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This Week in NEJM: Feb 16, 2012

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In NEJM this week, researchers in Europe and Canada report a study on the use of semuloparin for thromboprophylaxis in cancer patients receiving chemotherapy. The team randomly assigned 1,608 patients with metastatic or locally advanced solid tumors to receive either subcutaneous semuloparin or placebo in addition to chemotherapy. They found that venous thromboembolism occurred in 1.2 percent of patients who had received semuloparin compared with 3.4 percent in the placebo group. "Semuloparin reduces the incidence of thromboembolic events in patients receiving chemotherapy for cancer, with no apparent increase in major bleeding," the authors write.

In a related editorial in NEJM this week, the State University of New York at Buffalo's Elie Akl and McMaster University's Holger Schünemann ask whether routine heparin for cancer patients might be one answer to the problem of venous thromboembolism. "The antithrombotic effect of heparins is established, and it is speculated that a direct antitumor effect of heparin might translate into a survival benefit in patients with cancer," the authors write. "This antitumor activity of heparins mechanistically includes the inhibition of cell–cell interaction by blocking cell-adhesion molecules (selectins), the inhibition of extracellular-matrix protease heparanase, and the inhibition of angiogenesis." The decision to include heparin in cancer treatment should be based on the patient's preferences and other clinical factors, they add. More research is also needed on whether treatment with heparin would have an effect on quality of life or tumor growth, and which cancers might respond best to such therapy.

Also in NEJM this week, researchers in the US and UK report on paraneoplastic thrombocytosis in ovarian cancer, and the association between platelet count and disease progression. The team analyzed data from 619 patients with epithelial ovarian cancer, and found that thrombocytosis was significantly associated with advanced disease and shortened survival. "These findings support the existence of a paracrine circuit wherein increased production of thrombopoietic cytokines in tumor and host tissue leads to paraneoplastic thrombocytosis, which fuels tumor growth," the authors write. "We speculate that countering paraneoplastic thrombocytosis either directly or indirectly by targeting these cytokines may have therapeutic potential."

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