. AZD2171, a pan-VEGF receptor tyrosine kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma patients. Cancer Cell 11, 83–95 (2007). This clinical study describes the ability of the pan-VEGFR inhibitor AZD1271 to normalize tumour vessels in recurrent patients with glioblastoma using MRI technology. FGF2 and SDF1α blood levels increased when tumours escaped treatment.
Bertolini, F., Mancuso, P., Shaked, Y. & Kerbel, R. S. Molecular and cellular biomarkers for angiogenesis in clinical oncology. Drug Discov. Today 12, 806–812 (2007).
Bertolini, F., Shaked, Y., Mancuso, P. & Kerbel, R. S. The multifaceted circulating endothelial cell in cancer: towards marker and target identification. Nature Rev. Cancer 6, 835–845 (2006).
Bocci, G. et al. Increased plasma vascular endothelial growth factor (VEGF) as a surrogate marker for optimal therapeutic dosing of VEGF receptor-2 monoclonal antibodies. Cancer Res. 64, 6616–6625 (2004).
Ebos, J. M., Lee, C. R., Christensen, J. G., Mutsaers, A. J. & Kerbel, R. S. Multiple circulating proangiogenic factors induced by sunitinib malate are tumor-independent and correlate with antitumor efficacy. Proc. Natl Acad. Sci. USA 104, 17069–17074 (2007).
Asahara, T. et al. Isolation of putative progenitor endothelial cells for angiogenesis. Science 275, 964–967 (1997).
Pollard, J. W. Tumour-educated macrophages promote tumour progression and metastasis. Nature Rev. Cancer 4, 71–78 (2004).
De Palma, M. et al. Tie2 identifies a hematopoietic lineage of proangiogenic monocytes required for tumor vessel formation and a mesenchymal population of pericyte progenitors. Cancer Cell 8, 211–226 (2005).
Hattori, K. et al. Placental growth factor reconstitutes hematopoiesis by recruiting VEGFR1+ stem cells from bone-marrow microenvironment. Nature Med. 8, 841–849 (2002).
Kaplan, R. N. et al. VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche. Nature 438, 820–827 (2005).
Bunt, S. K., Sinha, P., Clements, V. K., Leips, J. & Ostrand-Rosenberg, S. Inflammation induces myeloid-derived suppressor cells that facilitate tumor progression. J. Immunol. 176, 284–290 (2006).
Yang, L. et al. Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis. Cancer Cell 6, 409–421 (2004).
Grunewald, M. et al. VEGF-induced adult neovascularization: recruitment, retention, and role of accessory cells. Cell 124, 175–189 (2006).
Du, R. et al. HIF1α induces the recruitment of bone marrow-derived vascular modulatory cells to regulate tumor angiogenesis and invasion. Cancer Cell 13, 206–220 (2008). This study reveals that monocytic cells from the bone marrow are sufficient to drive neovascularization in GBM. Impairment of VEGF signalling leads to an adaptive pro-invasive tumour phenotype, which can be directly blocked by VEGF.
Ceradini, D. J. et al. Progenitor cell trafficking is regulated by hypoxic gradients through HIF-1 induction of SDF-1. Nature Med. 10, 858–864 (2004).
De Falco, E. et al. SDF-1 involvement in endothelial phenotype and ischemia-induced recruitment of bone marrow progenitor cells. Blood 104, 3472–3482 (2004).
Aghi, M., Cohen, K. S., Klein, R. J., Scadden, D. T. & Chiocca, E. A. Tumor stromal-derived factor-1 recruits vascular progenitors to mitotic neovasculature, where microenvironment influences their differentiated phenotypes. Cancer Res. 66, 9054–9064 (2006).
Dewhirst, M. W., Cao, Y. & Moeller, B. Cycling hypoxia and free radicals regulate angiogenesis and radiotherapy response. Nature Rev. Cancer 8, 425–437 (2008).
Shaked, Y. et al. Therapy-induced acute recruitment of circulating endothelial progenitor cells to tumors. Science 313, 1785–1787 (2006). This study reveals that influx of bone marrow-derived endothelial progenitors is an essential step in re-neovascularization of tumours that have undergone treatments with vascular disrupting agents.
Sathornsumetee, S. et al. Tumor angiogenic and hypoxic profiles predict radiographic response and survival in malignant astrocytoma patients treated with bevacizumab and irinotecan. J. Clin. Oncol. 26, 271–278 (2008).
Allt, G. & Lawrenson, J. G. Pericytes: cell biology and pathology. Cells Tissues Organs 169, 1–11 (2001).
Gerhardt, H. & Betsholtz, C. Endothelial–pericyte interactions in angiogenesis. Cell Tissue Res. 314, 15–23 (2003).
Bergers, G. & Song, S. The role of pericytes in blood-vessel formation and maintenance. Neuro Oncol. 7, 452–464 (2005).
Jain, R. K. & Booth, M. F. What brings pericytes to tumor vessels? J. Clin. Invest. 112, 1134–1136 (2003).
Jain, R. K. Normalization of tumor vasculature: an emerging concept in antiangiogenic therapy. Science 307, 58–62 (2005).
Mancuso, M. R. et al. Rapid vascular regrowth in tumors after reversal of VEGF inhibition. J. Clin. Invest. 116, 2610–2621 (2006).
Kamba, T. & McDonald, D. M. Mechanisms of adverse effects of anti-VEGF therapy for cancer. Br. J. Cancer 96, 1788–1795 (2007).
Baluk, P., Hashizume, H. & McDonald, D. M. Cellular abnormalities of blood vessels as targets in cancer. Curr. Opin. Genet. Dev. 15, 102–111 (2005).
Benjamin, L., Hemo, I. & Keshet, E. A plasticity window for blood vessel remodelling is defined by pericyte coverage of the preformed endothelial network and is regulated by PDGF-B and VEGF. Development 125, 1591–1598 (1998).
Darland, D. C. et al. Pericyte production of cell-associated VEGF is differentiation-dependent and is associated with endothelial survival. Dev. Biol. 264, 275–288 (2003).
Song, S., Ewald, A. J., Stallcup, W., Werb, Z. & Bergers, G. PDGFRβ+ perivascular progenitor cells in tumours regulate pericyte differentiation and vascular survival. Nature Cell Biol. 7, 870–879 (2005).
Hirschi, K. K. & D'Amore, P. A. Control of angiogenesis by the pericyte: molecular mechanisms and significance. EXS 79, 419 (1997).
Orlidge, A. & D'Amore, P. A. Inhibition of capillary endothelial cell growth by pericytes and smooth muscle cells. J. Cell. Biol. 105, 1455–1462 (1987).
Pietras, K. & Hanahan, D. A multitargeted, metronomic, and maximum-tolerated dose “chemo-switch” regimen is antiangiogenic, producing objective responses and survival benefit in a mouse model of cancer. J. Clin. Oncol. 23, 939–952 (2005).
Sun, J. et al. Inhibiting angiogenesis and tumorigenesis by a synthetic molecule that blocks binding of both VEGF and PDGF to their receptors. Oncogene 24, 4701–4709 (2005).
Xian, X. et al. Pericytes limit tumor cell metastasis. J. Clin. Invest. 116, 642–651 (2006). This study demonstrates that disruption of pericyte coverage from tumour vessels can elicit increased metastasis in a transgenic model of pancreatic islet carcinogenesis.
Norden, A. D. et al. Bevacizumab for recurrent malignant gliomas: efficacy, toxicity, and patterns of recurrence. Neurology 70, 779–787 (2008).
Narayana, A. et al. Anti-angiogenic therapy using bevacizumab in recurrent high grade glioma: impact on local control and survival. J. Neurosurg. (in the press).
Berger, M. S. & Wilson, C. B. The Gliomas (W.B. Saunders, Philadelphia, 1999).
Kunkel, P. et al. Inhibition of glioma angiogenesis and growth in vivo by systemic treatment with a monoclonal antibody against vascular endothelial growth factor receptor-2. Cancer Res. 61, 6624–6628 (2001).
Hida, K. et al. Tumor-associated endothelial cells with cytogenetic abnormalities. Cancer Res. 64, 8249–8255 (2004).
Lesslie, D. P. et al. Vascular endothelial growth factor receptor-1 mediates migration of human colorectal carcinoma cells by activation of Src family kinases. Br. J. Cancer 94, 1710–1717 (2006).
Relf, M. et al. Expression of the angiogenic factors vascular endothelial cell growth factor, acidic and basic fibroblast growth factor, tumor growth factor β-1, platelet-derived endothelial cell growth factor, placenta growth factor, and pleiotrophin in human primary breast cancer and its relation to angiogenesis. Cancer Res. 57, 963–969 (1997).
Marty, M. & Pivot, X. The potential of anti-vascular endothelial growth factor therapy in metastatic breast cancer: clinical experience with anti-angiogenic agents, focusing on bevacizumab. Eur. J. Cancer 44, 912–920 (2008).
Miller, K. et al. Paclitaxel plus bevacizumab versus paclitaxel alone for metastatic breast cancer. N. Engl. J. Med. 357, 2666–2676 (2007).
Sofuni, A. et al. Differential diagnosis of pancreatic tumors using ultrasound contrast imaging. J. Gastroenterol. 40, 518–525 (2005).
Schneider, G. & Schmid, R. M. Genetic alterations in pancreatic carcinoma. Mol. Cancer 2, 15 (2003).
Cowgill, S. M. & Muscarella, P. The genetics of pancreatic cancer. Am. J. Surg. 186, 279–286 (2003).
Yu, J. L. et al. Heterogeneous vascular dependence of tumor cell populations. Am. J. Pathol. 158, 1325–1334 (2001).
Yu, J. L., Rak, J. W., Coomber, B. L., Hicklin, D. J. & Kerbel, R. S. Effect of p53 status on tumor response to antiangiogenic therapy. Science 295, 1526–1528 (2002).
Kaur, B., Tan, C., Brat, D. J., Post, D. E. & Van Meir, E. G. Genetic and hypoxic regulation of angiogenesis in gliomas. J. Neurooncol. 70, 229–243 (2004).
Sessa, C., Guibal, A., Del Conte, G. & Ruegg, C. Biomarkers of angiogenesis in the development of antiangiogenic therapies in oncology: tools or decorations? Nature Clin. Pract. Oncol. 5, 378–391 (2008).
Wang, X. et al. Potent and selective inhibitors of the Met [hepatocyte growth factor/scatter factor (HGF/SF) receptor] tyrosine kinase block HGF/SF-induced tumor cell growth and invasion. Mol. Cancer Ther. 2, 1085–1092 (2003).
Feng, Y. & Dimitrov, D. S. Monoclonal antibodies against components of the IGF system for cancer treatment. Curr. Opin. Drug Discov. Devel. 11, 178–185 (2008).
Giaccia, A., Siim, B. G. & Johnson, R. S. HIF-1 as a target for drug development. Nature Rev. Drug Discov. 2, 803–811 (2003).
Tan, C. et al. Identification of a novel small-molecule inhibitor of the hypoxia-inducible factor 1 pathway. Cancer Res. 65, 605–612 (2005).
Sarker, D. et al. A phase I pharmacokinetic and pharmacodynamic study of TKI258, an oral, multitargeted receptor tyrosine kinase inhibitor in patients with advanced solid tumors. Clin. Cancer Res. 14, 2075–2081 (2008).
Garrett, C. R. et al. A phase I study of BMS-582664 (brivanib alaninate), an oral dual inhibitor of VEGFR and FGFR tyrosine kinases, in combination with full-dose cetuximab in patients (pts) with advanced gastrointestinal malignancies (AGM) who failed prior therapy. J. Clin. Oncol. 2007 ASCO Annu. Meeting Proc. Pt I 25, 14018 (2007).
Von Pawel, J. et al. A double blind phase II study of BIBF 1,120 in patients suffering from relapsed advanced non-small cell lung cancer (NSCLC). J. Clin. Oncol. 2007 ASCO Annu. Meeting Proc. Pt I 25, 7635 (2007).