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In this study, we uncover three different modes of\n                    <jats:italic>ERG<\/jats:italic>\n                    amplification in AML\u2010CK. Importantly, we present evidence to show that\n                    <jats:italic>ERG<\/jats:italic>\n                    amplification is distinct from intrachromosomal amplification of chromosome 21 (iAMP21), a hallmark segmental amplification frequently encompassing\n                    <jats:italic>RUNX1<\/jats:italic>\n                    and\n                    <jats:italic>ERG<\/jats:italic>\n                    in a subset of high\u2010risk B\u2010lymphoblastic leukemia. We also characterize the association with\n                    <jats:italic>TP53<\/jats:italic>\n                    aberrations and other chromosomal aberrations, including chromothripsis. Lastly, we show that\n                    <jats:italic>ERG<\/jats:italic>\n                    amplification can initially emerge as subclonal events in low\u2010grade myeloid neoplasms. These findings demonstrate that\n                    <jats:italic>ERG<\/jats:italic>\n                    amplification is a recurrent secondary driver event in AML and raise the tantalizing possibility of\n                    <jats:italic>ERG<\/jats:italic>\n                    as a therapeutic target.\n                  <\/jats:p>","DOI":"10.1002\/gcc.23027","type":"journal-article","created":{"date-parts":[[2022,1,27]],"date-time":"2022-01-27T04:05:40Z","timestamp":1643256340000},"page":"399-411","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["<scp>\n                      <i>ERG<\/i>\n                    <\/scp>\n                    amplification is a secondary recurrent driver event in myeloid malignancy with complex karyotype and\n                    <scp>\n                      <i>TP53<\/i>\n                    <\/scp>\n                    mutations"],"prefix":"10.1002","volume":"61","author":[{"given":"Winston Y.","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Pathology, Michigan Medicine University of Michigan  Ann Arbor Michigan USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Efrain A.","family":"Gutierrez\u2010Lanz","sequence":"additional","affiliation":[{"name":"Department of Pathology, Michigan Medicine University of Michigan  Ann Arbor Michigan USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Pathology, Michigan Medicine University of Michigan  Ann Arbor Michigan USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"McClintock","sequence":"additional","affiliation":[{"name":"Department of Pathology, Michigan Medicine University of Michigan  Ann Arbor Michigan USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"May 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