{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T00:13:46Z","timestamp":1779236026348,"version":"3.51.4"},"reference-count":33,"publisher":"American Society for Clinical Investigation","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,7,7]]},"abstract":"<jats:p>\n                    The tumor suppressor p53 blocks tumor progression in multiple tumor types. Radiation-induced cancer following exposure to radiation therapy or space travel may also be regulated by p53 because p53 has been proposed to respond to DNA damage to suppress tumorigenesis. Here, we investigate the role of p53 in lung carcinogenesis and lymphomagenesis in\n                    <jats:italic>\n                      LA-1 Kras\n                      <jats:sup>G12D<\/jats:sup>\n                    <\/jats:italic>\n                    mice with\n                    <jats:italic>wild-type<\/jats:italic>\n                    <jats:italic>p53<\/jats:italic>\n                    or an extra copy of\n                    <jats:italic>p53<\/jats:italic>\n                    (\n                    <jats:italic>super p53<\/jats:italic>\n                    ) exposed to fractionated total body irradiation with low linear energy transfer (low-LET) X-rays or high-LET iron ions and compared tumor formation in these mice with unirradiated controls. We found that an additional copy of\n                    <jats:italic>p53<\/jats:italic>\n                    suppressed both Kras-driven lung tumor and lymphoma development in the absence of radiation. However, an additional copy of\n                    <jats:italic>p53<\/jats:italic>\n                    did not affect lymphoma development following low- or high-LET radiation exposure and was unable to suppress radiation-induced expansion of thymocytes with mutated\n                    <jats:italic>Kras<\/jats:italic>\n                    . Moreover, radiation exposure increased lung tumor size in\n                    <jats:italic>super p53<\/jats:italic>\n                    but not\n                    <jats:italic>wild-type p53<\/jats:italic>\n                    mice. These results demonstrate that although\n                    <jats:italic>p53<\/jats:italic>\n                    suppresses the development of spontaneous tumors expressing Kras\n                    <jats:sup>G12D<\/jats:sup>\n                    , in the context of exposure to ionizing radiation, an extra copy of\n                    <jats:italic>p53<\/jats:italic>\n                    does not protect against radiation-induced lymphoma and may promote Kras\n                    <jats:sup>G12D<\/jats:sup>\n                    mutant lung cancer.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.86698","type":"journal-article","created":{"date-parts":[[2016,7,6]],"date-time":"2016-07-06T11:00:57Z","timestamp":1467802857000},"source":"Crossref","is-referenced-by-count":17,"title":["An extra copy of p53 suppresses development of spontaneous Kras-driven but not radiation-induced cancer"],"prefix":"10.1172","volume":"1","author":[{"given":"Everett J.","family":"Moding","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Cancer Biology and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hooney D.","family":"Min","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Duke University, Durham, North Carolina, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katherine D.","family":"Castle","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Cancer Biology and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Moiez","family":"Ali","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Cancer Biology and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Loretta","family":"Woodlief","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Duke University, Durham, North Carolina, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nerissa","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Duke University, Durham, North Carolina, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Duke University, Durham, North Carolina, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yongbaek","family":"Kim","sequence":"additional","affiliation":[{"name":"Laboratory of Veterinary Clinical Pathology, College of Veterinary Medicine, Seoul National University, Seoul, South Korea."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chang-Lung","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Duke University, Durham, North Carolina, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David G.","family":"Kirsch","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Cancer Biology and"},{"name":"Department of Radiation Oncology, Duke University, Durham, North Carolina, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"232","published-online":{"date-parts":[[2016,7,7]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-10-4563"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ng747"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccr.2012.11.014"},{"issue":"5","key":"B4","first-page":"412","article-title":"Role of p53 in regulating tissue response to radiation by mechanisms independent of apoptosis","volume":"2","author":"Lee","year":"2013","journal-title":"Transl Cancer 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