My current research interests in the Department of Interdisciplinary Oncology, LSUHSC focus on the role of the anticoagulant Protein S (PS) in regulation of Thrombosis and Hemophilia, Currently, we identified a new role of PS in regulating Pancreatic Cancer.
Recently, I have been actively involved in collaborative research work with Dr. Samarpan Majumder, Dept. of Genetics, LSUHSC, where we are investigating the role PS), in pancreatic ductal adenocarcinoma (PDAC). PDAC patients have a much higher relative risk of developing cancer associated thrombosis (CAT) compared to other cancers and many PDAC patients have significantly low PS level. CAT is a concept whereby cancer cells promote thromboembolism, primarily venous thromboembolism (VTE). VTE in cancer patients remains an underestimated major health problem. Cancer increases the risk of thromboembolism anywhere from 4- to 7-fold to as much as 40- to 60-fold, depending on the type and stage of the malignancy. In fact, as many as 10 to 20% of deaths in adults with cancer are directly related to thromboembolism rather than the malignancy itself making thromboembolism the second leading cause of death in patients with cancer. Of all cancer types, PDAC is associated with the highest risk of developing VTE. About one in five patients with PDAC develops VTE. Emerging clinical data strongly suggest that anticoagulant treatments may improve cancer patient survival by decreasing thromboembolic complications as well as by anticancer effects, but few data is available in PC patients due to their short life expectancy. The aggressive and invasive properties of PDAC coupled with poor diagnostic options contribute to the high mortality rate since most patients are present with late-stage disease. The scope and significance of PS supplementation as a primary treatment modality to minimize tumor hypoxia and improve underlying cancer associated thrombosis (CAT) risk in PC is high.
