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JCI online early table of contents: April 13, 2009
Date:4/13/2009

who really do not require treatment and should not be exposed to the considerable side effects of therapy, from men who have disease that requires treatment. However, Antonella Farsetti and colleagues, at Regina Elena Cancer Institute, Italy, hope that by using cultured cells from men with prostate cancer to define a molecular mechanism underlying the most aggressive form of prostate cancer, specifically a pathway involving the proteins eNOS, HIF-2-alpha, and ER-beta, they might have generated data that will help develop diagnostic approached that can determine which individuals have aggressive disease.

TITLE: Endothelial NOS, estrogen receptorbeta, and HIFs cooperate in the activation of a prognostic transcriptional pattern in aggressive human prostate cancer

AUTHOR CONTACT:
Antonella Farsetti
Regina Elena Cancer Institute, Rome, Italy.
Phone: 39-06-5266-2531; Fax: 39-06-41805-26; E-mail: afarsetti@gmail.com.

View the PDF of this article at: https://www.the-jci.org/article.php?id=35079


METABOLIC DISEASE: New insights into hardening of the arteries

Atherosclerosis, or hardening of the arteries, is a disease of the major arterial blood vessels that is a common cause of heart attack and stroke. The uptake of molecules comprised of both protein and fat-soluble substances such as cholesterol (lipoproteins) by cells known as macrophages is vital to the development of atherosclerosis; however, the method of lipoprotein uptake in vivo remains poorly defined. In a new study, Howard S. Kruth and his colleagues at the National Heart, Lung, and Blood Institute, Maryland, found that cultured human and mouse macrophages took up fluorescent lipoprotein-sized nanoparticles by a process known as pintocytosis. They also found that when mice susceptible to atherosclerosis were injected with these particle
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Contact: Karen Honey
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215-573-1850
Journal of Clinical Investigation
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