Matches in UGent Biblio for { <https://biblio.ugent.be/publication/3126734#aggregation> ?p ?o. }
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- aggregation classification "A1".
- aggregation creator B510419.
- aggregation creator B510420.
- aggregation creator B510421.
- aggregation creator B510422.
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- aggregation creator person.
- aggregation date "2008".
- aggregation format "application/pdf".
- aggregation hasFormat 3126734.bibtex.
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- aggregation isPartOf urn:issn:0887-6924.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Cooperative genetic defects in TLX3 rearranged pediatric T-ALL".
- aggregation abstract "T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes. About 20% of pediatric T-ALL cases are characterized by TLX3 expression due to a cryptic translocation t(5; 14)(q35; q32). Although a number of collaborating genetic events have been identified in TLX3 rearranged T-ALL patients (NOTCH1 mutations, p15/p16 deletions, NUP214-ABL1 amplifications), further elucidation of additional genetic lesions could provide a better understanding of the pathogenesis of this specific T-ALL subtype. In this study, we used array-CGH to screen TLX3 rearranged T-ALL patients for new chromosomal imbalances. Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del(19)(p13.2). From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases. In addition, 19 other genetic lesions were detected once in TLX3 rearranged T-ALL cases, including a cryptic WT1 deletion and a deletion covering the FBXW7 gene, an U3-ubiquitin ligase that mediates the degradation of NOTCH1, MYC, JUN and CyclinE. This study provides a genome-wide overview of copy number changes in TLX3 rearranged T-ALL and offers great new challenges for the identification of new target genes that may play a role in the pathogenesis of T-ALL.".
- aggregation authorList BK855604.
- aggregation endPage "770".
- aggregation issue "4".
- aggregation startPage "762".
- aggregation volume "22".
- aggregation aggregates 3195330.
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