{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T09:11:09Z","timestamp":1792055469971,"version":"4.4.0"},"reference-count":28,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2006,3,10]],"date-time":"2006-03-10T00:00:00Z","timestamp":1141948800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2006,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>BACKGROUND<\/jats:title>\n                    <jats:p>\n                      The t(3;21)(q26;q22) translocation is associated with myeloid leukemias and results in a chimeric oncoprotein containing\n                      <jats:italic>AML1\/RUNX1<\/jats:italic>\n                      variably fused to\n                      <jats:italic>EAP, MDS1,<\/jats:italic>\n                      and\/or\n                      <jats:italic>EVI1<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      The current study describes what to the authors' knowledge is the first large case series reported to date of 26 t(3;21)(q26;q22)\u2010associated leukemias, in which 24 cases arose after chemotherapy. Conventional G\u2010band karyotyping and flow cytometry immunophenotyping were performed. Reverse transcriptase\u2013polymerase chain reaction (RT\u2013PCR) was performed to detect fusion transcripts between\n                      <jats:italic>AML1<\/jats:italic>\n                      and\n                      <jats:italic>EAP, MDS1<\/jats:italic>\n                      , or\n                      <jats:italic>EVI1<\/jats:italic>\n                      , followed by DNA sequencing.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>In all 16 patients with chronic myeloproliferative disorders, including 14 with chronic myelogenous leukemia (CML), the occurrence of t(3;21) heralded myeloid blast transformation. Fifteen (93%) patients had been previously treated with hydroxyurea. Eight patients with chronic myeloproliferative disorders (CMPD) were found to have t(3;21) with t(9;22) as the sole cytogenetic abnormality; in 5 other patients this was accompanied by trisomy 8. Among 10 cases of t(3;21)\u2010associated acute myeloid leukemia, 8 were secondary tumors after chemotherapy for other neoplasms that had been treated with regimens including fludarabine and 5\u2013fluorouracil in 3 patients each and etoposide in 2 patients. The immunophenotype of the blasts in all 22 tested cases was similar, with uniform expression of myeloid markers and CD34 and variable expression of CD7 and CD9, but minimal morphological myeloid maturation. Dysplastic micromegakaryocytes and bone marrow fibrosis were observed predominantly in CMPD cases. RT\u2013PCR followed by DNA sequencing showed that the AML1\u2010\/MDS1\u2010\/EVI1 (AME) fusion transcript was detected in all 5 cases assessed. Among the patients with CMPD, 8 died of disease (at a median of 6.5 mos) and 5 achieved disease remission with bone marrow transplantation. Among patients with acute myeloid leukemia\/myelodysplastic syndrome, 7 died of disease (at a median of 2 mos) and 2 had persistent leukemia with short follow\u2010up.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>Activation of AME through t(3;21) defines a highly aggressive, therapy\u2010related leukemic blast syndrome. Prior treatment with hydroxyurea or other antimetabolites is implicated as a contributory cause. Cancer 2006. \u00a9 2006 American Cancer Society.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cncr.21797","type":"journal-article","created":{"date-parts":[[2006,3,10]],"date-time":"2006-03-10T11:48:44Z","timestamp":1141991324000},"page":"1730-1738","source":"Crossref","is-referenced-by-count":51,"title":["t(3;21)(q26;q22) in myeloid leukemia"],"prefix":"10.1002","volume":"106","author":[{"given":"C.","family":"Cameron Yin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge","family":"Cortes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bedia","family":"Barkoh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kimberly","family":"Hayes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hagop","family":"Kantarjian","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dan","family":"Jones","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,3,10]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.1053\/shem.2002.36921"},{"key":"e_1_2_5_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0959-437X(02)00018-7"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrc840"},{"key":"e_1_2_5_5_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.16.7784"},{"key":"e_1_2_5_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06288.x"},{"key":"e_1_2_5_7_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.9.4004"},{"key":"e_1_2_5_8_2","volume-title":"World Health Organization classification of tumours. 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