|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Molecular mechanisms involved in the relapse of T-cell acute lymphoblastic leukemia (T-ALL) are not fully understood, although activating NOTCH1 signaling due to NOTCH1/FBXW7 alterations is a major oncogenic driver.
|
30387229 |
2019 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Our study suggests that NOTCH1/FBXW7 hotspot-mutated T-ALL cases had better response to ALL BFM-95 protocol.
|
29200162 |
2018 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Meta-analysis of the clinical characteristics and prognostic relevance of NOTCH1 and FBXW7 mutation in T-cell acute lymphoblastic leukemia.
|
29029518 |
2017 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
PTEN gene inactivation by mutation or deletion is common in pediatric T-cell acute lymphoblastic leukemia (T-ALL), but the impact on outcome is unclear, particularly in patients with NOTCH1/FBXW7 mutations.
|
26220040 |
2016 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Using an integrative approach combining genomic and transcriptomic data, we molecularly characterized 30 pediatric T-ALLs and identified common recurrent T-ALL targets such as FBXW7, JAK1, JAK3, PHF6, KDM6A and NOTCH1 as well as novel candidate T-ALL driver mutations including the p.R35L missense mutation in splicesome factor U2AF1 found in 3 patients and loss of function mutations in the X-linked tumor suppressor genes MED12 (frameshit mutation p.V167fs, splice site mutation g.chrX:70339329T>C, missense mutation p.R1989H) and USP9X (nonsense mutation p.Q117*).
|
27602765 |
2016 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
FBXW7 mutations were detected in 5 of the 50 (10%) T-ALL patients.
|
25493453 |
2015 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
This study revealed differences in the mutational profiles of pediatric and adult T-ALL and suggests mutant FBXW7 as an independent prognostic indicator for inferior survival in pediatric T-ALL.
|
26341754 |
2015 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In T-cell acute lymphoblastic leukemia (T-ALL), elevated MYB levels can arise directly through T-cell receptor-mediated MYB translocations, genomic MYB duplications or enhanced TAL1 complex binding at the MYB locus or indirectly through the TAL1/miR-223/FBXW7 regulatory axis.
|
25231743 |
2015 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Activation of the NOTCH pathway occurs commonly in T acute lymphoblastic leukemia (T-ALL) mainly due to mutations in NOTCH1 or alterations in FBW7 and is involved in the regulation of cell proliferation and survival.
|
25355291 |
2015 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Moreover, we observed the inverse correlation of miR-223 and FBXW7 expression in a panel of T-ALL patient-derived xenografts.
|
24727676 |
2014 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
A higher specific hazard of relapse was independently associated with postinduction MRD level ≥10(-4) and unfavorable genetic characteristics (ie, MLL gene rearrangement or focal IKZF1 gene deletion in BCP-ALL and no NOTCH1/FBXW7 mutation and/or N/K-RAS mutation and/or PTEN gene alteration in T-cell ALL).
|
24740809 |
2014 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
Biomarker
|
disease |
CTD_human |
c-Myc inhibition prevents leukemia initiation in mice and impairs the growth of relapsed and induction failure pediatric T-ALL cells.
|
24394663 |
2014 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
There was no difference in overall (P = 0.14) or event-free survival (EFS) (P = 0.10) in patients with T-ALL with mutation(s) in NOTCH1/FBXW7 compared with patients with T-ALL without mutations in any of these genes.
|
24424791 |
2014 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
FBXW7 regulates glucocorticoid response in T-cell acute lymphoblastic leukaemia by targeting the glucocorticoid receptor for degradation.
|
23228967 |
2013 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Overexpression of miR-223 also leads to marked down-regulation of FBXW7 protein expression, whereas knockdown of TAL1 leads to up-regulation of FBXW7 protein levels, with a marked reduction of its substrates MYC, MYB, NOTCH1, and CYCLIN E. We conclude that TAL1-mediated up-regulation of miR-223 promotes the malignant phenotype in T-ALL through repression of the FBXW7 tumor suppressor.
|
23857984 |
2013 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
In line with these genomic data, engineered deletion of Fbw7 in mouse T cells results in T-ALL, validating FBW7 as a T-ALL tumour suppressor.
|
21368833 |
2011 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Moreover, these miRNAs produce overlapping and cooperative effects on tumor suppressor genes implicated in the pathogenesis of T-ALL, including IKAROS (also known as IKZF1), PTEN, BIM, PHF6, NF1 and FBXW7.
|
21642990 |
2011 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Activation of the Notch pathway occurs commonly in T acute lymphoblastic leukemia (T-ALL) because of mutations in Notch1 or Fbw7 and is involved in the regulation of cell proliferation and survival.
|
21263446 |
2011 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Furthermore, it provides the rationale for targeted usage of Mcl-1 antagonists to treat Fbw7-deficient T-ALL patients.
|
21608150 |
2011 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
We investigated the prognostic implication of hyperactivation of NOTCH pathway resulting from mutations of NOTCH1 or FBXW7 in children with T-ALL enrolled in EORTC-CLG trials.
|
20861920 |
2010 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Reverse-phase protein microarray data confirmed that NOTCH1 and FBXW7 mutations resulted in increased intracellular NOTCH1 levels in primary T-ALL biopsies.
|
20861909 |
2010 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
NOTCH1 and FBXW7 were screened by a combination of denaturing high-performance liquid chromatography and sequencing in 88 adult patients with T-ALL treated on the UKALLXII/ECOG E2993 protocol and compared with clinical characteristics and outcome.
|
19635999 |
2009 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
We explored the impact of mutations in the NOTCH1, FBW7 and PTEN genes on prognosis and downstream signaling in a well-defined cohort of 47 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL).
|
19340001 |
2009 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
Biomarker
|
disease |
CTD_human |
Targeting the Notch1 and mTOR pathways in a mouse T-ALL model.
|
19246562 |
2009 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Three (5.4%) T-ALL and two (1.4%) T-NHL patients had mutations in both FBXW7 and NOTCH1.
|
19245433 |
2009 |