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Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine
by
Sarry, Audrey
, Filleron, Thomas
, Cassou, Manon
, Fornecker, Luc-Matthieu
, Plenecassagnes, Julien
, Luquet, Isabelle
, Simand, Célestine
, Prade, Naïs
, Bories, Pierre
, Bertoli, Sarah
, Largeaud, Laetitia
, Recher, Christian
, Lagarde, Stéphanie
, Cabarrou, Bastien
, De Mas, Véronique
, Delabesse, Eric
in
5-aza-2'-deoxycytidine
/ Acute myelocytic leukemia
/ Acute myeloid leukemia
/ Azacitidine
/ Biology and Life Sciences
/ Biomarkers
/ Bone marrow
/ Cancer
/ Cancer research
/ Cancer therapies
/ Chemotherapy
/ Classification
/ Cytogenetics
/ Deoxyribonucleic acid
/ DNA
/ Drug therapy
/ Gene mutation
/ Genetic aspects
/ Genetics
/ Health aspects
/ Hematology
/ Human genetics
/ Human health and pathology
/ Karyotypes
/ Leukemia
/ Life Sciences
/ Medical prognosis
/ Medicine and Health Sciences
/ Mutants
/ Mutation
/ Myeloid leukemia
/ p53 Protein
/ Patient outcomes
/ Patients
/ Pharmaceutical sciences
/ Pharmacology
/ Software
/ Subgroups
/ Tumor proteins
2020
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Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine
by
Sarry, Audrey
, Filleron, Thomas
, Cassou, Manon
, Fornecker, Luc-Matthieu
, Plenecassagnes, Julien
, Luquet, Isabelle
, Simand, Célestine
, Prade, Naïs
, Bories, Pierre
, Bertoli, Sarah
, Largeaud, Laetitia
, Recher, Christian
, Lagarde, Stéphanie
, Cabarrou, Bastien
, De Mas, Véronique
, Delabesse, Eric
in
5-aza-2'-deoxycytidine
/ Acute myelocytic leukemia
/ Acute myeloid leukemia
/ Azacitidine
/ Biology and Life Sciences
/ Biomarkers
/ Bone marrow
/ Cancer
/ Cancer research
/ Cancer therapies
/ Chemotherapy
/ Classification
/ Cytogenetics
/ Deoxyribonucleic acid
/ DNA
/ Drug therapy
/ Gene mutation
/ Genetic aspects
/ Genetics
/ Health aspects
/ Hematology
/ Human genetics
/ Human health and pathology
/ Karyotypes
/ Leukemia
/ Life Sciences
/ Medical prognosis
/ Medicine and Health Sciences
/ Mutants
/ Mutation
/ Myeloid leukemia
/ p53 Protein
/ Patient outcomes
/ Patients
/ Pharmaceutical sciences
/ Pharmacology
/ Software
/ Subgroups
/ Tumor proteins
2020
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Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine
by
Sarry, Audrey
, Filleron, Thomas
, Cassou, Manon
, Fornecker, Luc-Matthieu
, Plenecassagnes, Julien
, Luquet, Isabelle
, Simand, Célestine
, Prade, Naïs
, Bories, Pierre
, Bertoli, Sarah
, Largeaud, Laetitia
, Recher, Christian
, Lagarde, Stéphanie
, Cabarrou, Bastien
, De Mas, Véronique
, Delabesse, Eric
in
5-aza-2'-deoxycytidine
/ Acute myelocytic leukemia
/ Acute myeloid leukemia
/ Azacitidine
/ Biology and Life Sciences
/ Biomarkers
/ Bone marrow
/ Cancer
/ Cancer research
/ Cancer therapies
/ Chemotherapy
/ Classification
/ Cytogenetics
/ Deoxyribonucleic acid
/ DNA
/ Drug therapy
/ Gene mutation
/ Genetic aspects
/ Genetics
/ Health aspects
/ Hematology
/ Human genetics
/ Human health and pathology
/ Karyotypes
/ Leukemia
/ Life Sciences
/ Medical prognosis
/ Medicine and Health Sciences
/ Mutants
/ Mutation
/ Myeloid leukemia
/ p53 Protein
/ Patient outcomes
/ Patients
/ Pharmaceutical sciences
/ Pharmacology
/ Software
/ Subgroups
/ Tumor proteins
2020
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Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine
Journal Article
Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine
2020
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Overview
Hypomethylating agents are a classical frontline low-intensity therapy for older patients with acute myeloid leukemia. Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear. We analyzed the therapeutic course and outcome of 279 patients treated with azacitidine between 2007 and 2016, prospectively enrolled in our regional healthcare network. By screening 224 of them, we detected TP53 mutations in 55 patients (24.6%), including 53 patients (96.4%) harboring high-risk cytogenetics. The identification of any TP53 mutation was associated with worse overall survival but not with response to azacitidine in the whole cohort and in the subgroup of patients with adverse karyotype. Stratification of patients according to three recent validated functional classifications did not allow the identification of TP53 mutated patients who could benefit from azacitidine. Systematic TP53 mutant classification will deserve further exploration in the setting of patients treated with conventional therapy and in the emerging field of therapies targeting TP53 pathway.
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