Risk factors for cancer-associated VTE include certain cancer types (e.g. pancreatic adenocarcinoma), chemotherapy, and the use of erythropoiesis-stimulating agents, central venous catheters, and surgery. We studied the risk factors for cancer-associated VTE in our institution.
Thrombosis occurs at sites of injury to the vessel wall, by inflammatory processes leading to activation of platelets, platelet adherence to the vessel wall and the formation of a fibrin network. A thrombus that goes on to occlude a blood vessel is known as a thromboembolism.
Venous thromboembolism begins with deep vein thrombosis (DVT), which forms in the deep veins of the leg (calf) or pelvis. In some cases, the DVT becomes detached from the vein and is transported to the right-hand side of the heart, and from there to the pulmonary arteries, giving rise to a pulmonary embolism (PE). Certain factors predispose patients toward the development of venous thromboembolism (VTE), including surgery, trauma, hospitalization, immobilization, cancer, long-haul travel, increased age, obesity, major medical illness and previous VTE; in addition, there may also be a genetic component to VTE. VTE is responsible for a substantial number of deaths per annum in Europe. Anticoagulants are the mainstay of both VTE treatment and VTE prevention, and many professional organizations have published guidelines on the appropriate use of anticoagulant therapies for VTE. Treatment of VTE aims to prevent morbidity and mortality associated with the disease, and any long-term complications such as VTE recurrence or post-thrombotic syndrome. Generally, guidelines recommend the use of low molecular weight heparins (LMWH), unfractionated heparin (UFH) or fondaparinux for the pharmacological prevention and treatment of VTE, with the duration of therapy varying according to the baseline characteristics and risk profile of the individual. Despite evidence showing that the use of anticoagulation prevents VTE, the availability of several convenient, effective anticoagulant therapies and the existence of clear guideline recommendations, thromboprophylaxis is underused, particularly in patients not undergoing surgery.
Greater adherence to guideline-recommended therapies, such as LMWH, which can be administered on an outpatient basis, should reduce the mortality associated with this preventable disease.
Protein S is a vitamin K-dependent anticoagulant protein. It functions as a cofactor of activated protein C to inactivate activated factor V (FVa) and activated factor VIII (FVIIIa). Its deficiency is a rare condition and can lead to deep vein thrombosis, pulmonary embolism or stroke. It is often treated with long-term anti-coagulant therapy.
Protein S deficiency may be hereditary or acquired; the latter is usually due to hepatic diseases or a vitamin K deficiency. Protein S deficiency manifests as an autosomal dominant trait; manifestations of thrombosis are observed in both heterozygous and homozygous genetic deficiencies of protein S. This case report is of DVT due to Protein S deficiency in a 53 year old male. Venous Doppler was used to diagnose DVT and free Protein S level measured by ELISA. IVC filter was placed on the third day of admission.
Anti-angiogenic therapies of solid cancers aim at specifically destroying the tumor vasculature in order to "asphyxiate" the tumors. Since few years, they represent a novel therapeutic tool, which allowed to significantly improve the survival of patients suffering from colon, breast, kidney and lung cancers. However, these therapies are limited in their efficacy by the appearance of tumor resistance phenomena.
In this review, I describe the molecular and cellular mechanisms of tumor angiogenesis with a special focus on the important roles played by hypoxia, the endothelial growth factor VEGF and the endothelial tip-cells located at the extremity of sprouting neo-vessels. I present the factors that respectively control the activation phase and the maturation phase of angiogenesis, as well as their mechanisms of action.
In a second part, the efficacy and the limits of anti-angiogenic therapies presently available on the market are described, and the recent elucidation of some molecular mechanisms of tumor resistance to anti-angiogenic therapies is reviewed.
While no real improvement in the long term survival has been obtained in lung cancer, during this decade a significant improvement in cancer control has been obtained by biology driven targeted therapy as with anti EGFR tyrosine kinase.
Two phases can be described in the knowledge of lung cancer biology: a first phase open in the 1980s describing the main molecular anomalies and impaired cell control mechanisms, and a second phase starting in the 2004-2005 giving rise to the therapeutic applications of this knowledge. A new molecular classification of lung cancer, particularly adenocarcinomas will soon be proposed for therapeutic application.