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Mechanisms of resistance to anti-angiogenic therapy and development of third-generation anti-angiogenic drug candidates.抗血管生成疗法的耐药机制及第三代抗血管生成候选药物的研发
Genes Cancer. 2010 Jan;1(1):12-25. doi: 10.1177/1947601909356574.
2
Compensatory angiogenesis and tumor refractoriness.代偿性血管生成与肿瘤难治性
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Evading tumor evasion: current concepts and perspectives of anti-angiogenic cancer therapy.逃避肿瘤的逃避:抗血管生成癌症治疗的当前概念和观点。
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The role of tumor microenvironment in resistance to anti-angiogenic therapy.肿瘤微环境在抗血管生成治疗耐药性中的作用。
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本文引用的文献

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Biomarkers of response and resistance to antiangiogenic therapy.抗血管生成治疗反应和耐药性的生物标志物。
Nat Rev Clin Oncol. 2009 Jun;6(6):327-38. doi: 10.1038/nrclinonc.2009.63.
2
PDGF-C induces maturation of blood vessels in a model of glioblastoma and attenuates the response to anti-VEGF treatment.血小板衍生生长因子C(PDGF-C)在胶质母细胞瘤模型中诱导血管成熟,并减弱对抗血管内皮生长因子(VEGF)治疗的反应。
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Accelerated metastasis after short-term treatment with a potent inhibitor of tumor angiogenesis.用强效肿瘤血管生成抑制剂进行短期治疗后转移加速。
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Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis.抗血管生成疗法会引发肿瘤的恶性进展,导致局部侵袭增加和远处转移。
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Silencing or fueling metastasis with VEGF inhibitors: antiangiogenesis revisited.用血管内皮生长因子抑制剂抑制或促进转移:重新审视抗血管生成
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Role of endothelial progenitors and other bone marrow-derived cells in the development of the tumor vasculature.内皮祖细胞及其他骨髓来源细胞在肿瘤血管生成中的作用。
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Heterozygous deficiency of PHD2 restores tumor oxygenation and inhibits metastasis via endothelial normalization.PHD2杂合性缺陷通过内皮细胞正常化恢复肿瘤氧合并抑制转移。
Cell. 2009 Mar 6;136(5):839-851. doi: 10.1016/j.cell.2009.01.020. Epub 2009 Feb 12.
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Arginase I-producing myeloid-derived suppressor cells in renal cell carcinoma are a subpopulation of activated granulocytes.肾细胞癌中产生精氨酸酶I的髓源性抑制细胞是活化粒细胞的一个亚群。
Cancer Res. 2009 Feb 15;69(4):1553-60. doi: 10.1158/0008-5472.CAN-08-1921. Epub 2009 Feb 5.
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Chemotherapy, bevacizumab, and cetuximab in metastatic colorectal cancer.转移性结直肠癌的化疗、贝伐单抗和西妥昔单抗
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10
Bevacizumab in combination with paclitaxel for HER-2 negative metastatic breast cancer: an economic evaluation.贝伐单抗联合紫杉醇治疗HER-2阴性转移性乳腺癌的经济学评估
Eur J Cancer. 2009 May;45(8):1397-406. doi: 10.1016/j.ejca.2008.12.016. Epub 2009 Jan 13.

抗血管生成疗法的耐药机制及第三代抗血管生成候选药物的研发

Mechanisms of resistance to anti-angiogenic therapy and development of third-generation anti-angiogenic drug candidates.

作者信息

Loges Sonja, Schmidt Thomas, Carmeliet Peter

机构信息

Vesalius Research Center (VRC), Leuven, Belgium.

出版信息

Genes Cancer. 2010 Jan;1(1):12-25. doi: 10.1177/1947601909356574.

DOI:10.1177/1947601909356574
PMID:21779425
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3092176/
Abstract

The concept of inhibiting tumor neovessels has taken the hurdle from the bench to the bedside and now represents an extra pillar of anticancer treatment. So far, anti-angiogenic therapy prolongs survival in the order of months in some settings while failing to induce a survival benefit in others, in part because of intrinsic refractoriness or evasive escape. This review provides an update on recent mechanisms via which tumor and stromal cells induce resistance and discusses recent evolutions in the (pre)clinical development of novel third-generation anti-angiogenic agents to overcome this problem.

摘要

抑制肿瘤新生血管的概念已跨越从实验室到临床应用的障碍,如今成为抗癌治疗的又一重要支柱。到目前为止,抗血管生成疗法在某些情况下能将生存期延长数月,而在其他情况下则无法带来生存获益,部分原因是存在内在难治性或逃避现象。本综述提供了关于肿瘤和基质细胞诱导耐药的最新机制的最新信息,并讨论了新型第三代抗血管生成药物在(临床前)临床开发中为克服这一问题的最新进展。