For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
25
views
16
references
 Top references
cited by
6
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      331
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Isomers Identification of 2-hydroxyglutarate acid disodium salt (2HG) by Terahertz Time-domain Spectroscopy

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          2-Hydroxyglutaric acid disodium salt (2HG) is a unique biomarker existing in glioma, which can be used for recognizing cancer development stage and identifying the boundary between the ordinary tissue and cancer tissue. However, the most efficient detection method for 2HG now is Magnetic Resonance Spectroscopy (MRS), whose testing time is at least twenty minutes and the variability of 2HG (continuous synthesis and decomposition) determines it cannot be used as the real-time image in medical surgery. In this paper, by using the Terahertz Time-domain Spectroscopy (THz-TDS) System, we investigate the vibration spectra of 2HG isomers and further distinguish their physical properties by using Density Functional Theory. The differences between isomers are mainly attributed to the proton transfer inside the carbon chain. These results indicate that terahertz technology can identify the isomers of 2HG accurate and fast, which has important significance for the further investigation of glioma and clinical surgery.

          Related collections

          Most cited references16

          • Record: found
          • Abstract: found
          • Article: found

          (R)-2-hydroxyglutarate is sufficient to promote leukemogenesis and its effects are reversible.

          Julie-Aurore Losman, Ryan Looper, Peppi Koivunen … (2013)
          Mutations in IDH1 and IDH2, the genes coding for isocitrate dehydrogenases 1 and 2, are common in several human cancers, including leukemias, and result in overproduction of the (R)-enantiomer of 2-hydroxyglutarate [(R)-2HG]. Elucidation of the role of IDH mutations and (R)-2HG in leukemogenesis has been hampered by a lack of appropriate cell-based models. Here, we show that a canonical IDH1 mutant, IDH1 R132H, promotes cytokine independence and blocks differentiation in hematopoietic cells. These effects can be recapitulated by (R)-2HG, but not (S)-2HG, despite the fact that (S)-2HG more potently inhibits enzymes, such as the 5'-methylcytosine hydroxylase TET2, that have previously been linked to the pathogenesis of IDH mutant tumors. We provide evidence that this paradox relates to the ability of (S)-2HG, but not (R)-2HG, to inhibit the EglN prolyl hydroxylases. Additionally, we show that transformation by (R)-2HG is reversible.
          Article 0 comments Cited 232 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Differentiation between glioma and radiation necrosis using molecular magnetic resonance imaging of endogenous proteins and peptides

            Jinyuan Zhou, Erik Tryggestad, Zhibo Wen … (2010)
            Distinguishing tumor recurrence from radiation necrosis following brain tumor therapy remains a major clinical challenge. Here we demonstrate the ability to distinguish these lesions using the amide proton transfer (APT) MRI signals of endogenous cellular proteins and peptides as an imaging biomarker. When comparing two orthotopic glioma models (SF188/V+ glioma and 9L gliosarcoma) with a radiation necrosis model in rats, viable glioma (hyperintense) and radiation necrosis (hypointense to isointense) could be clearly differentiated using APT MRI. When irradiating rats with U87MG gliomas, the APT signals in the irradiated tumors decreased significantly at 3 days and 6 days post-radiation. The amide protons detected by APT provide a unique and non-invasive MRI biomarker for assessing viable malignancy versus radiation necrosis and predicting tumor response to therapy.
            Article 0 comments Cited 104 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Disruption of wild-type IDH1 suppresses D-2-hydroxyglutarate production in IDH1-mutated gliomas.

              Zachary Reitman, GENGLIN JIN, Giselle Lopez … (2013)
              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. 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. These insights may aid in the development of therapeutic strategies to target IDH1-mutated cancers.
              Article 0 comments Cited 45 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Yan Peng: py@usst.edu.cn
                Yiming Zhu: ymzhu@usst.edu.cn
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 22 September 2017
                Publication date PMC-release: 22 September 2017
                Publication date Collection: 2017
                Volume: 7
                Affiliations
                [1 ]ISNI 0000 0000 9188 055X, GRID grid.267139.8, Shanghai Key Lab of Modern Optical System, University of Shanghai for Science and Technology, No. 516, Jungong Road, ; 200093 Shanghai, China
                [2 ]ISNI 0000 0000 9989 3072, GRID grid.450275.1, Shanghai Institute of Applied Physics, Chinese Academy of Sciences, ; 201800 Shanghai, China
                Article
                Publisher ID: 11527
                DOI: 10.1038/s41598-017-11527-z
                PMC ID: 5610270
                PubMed ID: 28939851
                SO-VID: fccd9c73-731e-4c69-ac12-60312c9dd625
                Copyright statement: © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

                Comments

                Comment on this article

                Similar content331

                See all similar

                Cited by6

                See all cited by

                Most referenced authors324

                See all reference authors