By a News Reporter-Staff News Editor at Cancer Gene Therapy Week -- Current study results on Biotechnology have been published. According to news reporting out of Durham, North Carolina, by NewsRx editors, research stated, "Point mutations at Arg132 of the cytoplasmic NADP(+)-dependent isocitrate dehydrogenase 1 (IDH1) occur frequently in gliomas and result in a gain of function to produce the 'oncometabolite' D-2-hydroxyglutarate (D-2HG). The mutated IDH1 allele is usually associated with a wild-type IDH1 allele (heterozygous) in cancer."
Our news journalists obtained a quote from the research from Duke University Medical Center, "Here, we identify 2 gliomas that underwent loss of the wild-type IDH1 allele but retained the mutant IDH1 allele following tumor progression from World Health Organization (WHO) grade III anaplastic astrocytomas to WHO grade IV glioblastomas. Intratumoral D-2HG was 14-fold lower in the glioblastomas lacking wild-type IDH1 than in glioblastomas with heterozygous IDH1 mutations. To characterize the contribution of wild-type IDH1 to cancer cell D-2HG production, we established an IDH1-mutated astrocytoma (IMA) cell line from a WHO grade III anaplastic astrocytoma. Disruption of the wild-type IDH1 allele in IMA cells by gene targeting resulted in an 87-fold decrease in cellular D-2HG levels, showing that both wild-type and mutant IDH1 alleles are required for D-2HG production in glioma cells. Expression of wild-type IDH1 was also critical for mutant IDH1-associated D-2HG production in the colorectal cancer cell line HCT116."
According to the news editors, the research concluded: "These insights may aid in the development of therapeutic strategies to target IDH1-mutated cancers."
For more information on this research see: Disruption of wild-type IDH1 suppresses D-2-hydroxyglutarate production in IDH1-mutated gliomas. Cancer Research, 2013;73(2):496-501. (American Association for Cancer Research - www.aacr.com; Cancer Research - cancerres.aacrjournals.org/)
Our news journalists report that additional information may be obtained by contacting G. Jin, The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation Institute and The Dept. of Pathology, Duke University Medical Center, Durham, North Carolina 27710, United States. Additional authors for this research include Z.J. Reitman, C.G. Duncan, I. Spasojevic, D.M. Gooden, B.A. Rasheed, R. Yang, G.Y. Lopez, Y. He, R.E. McLendon, D.D. Bigner and H. Yan (see also Biotechnology).
Keywords for this news article include: Biotechnology, Durham, Genetics, Oncology, United States, North Carolina, Cancer Gene Therapy, North and Central America, World Health Organization, Government Agencies Offices and Entities.
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