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JCI early table of contents for Nov. 12, 2012
Date:11/12/2012

he Journal of Clinical Investigation, researchers led by Constantinos Koumenis at the University of Pennsylvania found that the oncogene c-Myc activated the UPR to increase cell survival and reduce a cell recycling process known as autophagy. By blocking c-Myc activation of the UPR in mice, Koumenis and colleagues were able to prevent the development of lymphoma. These findings suggest that inhibition of UPR may be effective in cancers characterized by enhanced c-Myc expression, such as Burkitt's lymphoma, colorectal cancer, breast cancer, and melanoma.

TITLE:
ER stress-mediated autophagy promotes Myc-dependent transformation and tumor growth

AUTHOR CONTACT:
Constantinos Koumenis
Univ. Pennsylvania, Philadelphia, PA, USA
Phone: 215-898-0076; E-mail: koumenis@xrt.upenn.edu

View this article at: http://www.jci.org/articles/view/62973?key=46032c58d4d36f3b1fbc


Immune cells have differential effects on recovery after acute kidney injury

Acute kidney injury (AKI) is defined as an abrupt decrease in kidney function. The renal tubule cells are the primary targets for injury. During AKI, these cells either temporarily quit functioning or die altogether. There is increasing evidence that immune cells are the source of renal tubule damage; treatments that prevent these cells from reaching the renal tubule can reduce kidney injury. In a study published in the Journal of Clinical Investigation, researchers led by Raymond Harris at Vanderbilt University used a mouse model of AKI to study the activity of macrophages, a specific type of immune cell, in the renal tubule. They found that two different types of macrophages accumulated in the kidney. M1 macrophages enhanced inflammation and injury, while M2 macrophages promoted healing. Blocking the activity of CSF1, a growth f
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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