{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T13:48:56Z","timestamp":1761918536403},"reference-count":10,"publisher":"American Society of Hematology","issue":"5","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2004,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Aberrant expression of transcription factor oncogenes such as HOX11, HOX11L2, TAL1\/SCL, LYL1, LMO1, and LMO2 can be detected in lymphoblasts from up to 80% of patients with acute T-cell lymphoblastic leukemia (T-ALL). Transcriptional activation of these oncogenes in leukemic cells typically results from chromosomal rearrangements that place them next to highly active cis-acting transcriptional regulatory elements. However, biallelic activation of TAL1 in some T-ALL cases has been previously proposed. We have used allele-specific mRNA analysis to show that trans-acting mechanisms leading to biallelic overexpression of TAL1 are involved in 10 (42%) of 24 TAL1+ informative T-ALL cases, 2 (17%) of 12 HOX11+ informative cases, and 7 (64%) of 11 LMO2+ informative cases. We propose that aberrant expression of oncogenic transcription factors in a significant fraction of T-ALLs may result from loss of the upstream transcriptional mechanisms that normally down-regulate the expression of these oncogenes during T-cell development.<\/jats:p>","DOI":"10.1182\/blood-2003-07-2577","type":"journal-article","created":{"date-parts":[[2003,11,10]],"date-time":"2003-11-10T20:13:36Z","timestamp":1068495216000},"page":"1909-1911","update-policy":"http:\/\/dx.doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":101,"title":["Biallelic transcriptional activation of oncogenic transcription factors in T-cell acute lymphoblastic leukemia"],"prefix":"10.1182","volume":"103","author":[{"given":"Adolfo A.","family":"Ferrando","sequence":"first","affiliation":[{"name":"From the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; Department of Pediatric Oncology, Harvard Medical School, Boston, MA; Clinical Research Institute of Montre\u0301al, Montre\u0301al, QC, Canada; and Shannon McCormack Advanced Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA."}]},{"given":"Sabine","family":"Herblot","sequence":"additional","affiliation":[{"name":"From the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; Department of Pediatric Oncology, Harvard Medical School, Boston, MA; Clinical Research Institute of Montre\u0301al, Montre\u0301al, QC, Canada; and Shannon McCormack Advanced Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA."}]},{"given":"Teresa","family":"Palomero","sequence":"additional","affiliation":[{"name":"From the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; Department of Pediatric Oncology, Harvard Medical School, Boston, MA; Clinical Research Institute of Montre\u0301al, Montre\u0301al, QC, Canada; and Shannon McCormack Advanced Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA."}]},{"given":"Mark","family":"Hansen","sequence":"additional","affiliation":[{"name":"From the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; Department of Pediatric Oncology, Harvard Medical School, Boston, MA; Clinical Research Institute of Montre\u0301al, Montre\u0301al, QC, Canada; and Shannon McCormack Advanced Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA."}]},{"given":"Trang","family":"Hoang","sequence":"additional","affiliation":[{"name":"From the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; Department of Pediatric Oncology, Harvard Medical School, Boston, MA; Clinical Research Institute of Montre\u0301al, Montre\u0301al, QC, Canada; and Shannon McCormack Advanced Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA."}]},{"given":"Edward A.","family":"Fox","sequence":"additional","affiliation":[{"name":"From the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; Department of Pediatric Oncology, Harvard Medical School, Boston, MA; Clinical Research Institute of Montre\u0301al, Montre\u0301al, QC, Canada; and Shannon McCormack Advanced Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA."}]},{"given":"A. Thomas","family":"Look","sequence":"additional","affiliation":[{"name":"From the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; Department of Pediatric Oncology, Harvard Medical School, Boston, MA; Clinical Research Institute of Montre\u0301al, Montre\u0301al, QC, Canada; and Shannon McCormack Advanced Molecular Diagnostics Laboratory, Dana-Farber Cancer Institute, Boston, MA."}]}],"member":"234","reference":[{"key":"2020021220573172200_REF1","doi-asserted-by":"crossref","unstructured":"Ferrando AA, Look AT. Clinical implications of recurring chromosomal and associated molecular abnormalities in acute lymphoblastic leukemia. Semin Hematol. 2000;37: 381-395.","DOI":"10.1016\/S0037-1963(00)90018-0"},{"key":"2020021220573172200_REF2","doi-asserted-by":"crossref","unstructured":"Ferrando AA, Neuberg DS, Staunton J, et al. Gene expression signatures define novel oncogenic pathways in T cell acute lymphoblastic leukemia. Cancer Cell. 2002;1: 75-87.","DOI":"10.1016\/S1535-6108(02)00018-1"},{"key":"2020021220573172200_REF3","doi-asserted-by":"crossref","unstructured":"Kees UR, Heerema NA, Kumar R, et al. Expression of HOX11 in childhood T-lineage acute lymphoblastic leukaemia can occur in the absence of cytogenetic aberration at 10q24: a study from the Children's Cancer Group (CCG). Leukemia. 2003;17: 887-893.","DOI":"10.1038\/sj.leu.2402892"},{"key":"2020021220573172200_REF4","doi-asserted-by":"crossref","unstructured":"Bash RO, Hall S, Timmons CF, et al. Does activation of the TAL1 gene occur in a majority of patients with T-cell acute lymphoblastic leukemia? A pediatric oncology group study. Blood. 1995;86: 666-676.","DOI":"10.1182\/blood.V86.2.666.bloodjournal862666"},{"key":"2020021220573172200_REF5","doi-asserted-by":"crossref","unstructured":"Watt PM, Kumar R, Kees UR. Promoter demethylation accompanies reactivation of the HOX11 proto-oncogene in leukemia. Genes Chromosomes Cancer. 2000;29: 371-377.","DOI":"10.1002\/1098-2264(2000)9999:9999<::AID-GCC1050>3.0.CO;2-Y"},{"key":"2020021220573172200_REF6","doi-asserted-by":"crossref","unstructured":"Herblot S, Steff AM, Hugo P, Aplan PD, Hoang T. SCL and LMO1 alter thymocyte differentiation: inhibition of E2A-HEB function and pre-T alpha chain expression. Nat Immunol. 2000;1: 138-144.","DOI":"10.1038\/77819"},{"key":"2020021220573172200_REF7","unstructured":"Janssen JW, Ludwig WD, Sterry W, Bartram CR. SIL-TAL1 deletion in T-cell acute lymphoblastic leukemia. Leukemia. 1993;7: 1204-1210."},{"key":"2020021220573172200_REF8","doi-asserted-by":"crossref","unstructured":"Bash RO, Crist WM, Shuster JJ, et al. Clinical features and outcome of T-cell acute lymphoblastic leukemia in childhood with respect to alterations at the TAL1 locus: a Pediatric Oncology Group study. Blood. 1993;81: 2110-2117.","DOI":"10.1182\/blood.V81.8.2110.2110"},{"key":"2020021220573172200_REF9","unstructured":"Salvati PD, Ranford PR, Ford J, Kees UR. HOX11 expression in pediatric acute lymphoblastic leukemia is associated with T-cell phenotype. Oncogene. 1995;11: 1333-1338."},{"key":"2020021220573172200_REF10","doi-asserted-by":"crossref","unstructured":"Spits H. Development of alphabeta T cells in the human thymus. Nat Rev Immunol. 2002;2: 760-772.","DOI":"10.1038\/nri913"}],"container-title":["Blood"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/ashpublications.org\/blood\/article-pdf\/103\/5\/1909\/1695612\/zh800504001909.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"http:\/\/ashpublications.org\/blood\/article-pdf\/103\/5\/1909\/1695612\/zh800504001909.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2020,2,12]],"date-time":"2020-02-12T21:04:39Z","timestamp":1581541479000},"score":1,"resource":{"primary":{"URL":"https:\/\/ashpublications.org\/blood\/article\/103\/5\/1909\/18161\/Biallelic-transcriptional-activation-of-oncogenic"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2004,3,1]]},"references-count":10,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2004,3,1]]}},"URL":"https:\/\/doi.org\/10.1182\/blood-2003-07-2577","relation":{},"ISSN":["0006-4971","1528-0020"],"issn-type":[{"value":"0006-4971","type":"print"},{"value":"1528-0020","type":"electronic"}],"subject":[],"published":{"date-parts":[[2004,3,1]]}}}