Venous thromboembolism and cancer: a systematic review

Rodrigues, Celso Arrais; Ferrarotto, Renata; Filho, Roberto Kalil; Novis, Yana; Hoff, Paulo M.

doi:10.1007/s11239-010-0441-0

Cited by 44 publications

(42 citation statements)

References 116 publications

(171 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thromboembolic events (TEE) contribute significantly to cancer morbidity [1,2,3,4,5,6]. Cancer itself is a risk factor for TEE due to mechanisms such as tumor-induced vascular damage with pro-thrombotic effects, release of inflammatory cytokines, activation of the clotting cascade, expression of hemostatic proteins on tumor cells, inhibition of natural anticoagulants and reduced fibrinolysis [7,8].…”

Section: Introductionmentioning

confidence: 99%

High Rates of Thromboembolic Events in Patients with Germ Cell Cancer Undergoing Cisplatin-Based Polychemotherapy

Solari¹,

Krönig

Ihorst³

et al. 2016

Urol Int

View full text Add to dashboard Cite

Background: We examined whether or not extended prophylaxis with low molecular weight heparin (LMWH) would significantly reduce thromboembolic event (TEE) rates in germ cell cancer patients undergoing cisplatin-based chemotherapy. Patients and Methods: LMWH prophylaxis was given from the first day of chemotherapy until 21 days after completing the last chemotherapy cycle to 45 out of 93 (48.4%) patients (extended), and to 48 out of 93 (51.6%) patients during their hospitalization only (limited) between January 2008 and December 2013. Patients were analyzed retrospectively for TEEs such as deep vein thrombosis (DVT), pulmonary embolism (PE), myocardial infarction (MI) or peripheral arterial thrombosis. Results: A total of 22/93 (23.7%) patients experienced 30 TEE during chemotherapy: 12 out of 30 (40%) deep vein thrombosis, 4 out of 30 (13.3%) MI, 10 out of 30 (33.3%) PE and 4 out of 30 peripheral arterial thrombosis (13.3%). TEE rates in both groups did not differ significantly (extended: 26.7 vs. limited: 20.8%). Conclusions: The introduction of extended LMWH prophylaxis did not significantly reduce TEE rates in our patient cohort.

show abstract

Section: Introductionmentioning

confidence: 99%

High Rates of Thromboembolic Events in Patients with Germ Cell Cancer Undergoing Cisplatin-Based Polychemotherapy

Solari¹,

Krönig

Ihorst³

et al. 2016

Urol Int

View full text Add to dashboard Cite

show abstract

“…Thrombosis is considered an early clinical indication and frequent complication of cancer (1,2). Malignant tumors often exhibit increased expression of tissue factor and cancer procoagulant, which can be followed by activation of cell surface protease receptors and fibrin generation (3).…”

mentioning

confidence: 99%

Heparin Impairs Angiogenesis through Inhibition of MicroRNA-10b

Shen

Fang

et al. 2011

Journal of Biological Chemistry

View full text Add to dashboard Cite

Heparin, which has been used as an anticoagulant drug for decades, inhibits angiogenesis, whereas thrombin promotes tumor-associated angiogenesis. However, the mechanisms underlying the regulation of angiogenesis by heparin and thrombin are not well understood. Here, we show that microRNA-10b (miR-10b) is down-regulated by heparin and up-regulated by thrombin in human microvascular endothelial cells (HMEC-1). Overexpression of miR-10b induces HMEC-1 cell migration, tube formation, and angiogenesis, and downregulates homeobox D10 (HoxD10) expression via direct binding of miR-10b to the putative 3 UTR of HoxD10. In addition, HMEC-1 cell migration and tube formation are induced by HoxD10 knockdown, whereas angiogenesis is arrested when HoxD10 expression is increased after anti-miR-10b or heparin treatments. Furthermore, expression of miR-10b and its transcription factor Twist are up-regulated by thrombin, whereas HoxD10 expression is impaired by thrombin. Using quartz crystal microbalance analysis, we show that heparin binds to thrombin, thereby inhibiting thrombin-induced expression of Twist and miR-10b. However, the expression of miR-10b is not attenuated by heparin any more after thrombin expression is silenced by its siRNA. Interestingly, we find that heparin attenuates miR10b expression and induces HoxD10 expression in vivo to inhibit angiogenesis and impair the growth of MDA-MB-231 tumor xenografts. These results provide insight into the molecular mechanism by which heparin and thrombin regulate angiogenesis.Thrombosis is considered an early clinical indication and frequent complication of cancer (1, 2). Malignant tumors often exhibit increased expression of tissue factor and cancer procoagulant, which can be followed by activation of cell surface protease receptors and fibrin generation (3). In addition, tumor cells can interact with blood cells, particularly monocytes, macrophages, and platelets, leading to the generation of thrombin and thrombosis through the clotting cascade or platelet activation (4). Moreover, aggressive antitumor therapies such as chemotherapy, radiation, and surgery also increase the risk of thrombosis.Positive feedback signaling loops exist between tumor tissue and the coagulation system (5, 6). For instance, it is widely accepted that elements of the coagulation and fibrinolytic system may aid in cancer cell survival, proliferation, invasion, and metastasis, as well as tumor angiogenesis (7). Therefore, inhibition of the activation of coagulation could be a useful antitumor strategy. A number of studies have shown that anticoagulant drugs can extend survival in patients with certain types of cancer (8), and studies are currently ongoing to confirm the effects of anticoagulant therapy in a range of tumor types. However, the molecular mechanisms involved in the action of anticoagulants in this process are not well understood.Heparins, in particular those of low molecular weight, are effective in the prevention and treatment of thromboembolic events in cancer patients (9, 10). As early...

show abstract

“…As regards adverse events, 2 patients had cerebral ischemia during the treatment, but we know that cancer patients have an increased risk of venous thromboembolism (VTE) because malignancy is associated with a hypercoagulable state as a result of the release of inflammatory cytokines, the activation of the clotting system, a decrease in the level of natural anticoagulants and impaired fibrinolysis [17]. In particular, patients with primary brain tumors have a latent hypercoagulable state that predisposes them to thromboembolism.…”

Section: Discussionmentioning

confidence: 99%

Bevacizumab-Based Therapy for Patients with Brain Metastases from Non-Small-Cell Lung Cancer: Preliminary Results

et al. 2014

View full text Add to dashboard Cite

Background: Bevacizumab is a recombinant humanized monoclonal antibody that obstructs the vascular endothelial growth factor (VEGF) pathway.Despite its extensive employment in the treatment of primary tumors of the brain, experience of brain metastatic disease, a frequent complication in patients with lung cancer, is very limited. On the basis of the strong antiedemigenous effect and no risk of intracranial bleeding, we administered a bevacizumab-based chemotherapy to patients with non-small-cell lung cancer (NSCLC) and symptomatic metastatic brain lesions who were not suitable candidates for a specific local therapy. Methods: The patients received bevacizumab 7.5 mg/kg and cisplatin 75 mg/m² on day 1, and gemcitabine 1,250 mg/m² on days 1 and 8, every 21 days. Results: We studied 13 patients with clinical and radiological progressive brain metastases; the majority had a treatment-naïve disease. Bevacizumab-based chemotherapy was found to be well tolerated and effective: progression-free survival (PFS) was 9.1 months (range: 0.9-39.2+) and overall survival (OS) was 9.6 months (range 3-41.5+). Conclusions: Bevacizumab-based therapy proved to be feasible and safe. The PFS and the OS data are very encouraging as well as the symptomatic benefit due to bevacizumab's high capacity to provide a long-lasting decrease of perilesional edema.

show abstract

Venous thromboembolism and cancer: a systematic review

Cited by 44 publications

References 116 publications

High Rates of Thromboembolic Events in Patients with Germ Cell Cancer Undergoing Cisplatin-Based Polychemotherapy

High Rates of Thromboembolic Events in Patients with Germ Cell Cancer Undergoing Cisplatin-Based Polychemotherapy

Heparin Impairs Angiogenesis through Inhibition of MicroRNA-10b

Bevacizumab-Based Therapy for Patients with Brain Metastases from Non-Small-Cell Lung Cancer: Preliminary Results

Contact Info

Product

Resources

About