Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2138223 | Leukemia Research | 2010 | 4 Pages |
Abstract
The Ikaros (Ikzf1) gene, encoding a transcription regulator, is a major tumor suppressor in B-cell acute lymphoblastic leukemia (B-ALL). In the mouse, however, loss of Ikaros is primarily associated with T-ALL development. Whether Ikaros is also implicated in human T-ALL remains unclear. We studied Ikaros in 25 human T-ALL samples from diverse molecular subtypes at the mRNA, protein, sequence and genomic copy number level. We found that Ikaros was abnormal in only one sample: one allele was lost by genomic deletion, while proteins generated from the remaining allele were delocalized and concentrated at a single cytoplasmic structure. Thus, inactivation of Ikaros by deletion or mutation is rare in human T-ALL.
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Authors
Ambroise Marçais, Robin Jeannet, Lucie Hernandez, Jean Soulier, François Sigaux, Susan Chan, Philippe Kastner,