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Genome analysis reveals new protein associated with breast cancer progression
Date:4/17/2008

s its own cascade of gene targets.

Whites team set out to map out the many sequential genetic events that occur in breast cancer cells after estrogen binding, using a series of innovative technologies. They ultimately found that estrogen-stimulated c-MYC enhanced production of H2A.Z, which altered the positioning and activation of various genes in ways that increased the odds that a cancer would spread to the lymph nodes and ultimately to distant sites, often resulting in the patients death.

This is not a simple process. In tumor cells from patients with estrogen-dependent breast cancers, the researchers found estrogen affected 1,615 genetic regions. One of those was the promoter for the gene for c-MYC, which, when activated, could bind another set of overlapping 311 genetic regions.

Both estrogen and c-MYC interact with the gene for H2A.Z, leading to increased production of this protein in breast cancer cells. When the researchers looked at tumor tissue samples collected from 500 patients, they found that elevated levels of H2A.Z were highly correlated with the spread of the cancer to lymph nodes and decreased patient survival. Adding H2A.Z expression to other known risk factors provided significant prognostic information, the authors note, beyond what these factors alone provide.

Although it has been implicated in genomic stability and gene transcription, H2A.Z has never been reported to be associated with cancer, said White. We would not have found this clinically important factor without taking such a large-scale integrated approach.

We suspect this integrated systems approach will lead us to a number of previously unsuspected genes that play a role in disease initiation and progression, he said. Many of these could become targets for new treatments.


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Contact: John Easton
john.easton@uchospitals.edu
773-702-6241
University of Chicago Medical Center
Source:Eurekalert

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