|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Targeting acute myeloid leukemia with TP53-independent vosaroxin.
|
27615555 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
This study reviews molecular advances in understanding the role of p53 in MDS and AML, and explores potential therapeutic strategies in this era of personalized medicine.
|
27967292 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
In conclusion, the results suggest that there is no association between TP53 Arg72Pro polymorphism and the risk of leukemia, but the CC genotype may increase the risk of ALL TP53 Arg72Pro polymorphism CC genotype may increase the risk of ALL but is not associated with AML.
|
27053289 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Despite a similar effect on apoptosis and cell numbers, the absence of p53 and PUMA had diametrically opposed effects on progression to AML: absence of p53 accelerated leukemic progression, while absence of PUMA significantly delayed progression.
|
26742432 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Gene expression profiling in TP53 mutant KMB3 acute myeloid leukaemia (AML) cells showed that genes which protected cells from oxidative stress to be the most up-regulated.
|
26991755 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
MLN4924/belinostat coadministration synergistically induced AML cell apoptosis with or without p53 deficiency or FLT3-internal tandem duplication (ITD), whereas p53 short hairpin RNA (shRNA) knockdown or enforced FLT3-ITD expression significantly sensitized cells to the regimen.
|
26851293 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
These results suggest that screening for TP53 mutations at diagnosis is useful for identifying older adults with AML who are least likely to respond to chemotherapy, although the presence of this mutation alone does not seem to justify rejecting induction therapy.
|
26781615 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Mutational analysis of TP53 might be an important additional tool to predict outcome after HSCT in patients with adverse karyotype AML.
|
26771088 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
TP53 and Decitabine in Acute Myeloid Leukemia and Myelodysplastic Syndromes.
|
27959731 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Conversely, p53 mutations are rare in leukemias and are only observed in a small fraction of the patient population, predominately in patients with complex karyotype acute myeloid leukemia or hypodiploid acute lymphoblastic leukemia.
|
27327543 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
This activity appeared to be p53 dependent, and E6201-induced cytotoxicity was retained under hypoxic culture conditions and during coculture with mesenchymal stem cells that mimic the AML microenvironment.
|
26822154 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
The p53-KLF4-CEBPA axis is deregulated in AML but can be functionally restored by conventional chemotherapy and novel p53 activating treatments.
|
26408402 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Hydroxyurea synergizes with valproic acid in wild-type p53 acute myeloid leukaemia.
|
26812881 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Combination treatment with venetoclax and idasanutlin results in synergistic anti-tumor activity compared with the respective single-agent treatments in vitro, in p53 wild-type AML cell lines, and leads to strongly superior efficacy in vivo, in subcutaneous and orthotopic AML models.
|
27353420 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
In this study, a high MDM2 transcription level was observed (41.17%) regardless of p53 expression in patient with acute myeloid leukemia (AML).
|
27524244 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Whole-arm translocation of der(5;17)(p10;q10) with concurrent TP53 mutations in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): A unique molecular-cytogenetic subgroup.
|
27134073 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Here, we found that inhibition of the kinase ATR, which is the primary sensor of DNA replication stress, induced chromosomal breakage and death of mouse AML(MLL) cells (with an MLL-ENL fusion and a constitutively active N-RAS independently of p53.
|
27625305 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
Biomarker
|
disease |
BEFREE |
Patients with chromatin-spliceosome and TP53-aneuploidy AML had poor outcomes, with the various class-defining mutations contributing independently and additively to the outcome.
|
27276561 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
DNMT3a and TP53 mutations in AML have a pertinent prognostic and therapeutic value for patients and their addition enhances the current three gene panel.
|
26992835 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
TP53 mutations are highly and similarly prevalent in t-MDS and t-AML but mutations in genes other than TP53 were more frequent in t-AML than t-MDS.
|
25573287 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Three patients progressed to AML; one, with baseline TP53 mutation, achieved HI-E, partial CyR, and did not progress to AML.
|
25811676 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
For example, in acute myeloid leukemia (AML) higher epigenetic age-predictions are associated with increased incidence of mutations in RUNX1, WT1, and IDH2, whereas mutations in TET2, TP53, and PML-PARA translocation are more frequent in younger age-predictions.
|
26110659 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Mutational analysis further demonstrated that TP53 mutations are associated with complex karyotype AML, whereas ASXL1 and U2AF1 mutations are associated with AML with myelodysplasia-related changes.
|
25412851 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
TP53 mutation characteristics in therapy-related myelodysplastic syndromes and acute myeloid leukemia is similar to de novo diseases.
|
25952993 |
2015 |