The proto-oncogene Ets-1 is a member of the Ets family of transcription factors which share a unique DNA binding domain, the Ets domain. Ets binding sites have been described on the promoters or enhancers of many proteinases and several Ets members transcriptionally regulate such promoters in transient cotransfection assays. Ets-1 is involved in both normal and pathological functions. Ets-1 is expressed in a variety of cells, including endothelial cells, vascular smooth muscle cells and epithelial cells. Ets-1 regulates the expression of several angiogenic and extracellular matrix remodeling factors promoting an invasive phenotype. The Ets family of transcription factors may play a role in the disease progression of breast cancer. In tumors, including breast neoplasia, Ets-1 expression is indicative of poorer prognosis. This review will summarize the role of Ets-1 in both the tumor cells, and the tumor endothelial cells as it relates to breast tumor growth and spread.
This report characterizes risk factors in patients who suffer pulmonary embolus (PE) after insertion of vena caval filter (VCF) and formulates an organized diagnostic and therapeutic plan of management. Three hundred eighteen patients were included in a review of patients undergoing insertion of VCF from 1989 to 1995. Ten patients (six men and four women, ages 25–72 years) from this group (3.1%) experienced PE after VCF insertion. Risk factors for deep venous thrombosis were documented in these ten patients. Venacavography was performed after diagnosis of PE. Thrombus length measured from the apex of the filter was used to determine further therapy. Thrombus 5 cm or greater in length was treated with a second VCF (VCF-2). Smaller clots were treated with anticoagulation (AC). All patients treated with AC underwent repeat vena caval study (CT scan or venacavagram) 10 days to 18 months after treatment. PE occurred from 8 days to 5.5 years after original VCF insertion. Five patients suffered PE longer than 6 months (range, 21–66 months; mean, 39 months) after VCF insertion. Venacavagrams demonstrated thrombus in all ten patients with PE. Six patients were treated with VCF-2 and four patients with AC. Dissolution of thrombus was seen on follow-up in all patients given AC. All 10 patients harbored at least two risk factors for deep venous thrombosis. Malignancy was found in only two patients. Five patients were found to have procoagulant states characterized by decreased levels of anti-thrombin III or protein C or S. No postoperative deaths or early recurrent PE occurred. One patient experienced another PE 5 years after treatment with AC when she discontinued warfarin. Contraindications to AC appeared to be self-limited, and all patients were discharged on warfarin. No significant bleeding occurred during early follow-up. Our findings confirm the reliability and low complication rate for VCF. Patients experiencing PE after insertion of VCF mandate an aggressive diagnostic approach that should include venacavography and a search for identifiable risk factors including procoagulant state. Treatment with AC and insertion of a second VCF both give favorable results. All patients appear to benefit from short- or long-term warfarin therapy, and contraindications to AC frequently are self-limited. Therapy based on clot size warrants further study.
Acute pulmonary embolism (PE) can be devastating. It is classified into three categories based on clinical scenario, elevated biomarkers, radiographic or echocardiographic features of right ventricular strain, and hemodynamic instability. Submassive PE is diagnosed when a patient has elevated biomarkers, CT-scan, or echocardiogram showing right ventricular strain and no signs of hemodynamic compromise. Thromboemboli in the acute setting increase pulmonary vascular resistance by obstruction and vasoconstriction, resulting in pulmonary hypertension. This, further, deteriorates symptoms and hemodynamic status. Studies have shown that elevated biomarkers and right ventricular (RV) dysfunction have been associated with increased risk of mortality. Therefore, aggressive treatment is necessary to “unload” right ventricle. The treatment of submassive PE with thrombolysis is controversial, though recent data have favored thrombolysis over conventional anticoagulants in acute setting. The most feared complication of systemic thrombolysis is intracranial or major bleeding. To circumvent this problem, a newer and safer approach is sought. Ultrasound-accelerated thrombolysis is a relatively newer and safer approach that requires local administration of thrombolytic agents. Herein, we report a case series of five patients who underwent ultrasound-accelerated thrombolysis with notable improvement in symptoms and right ventricular function.
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