Originally published as JCO Early Release 10.1200/JCO.2009.22.7199 on September 8 2009

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Genetic Link Between Cancer and Thrombosis

From the Institute for Cancer Research and Treatment, University of Turin Medical School, Candiolo, Torino, Italy.

Corresponding author: Carla Boccaccio, MD, Institute for Cancer Research and Treatment, Str Prov 142, I-10060 Candiolo, Torino, Italy; e-mail: carla.boccaccio{at}ircc.it.

From the beginning of their lives, cancer cells exert a procoagulant activity in their microenvironment, which can extend systemically and become clinically evident as Trousseau's syndrome, the well-known association between tumor and thrombosis. It is becoming clear that the genetic mechanisms responsible for neoplastic transformation (activation of oncogenes such as RAS or MET, and inactivation of tumor suppressor genes such as p53 or PTEN) directly induce the expression of genes controlling hemostasis. Activation of blood coagulation results in a selective advantage for cancer cells, as fibrin provides a scaffold for anchorage and invasion, and coagulation proteins induce receptor-mediated intracellular signals promoting invasive growth. Targeting the tumor procoagulant activity can fight not only a dangerous tumor adverse effect, but also the core mechanisms of cancer onset and progression.

Supported by Italian Association for Cancer Research, Compagnia di S.Paolo, CRT Foundation, European Union Framework Programs (FP7 Microenvimet No. 201279 and SFMET No. 201640), Italian Ministry of University and Research, Regione Piemonte Ricerca Sanitaria Finalizzata.

Authors' disclosures of potential conflicts of interest and author contributions are found at the end of this article.

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