The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia

Pieter Van Vlierberghe, Martine Van Grotel, H. Berna Beverloo, Charles Lee, Tryggvi Helgason, Jessica Buijs-Gladdines, Monique Passier, Elisabeth R. Van Wering, Anjo J.P. Veerman, Willem A. Kamps, Jules P.P. Meijerink, Rob Pieters

Onderzoeksoutput: Bijdrage aan tijdschriftArtikelpeer review

141 Citaten (Scopus)

Samenvatting

To identify new cytogenetic abnormalities associated with leukemogenesis or disease outcome, T-cell acute lymphoblastic leukemia (T-ALL) patient samples were analyzed by means of the array-comparative genome hybridization technique (array-CGH). Here, we report the identification of a new recurrent and cryptic deletion on chromosome 11 (del(11)(p12p13)) in about 4% (6/138) of pediatric T-ALL patients. Detailed molecular-cytogenetic analysis revealed that this deletion activates the LMO2 oncogene in 4 of 6 del(11)(p12p13)-positive T-ALL patients, in the same manner as in patients with an LMO2 translocation (9/138). The LMO2 activation mechanism of this deletion is loss of a negative regulatory region upstream of LMO2, causing activation of the proximal LMO2 promoter. LMO2 rearrangements, including this del(11)(p12p13) and t(11;14) (p13;q11) or t(7;11)(q35;p13), were found in the absence of other recurrent cytogenetic abnormalities involving HOX11L2, HOX11, CALM-AF10, TAL1, MLL, or MYC. LMO2 abnormalities represent about 9% (13/138) of pediatric T-ALL cases and are more frequent in pediatric T-ALL than appreciated until now.

Originele taal-2Engels
Pagina's (van-tot)3520-3529
Aantal pagina's10
TijdschriftBlood
Volume108
Nummer van het tijdschrift10
DOI's
StatusGepubliceerd - 15 nov. 2006
Extern gepubliceerdJa

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