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Through genetic analysis, researchers used gene expression profiles to differentiate between several clinical phenotypes of VTE and distinguish high-risk patients from both low-risk patients and healthy controls, in a study published in Thrombosis Research.
Dr. Deborah A. Lewis of Duke University Medical Center and her associates used differential expression analysis to find several genes previously identified as potentially having a role in the development of thrombotic disorders, including SELP, KLKB1, ANXA5, andCD46. They then compared the genetic profiles of 107 patients, separated into low-, moderate-, or high-risk groups based on their clinical presentations of VTE, as well as 25 controls.
The most accurate comparisons were between the high-risk and low-risk groups, the high-risk group and the healthy controls, and the low-risk group and healthy controls, where the AUC levels were 0.81, 0.84 and 0.80 respectively.
“The profiles obtained … provide insights into approaches that might be useful in the identification of individuals with a single thrombotic event who are at highest risk for a recurrent VTE after completing a standard course of therapy,” the investigators wrote.
For the full article, click here (Thromb. Res. 2015 [doi:10.1016/j.thromres.2015.02.003]).
Through genetic analysis, researchers used gene expression profiles to differentiate between several clinical phenotypes of VTE and distinguish high-risk patients from both low-risk patients and healthy controls, in a study published in Thrombosis Research.
Dr. Deborah A. Lewis of Duke University Medical Center and her associates used differential expression analysis to find several genes previously identified as potentially having a role in the development of thrombotic disorders, including SELP, KLKB1, ANXA5, andCD46. They then compared the genetic profiles of 107 patients, separated into low-, moderate-, or high-risk groups based on their clinical presentations of VTE, as well as 25 controls.
The most accurate comparisons were between the high-risk and low-risk groups, the high-risk group and the healthy controls, and the low-risk group and healthy controls, where the AUC levels were 0.81, 0.84 and 0.80 respectively.
“The profiles obtained … provide insights into approaches that might be useful in the identification of individuals with a single thrombotic event who are at highest risk for a recurrent VTE after completing a standard course of therapy,” the investigators wrote.
For the full article, click here (Thromb. Res. 2015 [doi:10.1016/j.thromres.2015.02.003]).
Through genetic analysis, researchers used gene expression profiles to differentiate between several clinical phenotypes of VTE and distinguish high-risk patients from both low-risk patients and healthy controls, in a study published in Thrombosis Research.
Dr. Deborah A. Lewis of Duke University Medical Center and her associates used differential expression analysis to find several genes previously identified as potentially having a role in the development of thrombotic disorders, including SELP, KLKB1, ANXA5, andCD46. They then compared the genetic profiles of 107 patients, separated into low-, moderate-, or high-risk groups based on their clinical presentations of VTE, as well as 25 controls.
The most accurate comparisons were between the high-risk and low-risk groups, the high-risk group and the healthy controls, and the low-risk group and healthy controls, where the AUC levels were 0.81, 0.84 and 0.80 respectively.
“The profiles obtained … provide insights into approaches that might be useful in the identification of individuals with a single thrombotic event who are at highest risk for a recurrent VTE after completing a standard course of therapy,” the investigators wrote.
For the full article, click here (Thromb. Res. 2015 [doi:10.1016/j.thromres.2015.02.003]).