Los Angeles (Embargoed until March 17, 2002, 1pm, EST) Aggressive ovarian cancer may be linked to the presence of thrombocytosis, a blood disorder characterized by high platelet cell counts, report investigators at Cedars-Sinai Medical Center. The findings, presented at the annual meeting of the Society of Gynecologic Oncologists, may lead to the development of more targeted therapies and help physicians to offer their patients more effective treatment options.
Our findings show that thrombocytosis correlates with a more aggressive tumor biology in ovarian cancer and a poorer response to treatment, said Dr. Beth Karlan, Medical Director of the Womens Cancer Research Institute at Cedars-Sinai Medical Center and senior author of the study. Knowing which patients have this disorder in addition to their cancer, will enable us to select patients who might benefit from experimental and other treatment approaches.
Platelets, the smallest of the blood cells, are involved in clotting and enable the body to control bleeding. In normal conditions, platelet levels are regulated by factors in the bone marrow, but cancer cells may secrete substances that induce the marrow to produce platelets in excessively large quantities. In turn, platelets may then produce factors that cause cancer cells to grow or spread.
To determine whether thrombocytosis played a role in ovarian cancer tumor growth and metastasis, the investigators examined the records of 183 consecutive patients with and without thrombocytosis who had undergone surgery for advanced ovarian cancer. They found that 41 of the 183 patients demonstrated thrombocytosis prior to surgery and that those with the disorder had higher CA-125 levels, (a marker for ovarian cancer), more advanced stage disease, higher grade tumors, and a greater tendency of cancer that had spread to the lymph nodes.
These findings indicate that thrombocytosis is somehow linked to more aggressive ovarian cancer,
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Contact: Kelli Stauning
kelli.stauning@cshs.org
310-423-3674
Cedars-Sinai Medical Center
17-Mar-2002