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<script type="text/javascript" src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/jr.boots.min.js"> </script><title>[99mTc]Human telomerase reverse-transcriptase antisense mRNA oligonucleotide - Molecular Imaging and Contrast Agent Database (MICAD) - NCBI Bookshelf</title>
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<meta name="citation_title" content="[99mTc]Human telomerase reverse-transcriptase antisense mRNA oligonucleotide">
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<meta name="citation_date" content="2008/05/27">
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<meta name="citation_author" content="Arvind Chopra">
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<meta name="DC.Title" content="[99mTc]Human telomerase reverse-transcriptase antisense mRNA oligonucleotide">
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<meta name="og:description" content="Telomerase is an enzyme that synthesizes telomeric DNA at the terminal end of a chromosome, and its activation is one of the mechanisms for the progression of cancer (1). Telomerase, in conjunction with the telomere-binding proteins, maintains stability of the chromosomal terminal end by replicating the DNA, but inhibition of this activity results in a shortened telomere and ultimately leads to replicative senescence or even cell death (2). The repression and close regulation of this enzyme is considered to be one of the mechanisms for tumor suppression in humans, and there is much evidence that a shortened telomere is an indication for the development of a cancer or other degenerative disease, especially in older individuals (3-6). In addition, telomerases are specifically expressed in most cancer cell types and therefore are targets for the development of many anticancer drugs (2). Also, tumors are less likely to develop resistance to anti-telomerase drugs compared to other anticancer treatments because maintenance of the telomere and immortality is crucial for tumor progression (2). Several clinical trials for drugs, vaccines, and antibodies that target the telomerases as a treatment for cancer have been approved by the United States Food and Drug Administration.">
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id="jr-fip-info-p"><a id="jr-fip-prev" class="wsprkl btn" title="Jump to previuos match">◀</a><button id="jr-fip-matches">no matches yet</button><a id="jr-fip-next" class="wsprkl btn" title="Jump to next match">▶</a></nav></nav></div><div id="jr-epub-interstitial" class="hidden"></div><div id="jr-content"><article data-type="main"><div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><div class="fm-sec"><h1 id="_NBK23339_"><span class="title" itemprop="name">[<sup>99m</sup>Tc]Human telomerase reverse-transcriptase antisense mRNA oligonucleotide</span></h1><div itemprop="alternativeHeadline" class="subtitle whole_rhythm">[<sup>99m</sup>Tc]MAG3-ASON</div><p class="contribs">Chopra A.</p><p class="fm-aai"><a href="#_NBK23339_pubdet_">Publication Details</a></p></div></div><div class="jig-ncbiinpagenav body-content whole_rhythm" data-jigconfig="allHeadingLevels: ['h2'],smoothScroll: false" itemprop="text"><div class="iconblock whole_rhythm clearfix ten_col table-wrap" id="figMAG3ASON99mTcT1"><a href="/books/NBK23339/table/MAG3ASON99mTc.T1/?report=objectonly" target="object" title="Table" class="img_link icnblk_img" rid-ob="figobMAG3ASON99mTcT1"><img class="small-thumb" src="/corehtml/pmc/css/bookshelf/2.26/img/table-icon.gif" alt="Table Icon" /></a><div class="icnblk_cntnt"><h4 id="MAG3ASON99mTc.T1"><a href="/books/NBK23339/table/MAG3ASON99mTc.T1/?report=objectonly" target="object" rid-ob="figobMAG3ASON99mTcT1">Table</a></h4><p class="float-caption no_bottom_margin">
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<i>In vitro</i>
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Rodents
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</p></div></div><div id="MAG3ASON99mTc.Background"><h2 id="_MAG3ASON99mTc_Background_">Background</h2><p>[PubMed]</p><p>Telomerase is an enzyme that synthesizes telomeric DNA at the terminal end of a chromosome, and its activation is one of the mechanisms for the progression of cancer (<a class="bibr" href="#MAG3ASON99mTc.REF.1" rid="MAG3ASON99mTc.REF.1">1</a>). Telomerase, in conjunction with the telomere-binding proteins, maintains stability of the chromosomal terminal end by replicating the DNA, but inhibition of this activity results in a shortened telomere and ultimately leads to replicative senescence or even cell death (<a class="bibr" href="#MAG3ASON99mTc.REF.2" rid="MAG3ASON99mTc.REF.2">2</a>). The repression and close regulation of this enzyme is considered to be one of the mechanisms for tumor suppression in humans, and there is much evidence that a shortened telomere is an indication for the development of a cancer or other degenerative disease, especially in older individuals (<a href="#MAG3ASON99mTc.REF.3">3-6</a>). In addition, telomerases are specifically expressed in most cancer cell types and therefore are targets for the development of many anticancer drugs (<a class="bibr" href="#MAG3ASON99mTc.REF.2" rid="MAG3ASON99mTc.REF.2">2</a>). Also, tumors are less likely to develop resistance to anti-telomerase drugs compared to other anticancer treatments because maintenance of the telomere and immortality is crucial for tumor progression (<a class="bibr" href="#MAG3ASON99mTc.REF.2" rid="MAG3ASON99mTc.REF.2">2</a>). Several <a href="http://clinicaltrials.gov/ct2/results?term=telomerase" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">clinical trials</a> for drugs, vaccines, and antibodies that target the telomerases as a treatment for cancer have been approved by the United States Food and Drug Administration.</p><p>Telomerase consists of the telomerase RNA (hTR), the telomerase reverse-transcriptase (hTERT), and the associated proteins (<a class="bibr" href="#MAG3ASON99mTc.REF.1" rid="MAG3ASON99mTc.REF.1">1</a>). Although hTR is expressed without telomerase activity both in normal cells and in malignant cells, only tumor cells express hTERT. As a consequence, hTERT is the target for the development of many anticancer therapies (<a class="bibr" href="#MAG3ASON99mTc.REF.7" rid="MAG3ASON99mTc.REF.7">7</a>), and its expression levels may have prognostic value (<a class="bibr" href="#MAG3ASON99mTc.REF.8" rid="MAG3ASON99mTc.REF.8">8</a>). Investigators have used only indirect methods such as immunohistochemistry, reverse-transcription polymerase chain reaction (RT-PCR), fluorescence, bioluminescence, and radionuclide imaging to determine the expression levels of hTERT in various cell types with reasonable results (<a class="bibr" href="#MAG3ASON99mTc.REF.9" rid="MAG3ASON99mTc.REF.9">9</a>, <a class="bibr" href="#MAG3ASON99mTc.REF.10" rid="MAG3ASON99mTc.REF.10">10</a>). This approach may not, however, yield the exact nature of the change(s) that alter the genotype and, ultimately, the cell phenotype that result in the development of a cancer. Liu et al. envisioned that antisense oligonucleotides (ASON) would be an excellent <i>in vivo</i> tool to determine the level of expression of a gene during the early stages of tumor development because of their high specificity for binding to nucleotides (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>). The authors investigated the <i>in vitro</i> activity and biodistribution of ASON directed toward the hTERT gene and labeled with radioactive technetium (<sup>99m</sup>Tc) in mice bearing xenograft tumors.</p></div><div id="MAG3ASON99mTc.Synthesis"><h2 id="_MAG3ASON99mTc_Synthesis_">Synthesis</h2><p>[PubMed]</p><p>The conjugation and radiolabeling of the ASON and the sense oligonucleotides (SON) used for the following studies described by Liu et al. (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>). The ASON sequence was 5’-TAGAGACGTGGCTCTTGA-3’, and the SON nucleotide sequence was 5’-TCAAGAGCCACGTCTCTA-3’. Both oligonucleotides had a primary amine on the 3’ terminal phosphate group through a six-member methylene carbon spacer. For conjugation of the ASON with the <i>N</i>-hydroxysuccinimidyl (NHS) derivative of <i>S</i>-acetylmercaptoacetyltriglycine (<i>S</i>-acetyl NHS-MAG3), it was dissolved in <i>N</i>-(2-hydroxyethyl)piperazine-<i>N’</i>-(2-ethanesulfonic acid) (HEPES) buffer (pH 8.0), and a fresh solution of <i>S</i>-acetyl NHS-MAG3 in <i>N,N</i>-dimethylformamide was added dropwise to a final ratio of 20:1. The mixture was incubated at room temperature for 60–120 min, and the conjugated ASON was purified with chromatography on a Sephadex G25 column using sterile phosphate buffer (pH 7.2) as an eluent. The conjugated ASON was then aliquoted into vials, lyophilized, and stored at -20°C until needed. Conjugation and storage of the SON was the same as described for the ASON (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>).</p><p>For labeling with radioactive <sup>99m</sup>Tc, the MAG3-ASON was dissolved in ammonium acetate buffer (pH 5.2), and sodium tartrate was added to it (as a transchelator) until the pH reached 7.6 (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>). Then <sup>99m</sup>Tc-pertechnetate was added, and a stannous chloride solution was added immediately. The mixture was incubated for 15–30 min, and the labeled MAG3-ASON was purified with chromatography on a Sephadex G25 column with phosphate buffer (pH 7.2) as the eluent. Labeling stability of <sup>99m</sup>Tc-MAG3-ASON was determined at room temperature, in saline at room temperature, and in fresh human serum at 37°C for >24 h by paper chromatography. Stability of the labeled ASON in human serum was also determined with polyacrylamide gel electrophoresis after extraction by the phenol:chloroform method, followed by overnight ethanol precipitation at -20°C (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>).</p><p>Under the conditions used, the labeling efficiency of the reaction was reported to be 76 ± 5% (<i>n</i> = 5 labeling reactions) with a specific activity of 10.2 kBq/pmol (0.27 μCi/pmol) and a radiochemical purity of >96% after purification (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>). The Rf values for the various reaction components after paper chromatography are reported in Table 1 of the publication (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>). The stability of <sup>99m</sup>Tc-MAG3-ASON was reported to be >93% over a 24-h period at room temperature, in normal saline, and in fresh human serum at 37°C.</p></div><div id="MAG3ASON99mTc.In_Vitro_Studies_Tes"><h2 id="_MAG3ASON99mTc_In_Vitro_Studies_Tes_"><i>In Vitro</i> Studies: Testing in Cells and Tissues</h2><p>[PubMed]</p><p>The <i>in vitro</i> activity of <sup>99m</sup>Tc-MAG3-ASON was investigated in HepG2 cells (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>). The cells were exposed to <sup>99m</sup>Tc-MAG3-ASON or ASON, and the hTERT mRNA levels in these cells were determined with RT-PCR and compared with the levels in cells exposed to <sup>99m</sup>Tc-MAG3-SON or 10% fetal bovine serum (FBS). A significant reduction (<i>P</i> < 0.05) in the hTERT mRNA was observed in cells treated with <sup>99m</sup>Tc-MAG3-ASON or ASON compared with the cells exposed either to <sup>99m</sup>Tc-MAG3-SON or 10% FBS. No differences were reported in the hTERT mRNA levels of cells treated with <sup>99m</sup>Tc-MAG3-ASON or ASON. Similar observations were also reported for the 10% FBS-treated cells.</p></div><div id="MAG3ASON99mTc.Animal_Studies"><h2 id="_MAG3ASON99mTc_Animal_Studies_">Animal Studies</h2><div id="MAG3ASON99mTc.Rodents"><h3>Rodents</h3><p>[PubMed]</p><p>The biodistribution of <sup>99m</sup>Tc-MAG3-ASON and <sup>99m</sup>Tc-MAG3-SON was investigated in BALB/c <i>nu/nu</i> mice bearing MCF-7 cell xenograft tumors (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>). The animals were injected with the labeled ASON or the SON through the tail vein and killed 0.5, 1, 2, 4, and 6 h after the injection (<i>n</i> = 5 animals per time point for each oligonucleotide). The various organs were harvested from the animals, weighed, and counted for radioactivity. The radioactivity had a rapid clearance from blood circulation with 2.62 ± 0.167% of the injected dose/gram tissue (% ID/g) of <sup>99m</sup>Tc-MAG3-ASON remaining in the blood 0.5 h after administration. This level dropped to 1.051 ± 0.121% ID/g at 2 h. The level of <sup>99m</sup>Tc-MAG3-ASON (1.157 ± 0.182% ID/g) was significantly higher (<i>P</i> < 0.05) compared with <sup>99m</sup>Tc-MAG3-SON (0.503 ± 0.051% ID/g) in the tumors after 4 h with a tumor/muscle ratio of 8.8 and a tumor/blood ratio of 2 at 6 h. Among the various organs, maximum radioactivity was noticed in the kidneys for both the radiolabeled oligonucleotides, which indicates that the radiochemicals were cleared mainly through the urinary system.</p><p>Imaging of the mice 4–8 h after administration of the labeled oligonucleotides clearly revealed tumors only in mice injected with <sup>99m</sup>Tc-MAG3-ASON (<a class="bibr" href="#MAG3ASON99mTc.REF.11" rid="MAG3ASON99mTc.REF.11">11</a>). The tumors were not visible by imaging at any time after the administration of <sup>99m</sup>Tc-MAG3-SON. However, the renal route of elimination of the radiochemicals led to an accumulation of substantial radioactivity in the abdomen with both labeled nucleotides.</p></div><div id="MAG3ASON99mTc.Other_NonPrimate_Mam"><h3>Other Non-Primate Mammals</h3><p>[PubMed]</p><p>No references are currently available.</p></div><div id="MAG3ASON99mTc.NonHuman_Primates"><h3>Non-Human Primates</h3><p>[PubMed]</p><p>No references are currently available.</p></div></div><div id="MAG3ASON99mTc.Human_Studies"><h2 id="_MAG3ASON99mTc_Human_Studies_">Human Studies</h2><p>[PubMed]</p><p>No references are currently available.</p></div><div id="MAG3ASON99mTc.Supplemental_Informa"><h2 id="_MAG3ASON99mTc_Supplemental_Informa_">Supplemental Information</h2><p>[<a href="/books/n/micad/disclaimer/?report=reader">Disclaimers</a>]</p></div><div id="MAG3ASON99mTc.references"><h2 id="_MAG3ASON99mTc_references_">References</h2><dl class="temp-labeled-list"><dl class="bkr_refwrap"><dt>1.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.1">Kelland L. Targeting the limitless replicative potential of cancer: the telomerase/telomere pathway. <span><span class="ref-journal">Clin Cancer Res. </span>2007;<span class="ref-vol">
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<strong>13</strong>
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</span>(17):4960–3.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/17785545" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 17785545</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>2.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.2">Harley C.B. Telomerase and cancer therapeutics. <span><span class="ref-journal">Nat Rev Cancer. </span>2008;<span class="ref-vol">
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<strong>8</strong>
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</span>(3):167–79.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/18256617" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 18256617</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>3.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.3">Cawthon R.M. , Smith K.R. , O'Brien E. , Sivatchenko A. , Kerber R.A. Association between telomere length in blood and mortality in people aged 60 years or older. <span><span class="ref-journal">Lancet. </span>2003;<span class="ref-vol">
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<strong>361</strong>
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</span>(9355):393–5.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/12573379" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 12573379</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>4.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.4">Vulliamy T. , Marrone A. , Szydlo R. , Walne A. , Mason P.J. , Dokal I. Disease anticipation is associated with progressive telomere shortening in families with dyskeratosis congenita due to mutations in TERC. <span><span class="ref-journal">Nat Genet. </span>2004;<span class="ref-vol">
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<strong>36</strong>
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</span>(5):447–9.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/15098033" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 15098033</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>5.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.5">Fitzpatrick A.L. , Kronmal R.A. , Gardner J.P. , Psaty B.M. , Jenny N.S. , Tracy R.P. , Walston J. , Kimura M. , Aviv A. Leukocyte telomere length and cardiovascular disease in the cardiovascular health study. <span><span class="ref-journal">Am J Epidemiol. </span>2007;<span class="ref-vol">
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<strong>165</strong>
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</span>(1):14–21.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/17043079" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 17043079</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>6.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.6">Armanios M.Y. , Chen J.J. , Cogan J.D. , Alder J.K. , Ingersoll R.G. , Markin C. , Lawson W.E. , Xie M. , Vulto I. , Phillips J.A. , Lansdorp P.M. , Greider C.W. , Loyd J.E. Telomerase mutations in families with idiopathic pulmonary fibrosis. <span><span class="ref-journal">N Engl J Med. </span>2007;<span class="ref-vol">
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<strong>356</strong>
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</span>(13):1317–26.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/17392301" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 17392301</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>7.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.7">Deng Y. , Chang S. Role of telomeres and telomerase in genomic instability, senescence and cancer. <span><span class="ref-journal">Lab Invest. </span>2007;<span class="ref-vol">
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<strong>87</strong>
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</span>(11):1071–6.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/17767195" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 17767195</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>8.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.8">Lee K.H. , Rudolph K.L. , Ju Y.J. , Greenberg R.A. , Cannizzaro L. , Chin L. , Weiler S.R. , DePinho R.A. Telomere dysfunction alters the chemotherapeutic profile of transformed cells. <span><span class="ref-journal">Proc Natl Acad Sci U S A. </span>2001;<span class="ref-vol">
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<strong>98</strong>
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</span>(6):3381–6.</span> [<a href="/pmc/articles/PMC30662/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC30662</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/11248087" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 11248087</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>9.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.9">Massoud T.F. , Gambhir S.S. Molecular imaging in living subjects: seeing fundamental biological processes in a new light. <span><span class="ref-journal">Genes Dev. </span>2003;<span class="ref-vol">
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<strong>17</strong>
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</span>(5):545–80.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/12629038" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 12629038</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>10.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.10">Padmanabhan P. , Otero J. , Ray P. , Paulmurugan R. , Hoffman A.R. , Gambhir S.S. , Biswal S. , Ulaner G.A. Visualization of telomerase reverse transcriptase (hTERT) promoter activity using a trimodality fusion reporter construct. <span><span class="ref-journal">J Nucl Med. </span>2006;<span class="ref-vol">
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<strong>47</strong>
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</span>(2):270–7.</span> [<a href="/pmc/articles/PMC4141555/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC4141555</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/16455633" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 16455633</span></a>]</div></dd></dl><dl class="bkr_refwrap"><dt>11.</dt><dd><div class="bk_ref" id="MAG3ASON99mTc.REF.11">Liu M. , Wang R.F. , Zhang C.L. , Yan P. , Yu M.M. , Di L.J. , Liu H.J. , Guo F.Q. Noninvasive imaging of human telomerase reverse transcriptase (hTERT) messenger RNA with 99mTc-radiolabeled antisense probes in malignant tumors. <span><span class="ref-journal">J Nucl Med. </span>2007;<span class="ref-vol">
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<strong>48</strong>
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</span>(12):2028–36.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/18006621" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 18006621</span></a>]</div></dd></dl></dl></div><div id="bk_toc_contnr"></div></div></div><div class="fm-sec"><h2 id="_NBK23339_pubdet_">Publication Details</h2><h3>Author Information and Affiliations</h3><div class="contrib half_rhythm"><span itemprop="author">Arvind Chopra</span>, PhD<div class="affiliation small">
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National Center for Biotechnology Information, NLM, NIH, Bethesda, MD 20894,
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<span class="before-email-separator"></span><span class="email-label">Email: </span><a href="mailto:dev@null" data-email="vog.hin.mln.ibcn@dacim" class="oemail">vog.hin.mln.ibcn@dacim</a>
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</div></div><h3>Publication History</h3><p class="small">Created: <span itemprop="datePublished">May 7, 2008</span>; Last Update: <span itemprop="dateModified">May 27, 2008</span>.</p><h3>Copyright</h3><div><div class="half_rhythm"><a href="/books/about/copyright/">Copyright Notice</a></div></div><h3>Publisher</h3><p><a href="http://www.ncbi.nlm.nih.gov/" ref="pagearea=page-banner&targetsite=external&targetcat=link&targettype=publisher">National Center for Biotechnology Information (US)</a>, Bethesda (MD)</p><h3>NLM Citation</h3><p>Chopra A. [99mTc]Human telomerase reverse-transcriptase antisense mRNA oligonucleotide. 2008 May 7 [Updated 2008 May 27]. In: Molecular Imaging and Contrast Agent Database (MICAD) [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2004-2013. <span class="bk_cite_avail"></span></p></div><div class="small-screen-prev"><a href="/books/n/micad/EGFRnAb99mTc/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M75,30 c-80,60 -80,0 0,60 c-30,-60 -30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Prev</text></svg></a></div><div class="small-screen-next"><a href="/books/n/micad/Hypericin99mTc/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M25,30c80,60 80,0 0,60 c30,-60 30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Next</text></svg></a></div></article><article data-type="table-wrap" id="figobMAG3ASON99mTcT1"><div id="MAG3ASON99mTc.T1" class="table"><p class="large-table-link" style="display:none"><span class="right"><a href="/books/NBK23339/table/MAG3ASON99mTc.T1/?report=objectonly" target="object">View in own window</a></span></p><div class="large_tbl" id="__MAG3ASON99mTc.T1_lrgtbl__"><table><tbody><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Chemical name:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">[<sup>99m</sup>Tc]Human telomerase reverse-transcriptase antisense mRNA oligonucleotide</td><td rowspan="9" colspan="1" style="text-align:left;vertical-align:middle;"></td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Abbreviated name:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">[<sup>99m</sup>Tc]MAG3-ASON</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Synonym:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">ASON</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Agent Category:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Oligonucleotide</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Target:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Human reverse-transcriptase mRNA</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Target Category:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Binding to complimentary mRNA strand</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Method of detection:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Single-photon emission computed tomography (SPECT); gamma planar imaging</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Source of Signal/Contrast:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;"><sup>99m</sup>Tc</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Activation:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">No</td></tr><tr><td rowspan="1" colspan="1" style="text-align:right;vertical-align:top;">
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<b>Studies:</b>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">
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<ul class="simple-list"><li class="half_rhythm"><div>
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<img alt="Checkbox" src="/corehtml/pmc/css/bookshelf/2.26/img/studies.checkbox.png" />
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<i>In vitro</i>
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</div></li></ul>
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<ul class="simple-list"><li class="half_rhythm"><div>
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<img alt="Checkbox" src="/corehtml/pmc/css/bookshelf/2.26/img/studies.checkbox.png" /> Rodents
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</div></li></ul>
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</td><td rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Structure not available.</td></tr></tbody></table></div></div></article></div><div id="jr-scripts"><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/libs.min.js"> </script><script src="/corehtml/pmc/jatsreader/ptpmc_3.22/js/jr.min.js"> </script></div></div>
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