{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:39:10Z","timestamp":1791225550100,"version":"4.1.0"},"reference-count":60,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2010,1,13]],"date-time":"2010-01-13T00:00:00Z","timestamp":1263340800000},"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":[[2010,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>T\u2010cell acute lymphoblastic leukemia (T\u2010ALL) is the result of multiple oncogenic insults of thymocytes. Recently, new <jats:italic>ABL1<\/jats:italic> fusion genes have been identified that provide proliferation and survival advantage to lymphoblasts. These are the <jats:italic>NUP214\u2010ABL1<\/jats:italic> fusion gene, on amplified episomes, the unique case of <jats:italic>EML1\u2010ABL1<\/jats:italic> fusion due to a cryptic t(9;14)(q34;q32) and the seldom reported <jats:italic>BCR\u2010ABL1<\/jats:italic> and <jats:italic>ETV6\u2010ABL1<\/jats:italic> chimeric genes. The most frequent and strictly associated with T\u2010ALL is the <jats:italic>NUP214\u2010ABL1<\/jats:italic> fusion identified in 6% of cases, in both children and adults. Patients present with classical T\u2010ALL features. Cytogenetically, the fusion is cryptic but seen by FISH on amplified episomes or more rarely as a small hsr. The <jats:italic>ABL1<\/jats:italic> fusion is a late event associated with other genetic alterations like <jats:italic>NOTCH1<\/jats:italic> activating mutation, deletion of <jats:italic>CDKN2A<\/jats:italic> locus, and ectopic expression of <jats:italic>TLX1<\/jats:italic> or <jats:italic>TLX3<\/jats:italic>. The mechanism of activation of the NUP214\u2010ABL1 protein is unique and requires localization at the nucleopore complex and interaction with other nuclear pore proteins for crossphosphorylation and constitutive kinase activity. The ABL1 fusion proteins are sensitive to tyrosine kinase inhibitors, which can be included in future treatment strategy. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gcc.20743","type":"journal-article","created":{"date-parts":[[2010,1,13]],"date-time":"2010-01-13T15:45:53Z","timestamp":1263397553000},"page":"299-308","source":"Crossref","is-referenced-by-count":66,"title":["<i>ABL1<\/i> rearrangements in T\u2010Cell acute lymphoblastic leukemia"],"prefix":"10.1002","volume":"49","author":[{"given":"Anne","family":"Hagemeijer","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos","family":"Graux","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2010,1,13]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/nri2304"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.leu.2403654"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.3324\/haematol.13291"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.leu.2403357"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cancergencyto.2005.04.002"},{"key":"e_1_2_11_7_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-04-014514"},{"key":"e_1_2_11_8_1","doi-asserted-by":"publisher","DOI":"10.3324\/haematol.10865"},{"key":"e_1_2_11_9_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-12-064683"},{"key":"e_1_2_11_10_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V76.3.489.489"},{"key":"e_1_2_11_11_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.2406902"},{"key":"e_1_2_11_12_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-12-4897"},{"key":"e_1_2_11_13_1","first-page":"1116","article-title":"Genetic insights in the pathogenesis of T\u2010cell acute lymphoblastic leukemia","volume":"90","author":"de Keersmaecker K","year":"2005","journal-title":"Haematologica"},{"key":"e_1_2_11_14_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.leu.2404425"},{"key":"e_1_2_11_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2008.05.005"},{"key":"e_1_2_11_16_1","unstructured":"de KeersmaeckerK VerachtertH LanduytW de Wolf\u2010PeetersC VandenbergheP SchwallerJ MarynenP CoolsJ.2008b.EML1\u2010ABL1 is activated by coiled coil mediated oligomerization and induces T cell acute lymphoblastic leukemia or myeloproliferative disease in a mouse bone marrow transplant model. ABL1 Fusions in T cell Acute Lymphoblastic Leukemia Ph.D. Thesis. 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