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               <email> </email>
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            <copyright-statement>© 2017,</copyright-statement>
            <copyright-year>2017</copyright-year>
            <copyright-holder> </copyright-holder>
            <license xlink:href="https://creativecommons.org/licenses/by/4.0/">
               <license-p>This article is distributed under the terms of the <ext-link ext-link-type="uri"
                            xlink:href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution License</ext-link>, which permits unrestricted use and redistribution provided that the original author and source are credited.</license-p>
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         <abstract abstract-type="section">
            <sec>
               <title>Abstract</title>
               <p>Genomic, proteomic, transcriptomic, and epigenomic analyses of human tumors indicate that there are thousands of anomalies within each cancer genome compared to matched normal tissue. Based on these analyses it is evident that there are many undiscovered genetic drivers of cancer. Performing an unbiased forward genetic screen in human provides the tools to generate tumors and analyze their genetic composition, while reducing the background of passenger mutations. The transposon system is one such method  that can be inserted throughout the genome by the transposable element. </p>
               <p>A transposable element or  jumping genes (TE or transposon) is a <ext-link xlink:href="https://en.wikipedia.org/wiki/DNA_sequence">DNA sequence</ext-link> that can change its position within a <ext-link xlink:href="https://en.wikipedia.org/wiki/Genome">genome</ext-link>, sometimes creating or reversing <ext-link xlink:href="https://en.wikipedia.org/wiki/Mutation">mutations</ext-link> and altering the cell's <ext-link xlink:href="https://en.wikipedia.org/wiki/Genome_size">genome size</ext-link>. Transposable elements make up a large fraction of the genome and are responsible for much of the <ext-link xlink:href="https://en.wikipedia.org/wiki/C-value">mass of  DNA</ext-link> in a <ext-link xlink:href="https://en.wikipedia.org/wiki/Eukaryotic_cell">eukaryotic cell</ext-link>. There are at least two classes of TEs: Class I TEs or <ext-link xlink:href="https://en.wikipedia.org/wiki/Retrotransposon">retrotransposons</ext-link> generally function via <ext-link xlink:href="https://en.wikipedia.org/wiki/Reverse_transcription">reverse transcription</ext-link>, while Class II TEs or <ext-link xlink:href="https://en.wikipedia.org/wiki/DNA_transposon">DNA transposons</ext-link> encode the protein <ext-link xlink:href="https://en.wikipedia.org/wiki/Transposase">transposase</ext-link>, which they require for insertion and excision, and some of these TEs also encode other proteins. The most common transposable element in <ext-link xlink:href="https://en.wikipedia.org/wiki/Human">humans</ext-link> is the <ext-link xlink:href="https://en.wikipedia.org/wiki/Alu_sequence">Alu</ext-link>
                  <ext-link xlink:href="https://en.wikipedia.org/wiki/Alu_sequence"> sequence</ext-link>. It is approximately 300 bases long and can be found between 300,000 and one million times in the <ext-link xlink:href="https://en.wikipedia.org/wiki/Human_genome">human genome</ext-link>. <italic>Alu</italic> alone is estimated to make up 15–17% of the human genome. Transposon s are <ext-link xlink:href="https://en.wikipedia.org/wiki/Mutagen">mutagens</ext-link> and their movements are often the causes of genetic disease. They can damage the genome of their host cell in different ways. A transposon or a retrotransposon that inserts itself  into a functional gene will most likely disable that gene causing cancers. After a DNA transposon leaves a gene, the resulting gap will probably not repaired correctly.</p>
               <p>Diseases often caused by TEs include predisposition to <ext-link xlink:href="https://en.wikipedia.org/wiki/Cancer">cancer</ext-link>.  Since its inception the conditional  transposon mutagenesis system has been applied to many cancer types, identifying hundreds of candidate cancer genes, generating new cancer models, and providing insights into the genes and mechanisms of cancer progression. The development of transposons elements and its use for cancer gene discovery has been a boon for cancer functional genomics studies. It has led to the discovery of new and specific cancer drivers critical to human tumor development or maintenance such as field of transposons elements , and others.</p>
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            <title>Keywords</title>
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         <title>References</title>
         <p>[<xref ref-type="bibr" rid="bib1">1</xref>]. Bucher E, Reinders J, Mirouze M. "Epigenetic control of transposon transcription and mobility in Arabidopsis". Current Opinion in Plant Biology. 2012;15 (5): 503–10.</p>
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         <p>[<xref ref-type="bibr" rid="bib9">9</xref>]. Munoz-Lopez M, Macia A, Garcia-Canadas M, Badge RM, Garcia-Perez JL. An epi [c] genetic battle: LINE-1 retrotransposons and intragenomic conflict in humans. Mob Genet Elements. 2011;1(2):122-7.</p>
         <p>[<xref ref-type="bibr" rid="bib10">10</xref>]. Pray, Leslie A. "Transposons: The jumping genes". Nature Education. 2008;1(1): 204.</p>
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         <title>Competing interests</title>
         <fn fn-type="conflict" id="conf1">
            <p>The author declare that no competing interests exist.</p>
         </fn>
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         <title>References</title>
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