{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T13:55:25Z","timestamp":1761918925803},"reference-count":49,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,10,17]],"date-time":"2006-10-17T00:00:00Z","timestamp":1161043200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp; Cancer"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The dic(17;20) is a recurrent unbalanced translocation occurring rarely in myelodysplastic syndromes and acute myeloid leukemia. We have studied eleven cases with the dic(17;20) or a more complex derivative, all of which showed deletion of 17p and 20q material. The tumor suppressor gene <jats:italic>TP53<\/jats:italic> was not always lost, supporting a more distal gene as the target of these 17p deletions. All derivatives could be interpreted as having initially been formed as a dicentric chromosome, those with a larger amount of material between the centromeres having undergone further rearrangement to stabilize the chromosome while retaining proximal 17p and proximal 20q material. We propose that critical sequences on both 17p and 20q proximal to the sites of deletion must be retained during the critical 17p and 20q deletions. This would explain the excess of dicentric chromosomes resulting from 17;20 translocation, and the apparent stabilization of the unstable derivatives by further rearrangements which preserve 17p and 20q material. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gcc.20385","type":"journal-article","created":{"date-parts":[[2006,10,17]],"date-time":"2006-10-17T20:42:05Z","timestamp":1161117725000},"page":"27-36","source":"Crossref","is-referenced-by-count":12,"title":["A FISH comparison of variant derivatives of the recurrent dic(17;20) of myelodysplastic syndromes and acute myeloid leukemia: Obligatory retention of genes on 17p and 20q may explain the formation of dicentric chromosomes"],"prefix":"10.1002","volume":"46","author":[{"given":"Ruth N.","family":"MacKinnon","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cris","family":"Patsouris","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ilse","family":"Chudoba","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lynda J.","family":"Campbell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,10,17]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/gcc.20145"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.leu.2401594"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M204734200"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1203728"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2141.1976.tb03563.x"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2141.1991.tb04444.x"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/0165-4608(95)00316-9"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1002\/ajh.20366"},{"key":"e_1_2_6_10_1","first-page":"67","article-title":"The prognostic significance of deletion of the long arm of chromosome 20 in myeloid disorders","volume":"8","author":"Campbell LJ","year":"1994","journal-title":"Leukemia"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-4608(03)00102-X"},{"key":"e_1_2_6_12_1","doi-asserted-by":"crossref","first-page":"2138","DOI":"10.1182\/blood.V95.6.2138","article-title":"Deletions of chromosome 5q13.3 and 17p loci cooperate in myeloid neoplasms","volume":"95","author":"Castro PD","year":"2000","journal-title":"Blood"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.leu.2401654"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0145-2126(98)00177-5"},{"key":"e_1_2_6_15_1","first-page":"127","article-title":"Cytogenetics of myelodysplastic syndromes","volume":"33","author":"Fenaux P","year":"1996","journal-title":"Semin Hematol"},{"key":"e_1_2_6_16_1","doi-asserted-by":"crossref","first-page":"225","DOI":"10.1182\/blood.V94.1.225.413k24_225_232","article-title":"Isochromosome 17q in blast crisis of chronic myeloid leukemia and in other hematologic malignancies is the result of clustered breakpoints in 17p11 and is not associated with coding TP53 mutations","volume":"94","author":"Fioretos T","year":"1999","journal-title":"Blood"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.090013497"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2141.2000.01801.x"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0165-4608(96)00172-0"},{"key":"e_1_2_6_20_1","doi-asserted-by":"publisher","DOI":"10.1002\/gcc.2870080402"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1206304"},{"key":"e_1_2_6_22_1","first-page":"370","article-title":"Myelodysplastic syndromes and acute myeloid leukemia with 17p deletion. 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