{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:17:18Z","timestamp":1784557038243,"version":"3.55.0"},"reference-count":62,"publisher":"Bioscientifica","issue":"3","content-domain":{"domain":["erc.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:p>\n                    Ionizing radiation (IR) exposure increases the risk of thyroid cancer and other cancer types. Chromosomal rearrangements, such as\n                    <jats:italic>RET\/PTC<\/jats:italic>\n                    , are characteristic features of radiation-associated thyroid cancer and can be induced by radiation\n                    <jats:italic>in vitro<\/jats:italic>\n                    . IR causes double-strand breaks (DSBs), suggesting that such damage leads to\n                    <jats:italic>RET\/PTC<\/jats:italic>\n                    , but the rearrangement mechanism has not been established. To study the mechanism, we explored the possibility of inducing\n                    <jats:italic>RET\/PTC<\/jats:italic>\n                    by electroporation of restriction endonucleases (REs) into HTori-3 human thyroid cells. We used five REs, which induced DSB in a dose-dependent manner similar to that seen with IR. Although all but one RE caused DSB in one or more of the three genes involved in\n                    <jats:italic>RET\/PTC<\/jats:italic>\n                    , rearrangement was detected only in cells electroporated with either PvuII (25 and 100\u200aU) or StuI (100 and 250\u200aU). The predominant rearrangement type was\n                    <jats:italic>RET\/PTC3<\/jats:italic>\n                    , which is characteristic of human thyroid cancer arising early after Chernobyl-related radioactive iodine exposure. Both enzymes that produced\n                    <jats:italic>RET\/PTC<\/jats:italic>\n                    had restriction sites only in one of the two fusion partner genes. Moreover, the two enzymes that produced\n                    <jats:italic>RET\/PTC<\/jats:italic>\n                    had restriction sites present in clusters, which was not the case for RE that failed to induce\n                    <jats:italic>RET\/PTC<\/jats:italic>\n                    . In summary, we establish a model of DSB induction by RE and report for the first time the formation of carcinogenic chromosomal rearrangements, predominantly\n                    <jats:italic>RET\/PTC3<\/jats:italic>\n                    , as a result of DSB produced by RE. Our data also raise a possibility that\n                    <jats:italic>RET\/PTC<\/jats:italic>\n                    rearrangement can be initiated by a complex DSB that is induced in one of the fusion partner genes.\n                  <\/jats:p>","DOI":"10.1530\/erc-11-0314","type":"journal-article","created":{"date-parts":[[2012,2,10]],"date-time":"2012-02-10T00:53:05Z","timestamp":1328835185000},"page":"271-281","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":16,"title":["Formation of carcinogenic chromosomal rearrangements in human thyroid cells after induction of double-strand DNA breaks by restriction 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