The many spaces of uPAR: delivery of theranostic agents and nanobins to multiple tumor compartments through a single target.
The many spaces of uPAR: delivery of theranostic agents and nanobins to multiple tumor compartments through a single target.
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DOI：
10.7150/thno.4953
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发表时间：
2013
期刊：
影响因子：
12.4
通讯作者：
Mazar AP
中科院分区：
文献类型：
--
作者：
O'Halloran TV;Ahn R;Hankins P;Swindell E;Mazar AP
The urokinase plasminogen activator (uPA) system is a proteolytic system comprised of uPA, a cell surface receptor for uPA (uPAR), and an inhibitor of uPA (PAI-1) and is implicated in many aspects of tumor growth and metastasis. The uPA system has been identified in nearly all solid tumors examined to date as well as several hematological malignancies. In adults, transient expression of the uPA system is observed during wound healing and inflammatory processes while only limited expression is identified in healthy, quiescent tissue. Members of the uPA system are expressed not only on cancer cells but also on tumor-associated stromal cells. These factors make the uPA system an ideal therapeutic target for cancer therapies. To date most therapeutics targeted at the uPA system have been inhibitors of either the uPA-uPAR interaction or uPA proteolysis but have not shown robust anti-tumor activity. There is now mounting evidence that uPAR participates in a complex signaling network central to its role in cancer progression, which provides a basis for the hypothesis that uPAR may be a marker for cancer stem cells. Several new uPAR-directed therapies have recently been developed based on this new information. A monoclonal antibody has been developed that disrupts the interactions of uPAR with signaling partners and is poised to enter the clinic. In addition, nanoscale drug delivery vehicles targeted to the uPA system using monoclonal antibodies, without disrupting the normal functioning of the system, are also in development. This review will highlight some of these new discoveries and the new uPA system-based therapeutic approaches that have arisen from them.
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影响因子：
5.2
作者：
Cortes-Dericks, Lourdes;Carboni, Giovanni L.;Karoubi, Golnaz
通讯作者：
Karoubi, Golnaz
影响因子：
8.8
作者：
Cantero D;Friess H;Deflorin J;Zimmermann A;Bründler MA;Riesle E;Korc M;Büchler MW
通讯作者：
Büchler MW
DOI：
10.1158/1078-0432.ccr-08-1631
发表时间：
2009-01-15
期刊：
Clinical cancer research : an official journal of the American Association for Cancer Research
影响因子：
--
作者：
Bin Hafeez B;Adhami VM;Asim M;Siddiqui IA;Bhat KM;Zhong W;Saleem M;Din M;Setaluri V;Mukhtar H
通讯作者：
Mukhtar H
影响因子：
82.9
作者：
HEISS, MM;ALLGAYER, H;SCHILDBERG, FW
通讯作者：
SCHILDBERG, FW
影响因子：
3.7
作者：
Gutova M;Najbauer J;Gevorgyan A;Metz MZ;Weng Y;Shih CC;Aboody KS
通讯作者：
Aboody KS