دورية أكاديمية
Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL)
| العنوان: | Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) |
|---|---|
| المؤلفون: | Akasaka, Takashi, Balasas, Theodore, Russell, Lisa J, Sugimoto, Kei-ji, Majid, Aneela, Walewska, Renata, Karran, E Loraine, Brown, David G, Cain, Kelvin, Harder, Lana, Gesk, Stefan, Martin-Subero, Jose Ignacio, Atherton, Mark G, Brüggemann, Monika, Calasanz, María José, Davies, Teresa, Haas, Oskar A, Hagemeijer-Hausman, Anne, Kempski, Helena, Lessard, Michel, Lillington, Debra M, Moore, Sarah, Nguyen-Khac, Florence, Radford-Weiss, Isabelle, Schoch, Claudia, Struski, Stéphanie, Talley, Polly, Welham, Melanie J, Worley, Helen, Strefford, Jon C, Harrison, Christine J, Siebert, Reiner, Dyer, Martin J S |
| بيانات النشر: | W.B. Saunders |
| سنة النشر: | 2007 |
| المجموعة: | KU Leuven: Lirias |
| مصطلحات موضوعية: | Burkitt Lymphoma, CCAAT-Enhancer-Binding Proteins, Centromere, Chromosomes, Human, Humans, Immunoglobulin Heavy Chains, In Situ Hybridization, Fluorescence, Multigene Family, Oncogenes, Polymerase Chain Reaction, Telomere, Translocation, Genetic |
| الوصف: | CCAAT enhancer-binding protein (CEBP) transcription factors play pivotal roles in proliferation and differentiation, including suppression of myeloid leukemogenesis. Mutations of CEBPA are found in a subset of acute myeloid leukemia (AML) and in some cases of familial AML. Here, using cytogenetics, fluorescence in situ hybridization (FISH), and molecular cloning, we show that 5 CEBP gene family members are targeted by recurrent IGH chromosomal translocations in BCP-ALL. Ten patients with t(8;14)(q11;q32) involved CEBPD on chromosome 8, and 9 patients with t(14;19)(q32;q13) involved CEBPA, while a further patient involved CEBPG, located 71 kb telomeric of CEBPA in chromosome band 19q13; 4 patients with inv(14)(q11q32)/t(14;14)(q11;q32) involved CEBPE and 3 patients with t(14;20)(q32;q13) involved CEBPB. In 16 patients the translocation breakpoints were cloned using long-distance inverse-polymerase chain reaction (LDI-PCR). With the exception of CEBPD breakpoints, which were scattered within a 43-kb region centromeric of CEBPD, translocation breakpoints were clustered immediately 5' or 3' of the involved CEBP gene. Except in 1 patient with t(14;14)(q11;q32), the involved CEBP genes retained germ-line sequences. Quantitative reverse transcription (RT)-PCR showed overexpression of the translocated CEBP gene. Our findings implicate the CEBP gene family as novel oncogenes in BCP-ALL, and suggest opposing functions of CEBP dysregulation in myeloid and lymphoid leukemogenesis. ; status: published |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 0006-4971 1528-0020 |
| العلاقة: | Blood vol:109 issue:8 pages:3451-61; https://lirias.kuleuven.be/handle/123456789/318764Test; http://bloodjournal.hematologylibrary.org/cgi/pmidlookup?view=long&pmid=17170124Test |
| الإتاحة: | https://lirias.kuleuven.be/handle/123456789/318764Test http://bloodjournal.hematologylibrary.org/cgi/pmidlookup?view=long&pmid=17170124Test |
| رقم الانضمام: | edsbas.E157C3FD |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 00064971 15280020 |
|---|