RESUMO
INTRODUCTION: Little is known about the clinical course and treatment decisions in patients with cancer-associated venous thromboembolism (VTE) beyond the initial treatment period of 3 to 6 months. This information is important for clinicians and patients to inform their decisions regarding duration of anticoagulation. MATERIALS AND METHODS: We reviewed health records from consecutive patients referred to our institution for cancer-associated VTE management between 2013 and 2015 to describe their clinical course and outcomes from 6 to 24 months following their index VTE. Details on patient and cancer characteristics, objectively documented recurrent venous thromboembolism (rVTE), clinically relevant bleeding (CRB) and overall mortality were captured. RESULTS: 524 patients met eligibility criteria and 322 were alive at 6 months after the index VTE. At 6 months, anticoagulation was continued in 222 patients (68.9%). During follow-up, there were 33 rVTE events in 30 patients (1-year cumulative incidence of 8.2%; 95% CI: 5.5%-11.6%), and 16 CRB events in 15 patients (1-year cumulative incidence of 4.1%; 95% CI: 2.3%-6.7%); 20 (60.6%) rVTE events and 13 (81.3%) CRB events occurred while on anticoagulation. One-year survival beyond 6 months was 73.7% (95% CI: 68.5%-78.2%). A higher proportion of patients with advanced cancer and receiving cancer treatment was found among those who continued anticoagulation beyond 6 months compared to those who stopped anticoagulation. CONCLUSIONS: Patients with cancer-associated VTE who are alive at 6 months after VTE diagnosis remain at high risk of rVTE, CRB and death.
Assuntos
Neoplasias , Tromboembolia Venosa , Anticoagulantes/uso terapêutico , Coagulação Sanguínea , Hemorragia , Humanos , Neoplasias/complicações , Recidiva , Fatores de Risco , Tromboembolia Venosa/complicações , Tromboembolia Venosa/tratamento farmacológicoRESUMO
Since its discovery in 1979, p53 has become the focus of intensive cancer-based research in laboratories around the world. The p53 protein mediates critical cellular functions including the response to genotoxic stress, differentiation, senescence, and apoptosis, and has been shown to be mutated in a large proportion of human cancers. These observations led many to speculate that targeting the p53 pathway would result in the development of successful anti-cancer treatments. In spite of this, 30 years later, p53 has yet to fulfill this promise. However, new insights into small molecule combination therapies, microRNA regulation, structuring of clinical trials, and potential involvement in stem cell regulation may help p53 reach its potential.