LSC17 score complements genetics and ...
Type de document :
Compte-rendu et recension critique d'ouvrage
Titre :
LSC17 score complements genetics and measurable residual disease in acute myeloid leukemia: an ALFA study
Auteur(s) :
Vasseur, Loic [Auteur]
Fenwarth, Laurène [Auteur]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Institut de Pathologie [CHU Lille]
Lambert, Jérôme [Auteur]
de Botton, Stéphane [Auteur]
Hôpital Edouard Herriot [CHU - HCL]
Figeac, Martin [Auteur]
Plateforme de génomique fonctionnelle et structurelle [Lille]
Villenet, Céline [Auteur]
Plateforme de génomique fonctionnelle et structurelle [Lille]
Heiblig, Maël [Auteur]
Université Claude Bernard Lyon 1 [UCBL]
Hospices Civils de Lyon [HCL]
Centre de Recherche en Cancérologie de Lyon [UNICANCER/CRCL]
Dumas, Pierre-Yves [Auteur]
Centre d'Immunologie de Marseille - Luminy [CIML]
CHU Bordeaux
Récher, Christian [Auteur]
Centre Hospitalier Universitaire de Toulouse [CHU Toulouse]
Berthon, Celine [Auteur]
Hôpital Claude Huriez [Lille]
Service des Maladies du Sang [CHU Lille] [SMS]
Lemasle, Emilie [Auteur]
Centre de Lutte Contre le Cancer Henri Becquerel Normandie Rouen [CLCC Henri Becquerel]
Lebon, Delphine [Auteur]
CHU Amiens-Picardie
HEMATIM - Hématopoïèse et immunologie - UR UPJV 4666 [HEMATIM]
Lambert, Juliette [Auteur]
Thérapie génique et contrôle de l'expansion cellulaire [UMR E007]
Terré, Christine [Auteur]
Celli-Lebras, Karine [Auteur]
Service d'Hémato-oncologie [CHU Saint-Louis]
Dombret, Hervé [Auteur]
Hôpital Saint-Louis
Preudhomme, Claude [Auteur]
Service d'Hématologie Cellulaire [Lille]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Institut de Pathologie [CHU Lille]
Cheok, Meyling [Auteur]
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Itzykson, Raphaël [Auteur]
Recherche clinique appliquée à l'hématologie [(EA_3518)]
Duployez, Nicolas [Auteur]
Service de pathologie [CHU Lille]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Institut Coeur Poumon [CHU Lille]
Fenwarth, Laurène [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Institut de Pathologie [CHU Lille]
Lambert, Jérôme [Auteur]
de Botton, Stéphane [Auteur]
Hôpital Edouard Herriot [CHU - HCL]
Figeac, Martin [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Plateforme de génomique fonctionnelle et structurelle [Lille]
Villenet, Céline [Auteur]
Plateforme de génomique fonctionnelle et structurelle [Lille]
Heiblig, Maël [Auteur]
Université Claude Bernard Lyon 1 [UCBL]
Hospices Civils de Lyon [HCL]
Centre de Recherche en Cancérologie de Lyon [UNICANCER/CRCL]
Dumas, Pierre-Yves [Auteur]
Centre d'Immunologie de Marseille - Luminy [CIML]
CHU Bordeaux
Récher, Christian [Auteur]
Centre Hospitalier Universitaire de Toulouse [CHU Toulouse]
Berthon, Celine [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Hôpital Claude Huriez [Lille]
Service des Maladies du Sang [CHU Lille] [SMS]
Lemasle, Emilie [Auteur]
Centre de Lutte Contre le Cancer Henri Becquerel Normandie Rouen [CLCC Henri Becquerel]
Lebon, Delphine [Auteur]
CHU Amiens-Picardie
HEMATIM - Hématopoïèse et immunologie - UR UPJV 4666 [HEMATIM]
Lambert, Juliette [Auteur]
Thérapie génique et contrôle de l'expansion cellulaire [UMR E007]
Terré, Christine [Auteur]
Celli-Lebras, Karine [Auteur]
Service d'Hémato-oncologie [CHU Saint-Louis]
Dombret, Hervé [Auteur]
Hôpital Saint-Louis
Preudhomme, Claude [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Service d'Hématologie Cellulaire [Lille]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Institut de Pathologie [CHU Lille]
Cheok, Meyling [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Institut pour la recherche sur le cancer de Lille [Lille] [IRCL]
Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Itzykson, Raphaël [Auteur]
Recherche clinique appliquée à l'hématologie [(EA_3518)]
Duployez, Nicolas [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Service de pathologie [CHU Lille]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Institut Coeur Poumon [CHU Lille]
Titre de la revue :
Blood advances
Pagination :
4024-4034
Éditeur :
The American Society of Hematology
Date de publication :
2023-05
ISSN :
2473-9529
Mot(s)-clé(s) en anglais :
Clinical Trials and Observations
Myeloid Neoplasia
Myeloid Neoplasia
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Whether the LSC17 gene expression can improve risk stratification in the context of NGS-based risk stratification and measurable residual disease (MRD) in AML patients treated intensively has not been explored. We analyzed ...
Lire la suite >Whether the LSC17 gene expression can improve risk stratification in the context of NGS-based risk stratification and measurable residual disease (MRD) in AML patients treated intensively has not been explored. We analyzed LSC17 in 504 adult patients prospectively treated in the ALFA-0702 trial. Multiple (cyto)genetic alterations were associated with changes in LSC17, such as higher LSC17 in patients with RUNX1 or TP53 mutations, and lower scores in those with CEBPA and NPM1 mutations. LSC17-high patients had a lower rate of complete response (CR) or CR with incomplete platelet recovery (CRp) after one induction course in a multivariable analysis (OR=0.41, p=0.0007) accounting for European LeukemiaNet 2022 (ELN22) risk groups, age, and white blood cell (WBC) count. The LSC17-high status was associated with shorter overall survival (OS) (3-year OS: 70.0% versus 52.7% in LSC17-low patients, p<0.0001). In a multivariable analysis considering ELN22, age and WBC count, LSC17-high patients had shorter disease-free survival (DFS) (HR=1.36, p=0.048) compared to LSC17-low patients. In 123 NPM1-mutated patients in CR/CRp with available MRD data, LSC17-high status predicted poorer DFS (HR=2.34, p=0.01) independently of age, WBC count, ELN22 risk, and NPM1-MRD. Combining MRD and LSC17 status identified a subset of 48% of NPM1 patients with LSC17-low status and negative NPM1-MRD with a 3-year OS from CR/CRp of 93.1% compared to 60.7% in those with LSC17-high status and/or positive NPM1-MRD (p=0.0001). Overall, LSC17 assessment refines genetic risk stratification in adult AML patients treated intensively. Combined with MRD, LSC17 identifies a subset of NPM1-mutated AML patients with excellent clinical outcome.Lire moins >
Lire la suite >Whether the LSC17 gene expression can improve risk stratification in the context of NGS-based risk stratification and measurable residual disease (MRD) in AML patients treated intensively has not been explored. We analyzed LSC17 in 504 adult patients prospectively treated in the ALFA-0702 trial. Multiple (cyto)genetic alterations were associated with changes in LSC17, such as higher LSC17 in patients with RUNX1 or TP53 mutations, and lower scores in those with CEBPA and NPM1 mutations. LSC17-high patients had a lower rate of complete response (CR) or CR with incomplete platelet recovery (CRp) after one induction course in a multivariable analysis (OR=0.41, p=0.0007) accounting for European LeukemiaNet 2022 (ELN22) risk groups, age, and white blood cell (WBC) count. The LSC17-high status was associated with shorter overall survival (OS) (3-year OS: 70.0% versus 52.7% in LSC17-low patients, p<0.0001). In a multivariable analysis considering ELN22, age and WBC count, LSC17-high patients had shorter disease-free survival (DFS) (HR=1.36, p=0.048) compared to LSC17-low patients. In 123 NPM1-mutated patients in CR/CRp with available MRD data, LSC17-high status predicted poorer DFS (HR=2.34, p=0.01) independently of age, WBC count, ELN22 risk, and NPM1-MRD. Combining MRD and LSC17 status identified a subset of 48% of NPM1 patients with LSC17-low status and negative NPM1-MRD with a 3-year OS from CR/CRp of 93.1% compared to 60.7% in those with LSC17-high status and/or positive NPM1-MRD (p=0.0001). Overall, LSC17 assessment refines genetic risk stratification in adult AML patients treated intensively. Combined with MRD, LSC17 identifies a subset of NPM1-mutated AML patients with excellent clinical outcome.Lire moins >
Langue :
Anglais
Vulgarisation :
Non
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