Save
Email
Print
ShareSep. 9, 2009 — Researchers at the National Cancer Institute have identified a gene that may play a role in breast cancer metastasis to the brain, according to a report in Molecular Cancer Research, a journal of the American Association for Cancer Research.
Diane Palmieri, Ph.D., a staff scientist at the NCI, said Hexokinase 2 overexpression was more highly expressed in brain metastasis in patients with breast cancer than in primary breast tumors.
"Importantly, this study was conducted in human tissue rather than animal models, so we are able to extrapolate data without the problems inherent in animal studies," said Palmieri.
Brunhilde Felding-Habermann, Ph.D., an associate professor at The Scripps Research Institute, said the findings are a major step forward in potential breast cancer treatments.
"Improvements in breast cancer therapy have made prognoses like brain metastasis a growing problem, and this research points to a potential target for future therapies," said Felding-Habermann.
Researchers performed analyses on both primary tumors and brain metastases. They found higher levels of Hexokinase 2 in brain metastases compared with unlinked primary tumors. Among resected brain metastases, these higher levels of Hexokinase 2 were linked with worse survival. The median survival for patients with high levels of Hexokinase 2 expression in their brain metastasis was 9.6 months compared with 17.5 months for those with lower expression.
Palmieri said that Hexokinase 2 plays a key role in glucose metabolism, which provides the energy tumors need to grow. It also impacts the cell survival process, apoptosis.
"Potential therapies would need to turn off this gene and thus starve the tumor of its growth potential," said Palmieri.
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by American Association for Cancer Research, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Note: If no author is given, the source is cited instead.
more 
