|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Patients with additional mutation at first sample showed a higher probability of developing cytopenia under HU therapy and a higher risk of AML (HR 12.2, 95% CI 2.6-57.1, p = 0.001) with mutations in ASXL1 (p < 0.0001), TP53 (p = 0.01), SRSF2 (p < 0.0001), IDH1/2 (p < 0.0001), and RUNX1 (p < 0.0001) being associated with a higher probability of AML.
|
29181548 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Multivariate analysis demonstrated that TP53 gene mutation in the DNA binding domain and outside the DNA binding domain was an independent poor prognostic factor for overall survival and relapse-free survival among the total cohort and it is also an unfavorable prognostic factor in FLT3-ITD-negative AML cases aged 70 years or below with intermediate cytogenetic prognosis.
|
28980058 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
We proposed that FLT3-ITD, NPM1 and TP53 be identified as markers for risk stratification of AML-M0 and M1.
|
29961066 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Granulocytes in AML-CK exhibited brighter expression of CD5, CD7, CD10 and CD14, with brighter CD3 also seen in AML-TP53.
|
30171088 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
All subjects with TP53 mutations (n = 21 out of 21 patients) and IDH1 and IDH2 (n = 15 out of 15 patients) mutations eventually developed AML in our study.
|
29988143 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
We conclude that p53 expression evaluated by immunohistochemistry in bone marrow biopsy specimens at the time of AML diagnosis may indicate distinct clinical characteristics in patients with normal diploid cytogenetics and is a potentially valuable tool that can enhance risk-stratification.
|
30117185 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Our study provides mechanistic insight to support further testing of ALRN-6924 as a therapeutic approach in AML and other cancers with wild-type p53.
|
29643228 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Tumor protein p53 (<i>TP53</i>) mutations are not only a risk factor in acute myeloid leukemia (AML) but also a potential biomarker for individualized treatment options.
|
29343974 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
The clinical and genomic characteristics of TP53 mutated AML are reviewed in this paper.
|
30466751 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
In summary, our data indicate that CITED2 functions in pathways regulating p53 activity and therefore represents an interesting target for AML therapy, since de novo AML cases are characterized by an inactivation of the p53 pathway or deregulation of apoptosis-related genes.
|
29072699 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Two new provisional entities, AML with mutated RUNX1 and AML with BCR- ABL1, have been included in the current update of the WHO classification of myeloid neoplasms and AML, and mutations in three genes- RUNX1, ASXL1, and TP53-have been added in the risk stratification of the 2017 European LeukemiaNet recommendations for AML.
|
28297624 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Acute myeloid leukemia (AML) is the most common malignant myeloid disorder in adults, and TP53 mutations or loss are frequently detected in patients with therapy-related AML or AML with complex karyotype.
|
28400619 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Our work indicates that genetic alterations of m<sup>6</sup>A regulatory genes may cooperate with TP53 and/or its regulator/downstream targets in the pathogenesis and/or maintenance of AML.
|
28153030 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Mechanistically, p53 activation negatively regulates the Ras/Raf/MEK/ERK pathway and activates GSK3 to modulate Mcl-1 phosphorylation and promote its degradation, thus overcoming AML resistance to Bcl-2 inhibition.
|
29232553 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Patients with p53 mutant AML are at an extremely high risk of relapse.
|
28211885 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
The resolution of the mechanisms underlying p53 dysfunction will better address the p53-targeted therapies that are currently considered for AML.
|
28607134 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Inactivated genes, such as <i>ASPP1, TP53, IKZF1</i> and <i>P15</i>, may correlate with poor prognosis in acute lymphoid leukemia (ALL), chronic lymphoid leukemia (CLL), chronic myelogenous leukemia (CML) and acute myeloid leukemia (AML), respectively.
|
28580304 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
In this issue of Cancer Cell, Pan et al. show that a combination therapy designed to reactivate the p53 tumor suppressor while antagonizing the anti-apoptotic function of Bcl-2 is highly active in preclinical models of refractory acute myeloid leukemia (AML).
|
29232547 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
In contrast to wild-type p53 AML (TP53<sup>wt</sup>), HCQ treatment did not trigger a BAX and PUMA-dependent apoptotic response in AMLs harboring TP53<sup>mut</sup>.
|
28703806 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
We examined a large AML cohort using proteomics, mutational profiling and network analyses, and showed that (1) p53 stabilization is universal in mutant TP53 samples, it is frequent in samples with wild-type TP53, and in both cases portends an equally dismal prognosis; (2) the p53 negative regulator Mdm2 is frequently overexpressed in samples retaining wild-type TP53 alleles, coupled with absence of p21 expression and dismal prognosis similar to that of cases with p53 stabilization; (3) AML samples display unique patterns of p53 pathway protein expression, which segregate prognostic groups with distinct cure rates; (4) such patterns of protein activation unveil potential AML vulnerabilities that can be therapeutically exploited.
|
27885271 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
The rationale for the investigation of those agents in AML and MDS is supported by an observed increased expression of programmed cell death 1 protein (PD-1) and ligand 1 (PD-L1) in the hematopoietic microenvironment of AML and MDS, and its association with low TP53 and a poor prognosis.
|
28643044 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
To further investigate the genetic interaction between p53 loss and endogenous Nras<sup>G12D/+</sup> in AML, we generated conditional Nras<sup>G12D/+</sup>p53<sup>-/-</sup> mice.
|
27815262 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Our bioinformatic analysis demonstrated that p53 pathway is differentially inactivated in different AML subtypes.
|
28340577 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
In this study, we evaluate the expression of p53 in core biopsies with acute myeloid leukemia and correlate the level of expression with acute myeloid leukemia subtype, TP53 mutation status, karyotype, and survival.
|
27934876 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Since Nup98 is a well-known regulator of the post-transcriptional modification of P53 target genes, and <i>P53</i> mutations are occasionally reported in AML, this translocant yeast strain can be used as a model to test the constitutive expression of human <i>P53</i>.
|
29034209 |
2017 |