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The cumulative recurrence rate of the children with non-functional subtypes of IKZF1 was significantly higher than that of those with functional types of IKZF1.
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heterozygous mutation decreases plasmacytoid dendritic cell numbers and expands conventional dendritic cells
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IKZF1 has a role in childhood B-cell precursor acute lymphoblastic leukemia
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this study shows that alteration in Ikaros expression promotes B-1 cell differentiation into phagocytes
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Our results demonstrate that the IKAROS promotes PHF2 expression, and suggest that PHF2 (low) expression works with the IKAROS gene deletion to drive oncogenesis of ALL
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present case provides the first definitive evidence on the ability of an IKAROS heterozygous mutation to cause both immunodeficiency and NOTCH1-driven T-ALL in humans
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Casein kinase II, glycogen synthase kinase-3, and Ikaros mediated regulation of leukemia has been summarized. (Review)
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Results found Ikaros directly binding the DNM2 promoter and suppresses DNM2 expression in ALL tumors and cell lines.
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there is a clear distinction between loss-of-function and dominant-negative IKZF1 deletions. Affected patients should thus be monitored for minimal residual disease carefully to detect incipient relapses at an early stage and they are potential candidates for alternative or intensified treatment regimes.
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IKZF1 gene deletion is associated with acute lymphoblastic leukemia.
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data reveal the mechanism by which chromatin remodeling and target gene expression are regulated by Ikaros alone and in complex with HDAC1 in B-ALL
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Ikaros regulates expression of the BCL6/BACH2 axis in acute lymphoblastic leukemia cells.
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high CRLF2 expression works with the IKZF1 deletion to drive oncogenesis of acute lymphoblastic leukemia
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expression of both CEBPE and IKZF1 in patient leukemic B cells was most similar to that in early stage B cells, believed to be the B-ALL cell-of-origin
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we identified IKZF1 as a novel regulator of glucocorticoid -induced transcriptional responses and a critical determinant of glucocorticoid -mediated cell death in normal and leukemic B cells
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We systematically screened 6 potentially functional SNPs in ARID5B and IKZF1 genes.
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Two families with a Common variable immunodeficiency-like syndrome with normal hematologic parameters and fetal hemoglobulin silencing with heterozygote IKZF1 mutations.
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IKZF1 rs10235796 C allele, IKZF1 rs6964969A>G, CDKN2A rs3731246 G>C, and CDKN2A rs3731246 C allele were signi fi cantly associated with Acute Lymphoblastic Leukemia in Yemenis of Arab-Asian descent. Borderline association found in IKZF1 rs4132601 T>G variant. No associations found with IKZF1 rs11978267 or rs7789635, DDC rs3779084; rs880028; rs7809758, CDKN2A rs3731217, CEBPE rs2239633; rs12434881
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Silence of IKZF1 expression in MHCC-LM3 and MHCC-97L cell lines revealed a approximately 1.84- and approximately 2.27-fold rise in MDIG mRNA levels.
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Data show that six patients had large interstitial deletions starting within intronic regions of COBL at diagnosis, which is ~611 Kb downstream of IKZF1, suggesting that COBL is a hotspot for IKZF1 deletion (DeltaIKZF1).
