The platelet contribution to cancer progression

被引:600
作者
Bambace, N. M. [1 ]
Holmes, C. E. [1 ]
机构
[1] Univ Vermont, Dept Med, Div Hematol & Oncol, Burlington, VT 05401 USA
关键词
angiogenesis; cancer; metastases; platelets; TCIPA; ENDOTHELIAL GROWTH-FACTOR; CELL LUNG-CANCER; VON-WILLEBRAND-FACTOR; INTERACTION IN-VITRO; P-SELECTIN; ACTIVATED PLATELETS; TUMOR ANGIOGENESIS; UP-REGULATION; STANDARDIZATION COMMITTEE; HEMOSTASIS SUBCOMMITTEE;
D O I
10.1111/j.1538-7836.2010.04131.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Traditionally viewed as major cellular components in hemostasis and thrombosis, the contribution of platelets to the progression of cancer is an emerging area of research interest. Complex interactions between tumor cells and circulating platelets play an important role in cancer growth and dissemination, and a growing body of evidence supports a role for physiologic platelet receptors and platelet agonists in cancer metastases and angiogenesis. Platelets provide a procoagulant surface facilitating amplification of cancer-related coagulation, and can be recruited to shroud tumor cells, thereby shielding them from immune responses, and facilitate cancer growth and dissemination. Experimental blockade of key platelet receptors, such as GP1b/IX/V, GPIIbIIIa and GPVI, has been shown to attenuate metastases. Platelets are also recognized as dynamic reservoirs of proangiogenic and anti-angiogenic proteins that can be manipulated pharmacologically. A bidirectional relationship between platelets and tumors is also seen, with evidence of 'tumor conditioning' of platelets. The platelet as a reporter of malignancy and a targeted delivery system for anticancer therapy has also been proposed. The development of platelet inhibitors that influence malignancy progression and clinical testing of currently available antiplatelet drugs represents a promising area of targeted cancer therapy.
引用
收藏
页码:237 / 249
页数:13
相关论文
共 178 条
[1]  
ABBASCIANO V, 1995, ONCOLOGY, V52, P381
[2]   Microparticles, thrombosis and cancer [J].
Aharon, Anat ;
Brenner, Benjamin .
BEST PRACTICE & RESEARCH CLINICAL HAEMATOLOGY, 2009, 22 (01) :61-69
[3]   Membrane type-1 matrix metalloproteinase stimulates tumour cell-induced platelet aggregation: role of receptor glycoproteins [J].
Alonso-Escolano, D ;
Strongin, AY ;
Chung, AW ;
Deryugina, EI ;
Radomski, MW .
BRITISH JOURNAL OF PHARMACOLOGY, 2004, 141 (02) :241-252
[4]   Inhibition of tumor cell-induced platelet aggregation and lung metastasis by the oral GpIIb/IIIa antagonist XV454 [J].
Amirkhosravi, A ;
Mousa, SA ;
Amaya, M ;
Blaydes, S ;
Desai, H ;
Meyer, T ;
Francis, JL .
THROMBOSIS AND HAEMOSTASIS, 2003, 90 (03) :549-554
[5]  
Amirkhosravi A, 1999, PLATELETS, V10, P285
[6]   TYPE-BETA TRANSFORMING GROWTH-FACTOR IN HUMAN-PLATELETS - RELEASE DURING PLATELET DEGRANULATION AND ACTION ON VASCULAR SMOOTH-MUSCLE CELLS [J].
ASSOIAN, RK ;
SPORN, MB .
JOURNAL OF CELL BIOLOGY, 1986, 102 (04) :1217-1223
[7]  
AVRAHAM H, 1994, BLOOD, V83, P2126
[8]   Platelet and osteoclast β3 integrins are critical for bone metastasis [J].
Bakewell, SJ ;
Nestor, P ;
Prasad, S ;
Tomasson, MH ;
Dowland, N ;
Mehrotra, M ;
Scarborough, R ;
Kanter, J ;
Abe, K ;
Phillips, D ;
Weilbaecher, KN .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (24) :14205-14210
[9]   The effect of P2Y-mediated platelet activation on the release of VEGF and endostatin from platelets [J].
Bambace, Nadia M. ;
Levis, Jamie E. ;
Holmes, Chris E. .
PLATELETS, 2010, 21 (02) :85-93
[10]   Mechanisms of cellular activation by platelet microparticles [J].
Barry, OP ;
FitzGerald, GA .
THROMBOSIS AND HAEMOSTASIS, 1999, 82 (02) :794-800