Drug resistance associated with antiangiogenesis therapy

被引：56

作者：

Eikesdal, Hans Petter

Kalluri, Raghu ^{[1
,2
,3
]}

机构：

[1] Beth Israel Deaconess Med Ctr, Div Matrix Biol, Ctr Life Sci, Dept Med, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA USA

[3] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA

来源：

SEMINARS IN CANCER BIOLOGY | 2009年 / 19卷 / 05期

基金：

美国国家卫生研究院;

关键词：

Cancer; Angiogenesis; Antiangiogenic therapy; Drug resistance mechanisms; MATRIX-METALLOPROTEINASE INHIBITORS; VASCULAR DISRUPTING AGENTS; ANTI-ANGIOGENIC AGENTS; GROWTH-FACTOR; BREAST-CANCER; TUMOR-GROWTH; ENDOTHELIAL-CELLS; IN-VIVO; VASCULOGENIC MIMICRY; BLOOD-VESSELS;

D O I：

10.1016/j.semcancer.2009.05.006

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Neovascularization is one of the hallmarks associated with tumor growth. In the recent years, a number of angiogenesis inhibitors have been approved for clinical use in cancer patients. However, the efficacy of antiangiogenic therapy is in most cases short-lasting, with likely drug resistance developing within a few months. It is becoming clear also that there are a subset of malignant tumors that are inherently resistant to angiogenesis inhibition. The knowledge regarding resistance mechanisms towards angiogenesis inhibitors is still evolving and here we propose some theories and in some cases provide experimental evidence. (C) 2009 Elsevier Ltd. All rights reserved.

引用

收藏

页码：310 / 317

页数：8

相关论文

共 139 条

[1]

Abdollahi A, 2003, CANCER RES, V63, P8890

[2] Endostatin's antiangiogenic signaling network [J].

Abdollahi, A ;

Hahnfeldt, P ;

Maercker, C ;

Gröne, HJ ;

Debus, J ;

Ansorge, W ;

Folkman, J ;

Hlatky, L ;

Huber, PE .

MOLECULAR CELL, 2004, 13 (05) :649-663

[3] PGE2 induces angiogenesis via MT1-MMP-mediated activation of the TGFβ/Alk5 signaling pathway [J].

Alfranca, Arantzazu ;

Manuel Lopez-Oliva, Juan ;

Genis, Laura ;

Lopez-Maderuelo, Dolores ;

Mirones, Isabel ;

Salvado, Dolores ;

Quesada, Antonio J. ;

Arroyo, Alicia G. ;

Miguel Redondo, Juan .

BLOOD, 2008, 112 (04) :1120-1128

[4] Lymphangiogenesis in development and human disease [J].

Alitalo, K ;

Tammela, T ;

Petrova, TV .

NATURE, 2005, 438 (7070) :946-953

[5] Targeting EGFR activity in blood vessels is sufficient to inhibit tumor growth and is accompanied by an increase in VEGFR-2 dependence in tumor endothelial cells [J].

Amin, Dhara N. ;

Bielenberg, Diane R. ;

Lifshits, Eugene ;

Heymach, John V. ;

Klagsbrun, Michael .

MICROVASCULAR RESEARCH, 2008, 76 (01) :15-22

[6] AZD2171, a pan-VEGF receptor tyrosine kinase inhibitor, normalizes tumor vasculature and alleviates edema in glioblastoma patients [J].

Batchelor, Tracy T. ;

Sorensen, A. Gregory ;

di Tomaso, Emmanuelle ;

Zhang, Wei-Ting ;

Duda, Dan G. ;

Cohen, Kenneth S. ;

Kozak, Kevin R. ;

Cahill, Daniel P. ;

Chen, Poe-Jou ;

Zhu, Mingwang ;

Ancukiewicz, Marek ;

Mrugala, Maciej M. ;

Plotkin, Scott ;

Drappatz, Jan ;

Louis, David N. ;

Ivy, Percy ;

Scadden, David T. ;

Benner, Thomas ;

Loeffler, Jay S. ;

Wen, Patrick Y. ;

Jain, Rakesh K. .

CANCER CELL, 2007, 11 (01) :83-95

[7] Vascular remodeling and clinical resistance to antiangiogenic cancer therapy [J].

Bender, JG ;

Cooney, EM ;

Kandel, JJ ;

Yamashiro, DJ .

DRUG RESISTANCE UPDATES, 2004, 7 (4-5) :289-300

[8]

Benelli R, 2003, INT J ONCOL, V22, P87

[9] Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal [J].

Benjamin, LE ;

Golijanin, D ;

Itin, A ;

Pode, D ;

Keshet, E .

JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (02) :159-165

[10] New approaches to assessing and treating early-stage colon and rectal cancers: Cooperative group strategies for assessing optimal approaches in early-stage disease [J].

Benson, Al B., III .

CLINICAL CANCER RESEARCH, 2007, 13 (22) :6913S-6918S

← 1 2 3 4 5 6 7 8 9 10 →