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Metabolite common among cancers

Date:
February 14, 2010
Source:
Rockefeller University Press
Summary:
Several distinct mutations found in a subset of patients with acute myelogenous leukemia result in excess production of the same metabolite, according to new research.

A study published online on February 8 in the Journal of Experimental Medicine reports that several distinct mutations found in a subset of patients with acute myelogenous leukemia (AML) result in excess production of the same metabolite.

The enzyme isocitrate dehydrogenase 1 (IDH1), which normally facilitates production of the metabolite {alpha}-ketoglutarate, is mutated in approximately 80% of secondary brain tumors. This mutant version of IDH1 promotes excess production of a different metabolite: R (-)-2-hydroxyglutarate (2-HG).

A team led by Tak Mak (Toronto) detected elevated concentrations of 2-HG in the serum of the approximately 8% of AML patients with mutations in IDH1. In addition, they identified a mutation in IDH2 -- the sister enzyme of IDH1 -- in some AML patients. These patients also had unusually high serum levels of 2-HG.

Additional work is needed to understand if and how 2-HG influences brain cancer and/or leukemia progression. However, as these mutations have so far only been found in cancer, they may prove useful as drug targets.

Reference: Gross, S., et al. 2010. J. Exp. Med. doi:10.1084/jem.20092506.


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The above story is based on materials provided by Rockefeller University Press. Note: Materials may be edited for content and length.


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Rockefeller University Press. "Metabolite common among cancers." ScienceDaily. ScienceDaily, 14 February 2010. <www.sciencedaily.com/releases/2010/02/100208092750.htm>.
Rockefeller University Press. (2010, February 14). Metabolite common among cancers. ScienceDaily. Retrieved July 31, 2014 from www.sciencedaily.com/releases/2010/02/100208092750.htm
Rockefeller University Press. "Metabolite common among cancers." ScienceDaily. www.sciencedaily.com/releases/2010/02/100208092750.htm (accessed July 31, 2014).

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