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Preview of articles to be published Jan. 3, 2012
Date:1/3/2012

imvastatin

AUTHOR CONTACT:
Nigel Mackman
University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Phone: 919 843 3961; Fax: 919 843 4896; E-mail: nmackman@med.unc.edu
View this article at: http://www.jci.org/articles/view/58969?key=b8d507e8dd483209c4ad

ACCOMPANYING COMMENTARY

TITLE: Teaching an old dog new tricks: potential antiatherothrombotic use for statins

AUTHOR CONTACT:

Roy L Silverstein
Medical College of Wisconsin, Milwaukee, WI, USA
Phone: (414) 805-0518; Fax: (414) 805-0524; E-mail: rsilverstein@mcw.edu
View this article at: http://www.jci.org/articles/view/61857?key=38138bc567017dc85bec


ONCOLOGY

Cooperation between two mutations drives ovarian cancer

Erroneous activation of signaling pathways that drive cell growth occurs in many human cancers. Mutations in one subunit of PI3K (encoded by PIK3CA) are frequent in human tumors, and these can lead to activation of the AKT signaling pathway. However, it was unclear whether this mutation was sufficient to drive tumor development. In this paper, Wayne Philips and his team, at the Peter MacCallum Cancer Center in Melbourne, Australia, generated a conditional knock-in mouse model of a common human Pik3ca mutation. They found that on its own, expression of this mutation in the mouse ovary induced premalignant hyperplasia of the ovarian surface epithelium (OSE), but not tumors. However, when the Pik3ca mutation was expressed in combination with deletion of the tumor suppressor Pten, mice developed ovarian serous adenocarcinomas and granulosa cell tumors. Pharmacological inhibition of PI3K/mTOR in these mice delayed tumor growth and prolonged su
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Contact: Karen Honey
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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