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JCI early table of contents for July 16, 2012
Date:7/16/2012

lly stable cancers raises the possibility that changes in few genes that regulate chromatin structure and gene expression are capable of driving cancer formation. Dr. Charles Roberts and colleauges at the Dana-Farber Cancer Institute in Boston sequenced the expressed genes of rhabdoid tumors, highly aggressive cancers of early childhood. These tumors typically exhibit loss of a protein known as SMARCB1, a subunit of the chromatin remodeling complex that is important in controlling gene transcription. The Roberts group identified an extremely low rate of mutations, with loss of SMARCB1 as the only recurrent event. Their results demonstrate that high mutation rates are typically associated with cancer development is not required in all tumors, particularly for cancers driven by mutation of a chromatin remodeling complex. Thus, remarkably simple genetic changes can underlie cancer development.

TITLE:

A remarkably simple genome underlies highly malignant pediatric rhabdoid cancers

AUTHOR CONTACT:

Charles Roberts

Dana-Farber Cancer Institute, Boston, MA, USA

Phone: 617-632-6497; Fax: 617-582-8096; E-mail: charles_roberts@dfci.harvard.edu

View this article at: http://www.jci.org/articles/view/64400?key=226866e0e308ef85783e

ONCOLOGY

PHD3-dependent hydroxylation of HCLK2 promotes the DNA damage response | Back to top

The DNA damage response (DDR) is a complex regulatory network that is critical for maintaining genome integrity. Posttranslational modifications are widely used to ensure strict spatiotemporal control of signal flow, but how the DDR responds to environmental cues, such as changes in ambient oxygen tension, remains poorly understood. Cam Patterson and colleagues at the University of North Carolina found that an essential component
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Contact: Sarah Jackson
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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