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  • 1
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    Mutational analysis reveals the origin and therapy-driven evolution of recurrent glioma (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-18
    Description: Tumor recurrence is a leading cause of cancer mortality. Therapies for recurrent disease may fail, at least in part, because the genomic alterations driving the growth of recurrences are distinct from those in the initial tumor. To explore this hypothesis, we sequenced the exomes of 23 initial low-grade gliomas and recurrent tumors resected from the same patients. In 43% of cases, at least half of the mutations in the initial tumor were undetected at recurrence, including driver mutations in TP53, ATRX, SMARCA4, and BRAF; this suggests that recurrent tumors are often seeded by cells derived from the initial tumor at a very early stage of their evolution. Notably, tumors from 6 of 10 patients treated with the chemotherapeutic drug temozolomide (TMZ) followed an alternative evolutionary path to high-grade glioma. At recurrence, these tumors were hypermutated and harbored driver mutations in the RB (retinoblastoma) and Akt-mTOR (mammalian target of rapamycin) pathways that bore the signature of TMZ-induced mutagenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998672/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998672/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Brett E -- Mazor, Tali -- Hong, Chibo -- Barnes, Michael -- Aihara, Koki -- McLean, Cory Y -- Fouse, Shaun D -- Yamamoto, Shogo -- Ueda, Hiroki -- Tatsuno, Kenji -- Asthana, Saurabh -- Jalbert, Llewellyn E -- Nelson, Sarah J -- Bollen, Andrew W -- Gustafson, W Clay -- Charron, Elise -- Weiss, William A -- Smirnov, Ivan V -- Song, Jun S -- Olshen, Adam B -- Cha, Soonmee -- Zhao, Yongjun -- Moore, Richard A -- Mungall, Andrew J -- Jones, Steven J M -- Hirst, Martin -- Marra, Marco A -- Saito, Nobuhito -- Aburatani, Hiroyuki -- Mukasa, Akitake -- Berger, Mitchel S -- Chang, Susan M -- Taylor, Barry S -- Costello, Joseph F -- 1T32CA15102201/CA/NCI NIH HHS/ -- K08 NS079485/NS/NINDS NIH HHS/ -- K08NS079485/NS/NINDS NIH HHS/ -- P01CA81403/CA/NCI NIH HHS/ -- P30 CA082103/CA/NCI NIH HHS/ -- P30CA82103/CA/NCI NIH HHS/ -- P50 CA097257/CA/NCI NIH HHS/ -- P50CA097257/CA/NCI NIH HHS/ -- R01 CA163336/CA/NCI NIH HHS/ -- R01 CA169316/CA/NCI NIH HHS/ -- R01CA163336/CA/NCI NIH HHS/ -- R01CA169316-01/CA/NCI NIH HHS/ -- R25NS070680/NS/NINDS NIH HHS/ -- T32 CA128583/CA/NCI NIH HHS/ -- T32GM008568/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 10;343(6167):189-93. doi: 10.1126/science.1239947. Epub 2013 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24336570" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents, Alkylating/*adverse effects/therapeutic use ; Brain/drug effects/pathology ; Brain Neoplasms/*drug therapy/genetics/*pathology ; DNA Helicases/genetics ; DNA Mutational Analysis ; Dacarbazine/adverse effects/*analogs & derivatives/therapeutic use ; Glioma/*drug therapy/genetics/*pathology ; Humans ; Mutagenesis/drug effects ; Neoplasm Grading ; Neoplasm Recurrence, Local/*chemically induced/drug therapy/*genetics ; Nuclear Proteins/genetics ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins c-akt/genetics ; TOR Serine-Threonine Kinases/genetics ; Transcription Factors/genetics ; Tumor Suppressor Protein p53/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Dual blockade of lipid and cyclin-dependent kinases induces synthetic lethality in malignant glioma (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-07-16
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 3
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    PI3K and CDK inhibitors induce apoptosis in glioma [Medical Sciences] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-08-01
    Description: Malignant glioma, the most common primary brain tumor, is generally incurable. Although phosphatidylinositol-3-kinase (PI3K) signaling features prominently in glioma, inhibitors generally block proliferation rather than induce apoptosis. Starting with an inhibitor of both lipid and protein kinases that induced prominent apoptosis and that failed early clinical development because of its broad target profile and overall toxicity, we identified protein kinase targets, the blockade of which showed selective synthetic lethality when combined with PI3K inhibitors. Prioritizing protein kinase targets for which there are clinical inhibitors, we demonstrate that cyclin-dependent kinase (CDK)1/2 inhibitors, siRNAs against CDK1/2, and the clinical CDK1/2 inhibitor roscovitine all cooperated with the PI3K inhibitor PIK-90, blocking the antiapoptotic protein Survivin and driving cell death. In addition, overexpression of CDKs partially blocked some of the apoptosis caused by PIK-75. Roscovitine and PIK-90, in combination, were well tolerated in vivo and acted in a synthetic-lethal manner to induce apoptosis in human glioblastoma xenografts. We also tested clinical Akt and CDK inhibitors, demonstrating induction of apoptosis in vitro and providing a preclinical rationale to test this combination therapy in patients.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Comparison of GLUT1, GLUT3, and GLUT4 mRNA and the subcellular distribution of their proteins in normal human muscle (2000)
    In:  Other Sources
    Details
    Publication Date: 2019-07-13
    Description: Basal, "insulin-independent" glucose uptake into skeletal muscle is provided by glucose transporters positioned at the plasma membrane. The relative amount of the three glucose transporters expressed in muscle has not been previously quantified. Using a combination of qualitative and quantitative ribonuclease protection assay (RPA) methods, we found in normal human muscle that GLUT1, GLUT3, and GLUT4 mRNA were expressed at 90 +/- 10, 46 +/- 4, and 156 +/- 12 copies/ng RNA, respectively. Muscle was fractionated by DNase digestion and differential sedimentation into membrane fractions enriched in plasma membranes (PM) or low-density microsomes (LDM). GLUT1 and GLUT4 proteins were distributed 57% to 67% in LDM, whereas GLUT3 protein was at least 88% in the PM-enriched fractions. These data suggest that basal glucose uptake into resting human muscle could be provided in part by each of these three isoforms.
    Keywords: Life Sciences (General)
    Type: Metabolism: clinical and experimental (ISSN 0026-0495); 49; 12; 1604-9
    Format: text
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