Gene | Score gda | Association Type | Type | Original DB | Sentence supporting the association | PMID | PMID Year | ||||
---|---|---|---|---|---|---|---|---|---|---|---|
|
0.370 | FusionGene | disease | ORPHANET | Identification of fusion genes and characterization of transcriptome features in T-cell acute lymphoblastic leukemia. | 29279377 | 2018 | ||||
|
0.370 | Biomarker | disease | BEFREE | Combined targeting of SET and tyrosine kinases provides an effective therapeutic approach in human T-cell acute lymphoblastic leukemia. | 27705940 | 2016 | ||||
|
0.370 | Biomarker | disease | BEFREE | SET-NUP214-positive patients were predominantly (10 [91%] of 11) T-cell receptor (TCR)-negative and strikingly associated with TCRγδ lineage T-ALLs, as defined by expression of TCRγδ, TCRδ and/or TCRγ rearrangements but no complete TCRβ variable diversity joining rearrangement in surface CD3/TCR-negative cases. | 24449214 | 2014 | ||||
|
0.370 | AlteredExpression | disease | BEFREE | We showed that SET expression was significantly upregulated in 96.5% of B-acute lymphoblastic leukemia (28 of 29; 16.6 fold) and 93% of T-acute lymphoblastic leukemia (28 of 30; 47.6 fold) patients. | 22677993 | 2012 | ||||
|
0.370 | GeneticVariation | disease | BEFREE | Overall, these results indicate that, in T-cell acute lymphoblastic leukemia, PHF6 mutations are a recurrent genetic abnormality associated with mutations of NOTCH1, JAK1 and rearrangement of SET-NUP214. | 21880637 | 2011 | ||||
|
0.370 | Biomarker | disease | BEFREE | Multiplex-polymerase chain reaction analysis and gene expression profiling of 129 further cases found five additional cases of TAF_I-NUP214-positive T-cell acute lymphoblastic leukemia. | 20065082 | 2010 | ||||
|
0.370 | AlteredExpression | disease | BEFREE | Of 141 human leukemia/lymphoma cell lines tested, only the T-ALL cell line LOUCY and the AML cell line MEGAL expressed the SET(TAF-Ibeta)-NUP214 fusion gene transcript. | 19166587 | 2009 | ||||
|
0.370 | Biomarker | disease | BEFREE | We conclude that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest. | 18299449 | 2008 |