[1] |
Kerbel RS. Tumor angiogenesis: past, present and the near future[J].Carcinogenesis, 2000, 21(3):505–515.
|
[2] |
Folkman J. Tumor angiogenesis: therapeutic implications[J]. N Engl J Med, 1971, 285(21):1182–1186.
|
[3] |
Ferrara N. Vascular endothelial growth factor as a target for anticancer therapy[J]. Oncologist, 2004, 9 suppl 1:2–10.
|
[4] |
Robinson CJ, Stringer SE. The splice variants of vascular endothelial growth factor (VEGF) and their receptors[J]. J Cell Sci, 2001, 114(5):853 –865.
|
[5] |
Roy H, Bhardwaj S, Ylä-Herttuala S. Biology of vascular endothelial growth factors[J]. FEBS Lett, 2006, 580(12):2879–2887.
|
[6] |
Leung DW, Cachianes G, Kuang WJ, et al. Vascular endothelial growth factor is a secretedangiogenic mitogen[J]. Science, 1989, 246(4935):1306–1309.
|
[7] |
Pajusola K, Aprelikova O, Korhonen J, et al. FLT4 receptor tyrosine kinase contains seven immunoglobulin-like loops and is expressed in multiple human tissues and cell lines[J]. Cancer Res, 1992, 52(20):5738–5743.
|
[8] |
Holmes K, Roberts OL, Thomas AM, et al. Vascular endothelial growth factor receptor-2: structure, function, intracellular signaling and therapeutic inhibition[J]. Cell Signal, 2007, 19(10):2003–2012.
|
[9] |
Chu E. An update on the current and emerging targeted agents in metastatic colorectal cancer[J]. Clin Colorectal Cancer, 2011, 11(1):1–13.
|
[10] |
Krauss G. Biochemistry of signal transduction and regulation[M]. 3rd ed. WILEY-VCH Verlag:Weinheim, 2003.
|
[11] |
Simó R, Sundstrom JM, Antonetti DA. Ocular anti-VEGF therapy for diabetic retinopathy: the role of VEGF in the pathogenesis of diabetic retinopathy[J]. Diabetes Care, 2014, 37(4):893–899.
|
[12] |
Takahashi T, Yamaguchi S, Chida K, et al. A single autophosphorylation site on KDR/Flk-1 is essential for VEGF-Adependent activation of PLC-gamma and DNA synthesis in vascular endothelial cells[J]. EMBO J, 2001, 20(11):2768–2778.
|
[13] |
Lee SL, Rouhi P, Dahl JL, et al. Hypoxia-induced pathological angiogenesis mediates tumor cell dissemination, invasion, and metastasis in a zebrafish tumor model[J]. Proc Natl Acad Sci U S A, 2009, 106(46):19485–19490.
|
[14] |
Liu W, Xu J, Wang M, et al. Tumor-derived vascular endothelial growth factor (VEGF)-a facilitates tumor metastasis through the VEGF-VEGFR1 signaling pathway[J]. Int J Oncol, 2011, 39(5):1213–1220.
|
[15] |
Hicklin DJ, Ellis LM. Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis[J]. J Clin Oncol, 2005, 23(5):1011–1027.
|
[16] |
Rosen LS. Clinical experience with angiogenesis signaling inhibitors: focus on vascular endothelial growth factor (VEGF) blockers[J]. Cancer Control, 2002, 9(2 suppl):36–44.
|
[17] |
Schmidt NO, Westphal M, Hagel C, et al. Levels of vascular endothelial growth factor, hepatocyte growth factor/scatter factor and basic fibroblast growth factor in human gliomas and their relation to angiogenesis[J]. Int J Cancer, 1999, 84(1):10–18.
|
[18] |
Pegram MD, Reese DM. Combined biological therapy of breast cancer using monoclonal antibodies directed against HER2/neu protein and vascular endothelial growth factor[J]. Semin Oncol, 2002, 29(32 suppl 11):29–37.
|
[19] |
Miao HQ, Hu K, Jimenez X, et al. Potent neutralization of VEGF biological activities with a fully human antibody Fab fragment directed against VEGF receptor 2[J]. Biochem Biophys Res Commun, 2006, 345(1):438–445.
|
[20] |
Liang X, Xu F, Li X, et al. VEGF signal system: the application of antiangiogenesis[J]. Curr Med Chemy, 2014, 21(7):894–910.
|
[21] |
Wang M, Zheng X, Ruan X, et al. Efficacy and safety of first-line chemotherapy plus bevacizumab in patients with metastatic colorectal cancer: a meta-analysis[J]. Chin Med J (Engl), 2014, 127(3):538–546.
|
[22] |
罗聪, 应杰儿. 贝伐单抗在结直肠癌靶向治疗中的研究进展[J]. 中国全科医学, 2011, 14(29):3407–3409.
|
[23] |
Du J, Lei B, Qin J, et al. Molecular modeling studies of vascular endothelial growth factor receptor tyrosine kinase inhibitors using QSAR and docking[J]. J Mol Graph Model, 2009, 27(5):642–654.
|
[24] |
Minguet J, Smith KH, Bramlage CP, et al. Targeted therapies for treatment of renal cell carcinoma: recent advances and future perspectives[J]. Cancer Chemother Pharmacol, 2015, [Epub ahead of print].
|
[25] |
Dreyer C, Sablin MP, Bouattour M, et al. Disease control with sunitinib in advanced intrahepatic cholangiocarcinoma resistant to gemcitabine-oxaliplatin chemotherapy[J]. World J Hepatol, 2015, 7(6):910–915.
|
[26] |
Choi KJ, Baik IH, Ye SK, et al. Molecular Targeted Therapy for Hepatocellular Carcinoma: Present Status and Future Directions[J]. Biol Pharm Bull, 2015, 38(7):986–991.
|
[27] |
Johnson PJ, Qin SK, Park JW, et al. Brivanib versus sorafenib as first-line therapy in patients with unresectable, advanced hepatocellular carcinoma:Results from the randomized phase III BRISK-FL study[J]. J Clin Oncol, 2013, 31(28):3517–24.
|
[28] |
Lai L, Liu J, Zhai D, et al. Plumbagin inhibits tumour angiogenesis and tumour growth through the rassignalling pathway following activation of the VEGF receptor-2[J]. Br J Pharmacol, 2012, 165(4b):1084–1096.
|
[29] |
Gibney GT, Gauthier G, Ayas C, et al. Treatment patterns and outcomes in BRAF V600E-mutant melanoma patients with brain metastases receiving vemurafenib in the real-world setting[J]. Cancer Med, 2015,[Epub ahead of print].
|
[30] |
Chelouche-Lev D, Miller CP, Tellez C, et al. Different signalling pathways regulate VEGF and IL-8 expression in breast cancer: implications for therapy[J]. Eur J Cancer, 2004, 40(16):2509–2518.
|
[31] |
Dry JR, Pavey S, Pratilas CA, et al. Transcriptional pathway signatures predict MEK addiction and response to selumetinib (AZD6244)[J]. Cancer Res, 2010, 70(6):2264–2273.
|
[32] |
American Society of Clinical Oncology (ASCO). 2012 ASCO Annual Meeting: METRIC phase III study: Efficacy of trametinib (T), a potent and selective MEK inhibitor (MEKi), in progressionfreesurvival (PFS) and overall survival (OS), compared with chemotherapy (C) in patients (pts) with BRAFV600E/K mutant advanced or metastatic melanoma (MM). Accessed 2012].
URL
|
[33] |
Rizos H, Menzies AM, Pupo GM, et al. BRAF inhibitor resistance mechanisms in metastatic melanoma: spectrum and clinical impact[J]. Clin Cancer Res, 2014, 20(7):1965–1977.
|
[34] |
Larkin J, Ascierto PA, Dréno B, et al. Combined vemurafenib and cobimetinib in BRAF-mutated melanoma[J]. N Engl J Med, 2014, 371(20):1867–1876.
|
[35] |
Long GV, Stroyakovskiy D, Gogas H, et al. Combined BRAF and MEK inhibition versus BRAF inhibition alone in melanoma[J]. N Engl J Med, 2014, 371(20):1877–1888.
|
[36] |
Robert C, Karaszewska B, Schachter J, et al. Improved overall survival in melanoma with combined dabrafenib and trametinib[J]. N Engl J Med, 2015, 372(1):30–39.
|
[37] |
Song Y, Dai F, Zhai D, et al. Usnic acid inhibits breast tumor angiogenesis and growth by suppressing VEGFR2-mediated AKT and ERK1/2 signaling pathways[J]. Angiogenesis, 2012, 15(3):421–432.
|
[38] |
Liu LZ, Li C, Chen Q, et al. MiR-21 induced angiogenesis through AKT and ERK activation and HIF-1alpha expression[J]. PLoS One, 2011, 6(4):e19139.
|
[39] |
Li C, Xin P, Xiao H, et al. The dual PI3K/mTOR inhibitor NVP-BEZ235 inhibits proliferation and induces apoptosis of burkitt lymphoma cells[J]. Cancer Cell Int, 2015, 15:65.
|
[40] |
Agarwal E, Chaudhuri A, Leiphrakpam PD, et al. Akt inhibitor MK-2206 promotes anti-tumor activity and cell death by modulation of AIF and Ezrin in colorectal cancer[J]. BMC Cancer, 2014, 14:145.
|
[41] |
Banumathi E, O’Connor A, Gurunathan S, et al. VEGF-induced retinal angiogenic signaling is critically dependent on Ca2+ signaling by Ca2+/calmodulin-dependent protein kinase II[J]. Invest Ophthalmol Vis Sci, 2011, 52(6):3103–3111.
|
[42] |
Pieramici D, Rabena M. Anti-VEGF therapy: comparison of current and future agents[J]. Eye (Lond), 2008, 22(10):1330–1336.
|
[43] |
Sitohy B, Nagy JA, Dvorak HF. Anti-VEGF/VEGFR therapy for cancer: reassessing the target[J]. Cancer Res, 2012, 72(8):1909–1914.
|
[44] |
BD. Advanced Information: RNA interference. Nobel Media AB: nobelprize.org [website on Internet].Available from: Accessed 8 November 2012].
URL
|
[45] |
Chen S, Feng J, Ma L, et al. RNA interference technology for anti-VEGF treatment[J]. Expert Opin Drug Deliv, 2014, 11(9):1471–1480.
|
[46] |
Chekhonin VP, Shein SA, Korchagina AA, et al. VEGF in tumor progression and targeted therapy[J]. Curr Cancer Drug Targets, 2013, 13(4):423–443.
|
[47] |
Batchelor TT, Sorensen AG, di Tomaso E, et al. AZD2171, a pan-VEGF receptor tyrosine kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma patients[J]. Cancer Cell, 2007, 11(1):83–95.
|
[48] |
Fan F, Samuel S, Gaur P, et al. Chronic exposure of colorectal cancer cells to bevacizumab promotes compensatory pathways that mediate tumour cell migration[J]. Br J Cancer, 2011, 104(8):1270–1277.
|
[49] |
Du R, Lu KV, Petritsch C, et al. HIF1 alpha induces the recruitment of bone marrow-derived vascular modulatory cells to regulate tumor angiogenesis and invasion[J]. Cancer Cell, 2008, 13(3):206–220.
|
[50] |
Hu YL, DeLay M, Jahangiri A, et al. Hypoxia-induced autophagy promotes tumor cell survival and adaptation to antiangiogenic treatment in glioblastoma[J]. Cancer Res, 2012, 72(7):1773–1783.
|
[51] |
Pàez-Ribes M, Allen E, Hudock J, et al. Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis[J]. Cancer Cell, 2009, 15(3):220–231.
|
[52] |
Ebos JM, Lee CR, Cruz-Munoz W, et al. Accelerated metastasis after shortterm treatment with a potent inhibitor of tumor angiogenesis[J]. Cancer Cell, 2009, 15(3):232–239.
|
[53] |
Sakariassen PØ, Prestegarden L, Wang J, et al. Angiogenesis-independent tumor growth mediated by stem-likecancer cells[J]. Proc Natl Acad Sci U S A, 2006, 103(44):16466–16471.
|
[54] |
Kondo Y, Kanzawa T, Sawaya R, et al. The role of autophagy in cancer development and response to therapy[J]. Nat Rev Cancer, 2005, 5(9):726–734.
|
[55] |
Hu YL, Jahangiri A, Delay M, et al. Tumor cell autophagy as an adaptive response mediating resistance to treatments such as antiangiogenictherapy[J]. Cancer Res, 2012, 72(17):4294–4299.
|
[56] |
Wu X, Northcott PA, Dubuc A, et al. Clonal selection drives genetic divergence of metastatic medulloblastoma[J]. Nature, 2012, 482(7386):529–533.
|