Thrombotic Events in Patients With Cancer Receiving Antiangiogenesis Agents
University of Utah, Division of Hematology, Blood/Marrow Transplant and Myeloma Program, Salt Lake City, UT, USA. Journal of Clinical Oncology
(Impact Factor: 18.43).
09/2009; 27(29):4865-73. DOI: 10.1200/JCO.2009.22.3875
Tumor-associated neoangiogenesis has recently become a suitable target for antineoplastic drug development. In this overview, we discuss specific drug-associated hemostatic complications, the already known pathogenetic mechanisms involved, and the effect of varying antithrombotic strategies. Multiple agents with angiogenic inhibitory capacity (thalidomide, lenalidomide, bevacizumab, sunitinib, sorafenib, and sirolimus) have obtained US Food and Drug Administration approval, and many others have entered clinical trials. Arterial and venous thromboembolism and hemorrhage have emerged as significant toxicities associated with the use of angiogenesis inhibitors. We present a detailed analysis of the literature on thrombotic complication of antiangiogenic drugs. Close attention to hemostatic complications during antiangiogenic treatment is warranted. Further studies are required to better understand the pathophysiologic mechanisms involved and to define a safe prophylactic strategy.
Available from: Fabio Martinelli
- "The most thrombogenic chemotherapeutic agents are fluorouracil, cisplatin and paclitaxel (Khorana et al., 2005, 2013). A pro-thrombotic effect is recognized also for hormonal agents such as tamoxifene (Blom et al., 2005; Cuzick et al., 2007) and for antiangiogenetic agents, including monoclonal antibodies and tyrosine kinase inhibitors (Zangari et al., 2009; Raschi and De Ponti, 2012). "
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ABSTRACT: BACKGROUND Compared with the general population, cancer patients have a higher risk of venous thromboembolism as well as arterial thrombotic
events such as stroke, myocardial infarction and peripheral arterial embolism. Therefore a possible concern for women with
malignancies undergoing ovarian stimulation for fertility preservation is the increased risk of venous or arterial thrombosis.
Human Reproduction Update 07/2014; 20(6). DOI:10.1093/humupd/dmu035 · 10.17 Impact Factor
Available from: Adriana Albu
- "The risk is additionally increased if chemotherapy is combined with steroids (Shen et al, 2011) or erythropoietin (Bennet et al, 2008). The inhibitors of angiogenesis (thalidomide, lenalidomide, bevacizumab, sunitinib, sorafenib, and sirolimus) used as novel antineoplasic therapy are associated with an increase in arterial and venous thromboembolism and hemorrhage (Zangari et al, 2009). Gemcitabine is a deoxycytidine analogue related to cytarabine, that has been shown to improve evolution in patients with advanced PC. Deep venous thrombosis was found in one study in 3.2% of patients treated with gemcitabine (Kaye,1994). "
Pancreatic Cancer - Clinical Management, 03/2012; , ISBN: 978-953-51-0394-3
Available from: Nigel S Key
- "As a result, abnormal apoptosis of endothelial cells leads to the exposure of highly prothrombotic basement membrane (Zangari et al, 2009). In addition, the prothrombotic effect may result from reduced levels of prostaglandin 1-2 and NO, leading to increased platelet activation (Zangari et al, 2009). Table III. "
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ABSTRACT: The pathophysiology of pulmonary hypertension (PHT) in sickle cell disease (SCD) is probably multifactorial. Soluble fms-like tyrosine kinase-1 (sFLT-1) is a member of the vascular endothelial growth factor receptor (VEGFR) family. By adhering to and inhibiting VEGF and placenta growth factor, it induces endothelial dysfunction. We sought to evaluate the association of sFLT-1 with clinical complications of SCD. We confirmed that sFLT-1 was significantly elevated in SCD patients compared to healthy, race-matched control subjects. The level of sFLT-1 was significantly higher in patients with PHT, but no association was observed between sFLT-1 and the frequency of acute pain episodes or history of acute chest syndrome. sFLT-1 was correlated with various measures of haemolysis, erythropoietin and soluble vascular cell adhesion molecule-1. By inducing endothelial dysfunction, sFLT-1 may contribute to the pathogenesis of SCD-associated PHT, although this effect does not appear to be independent of haemolysis.
British Journal of Haematology 02/2011; 152(4):485-91. DOI:10.1111/j.1365-2141.2010.08410.x · 4.71 Impact Factor
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