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Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Overall survival based on (A) NPM1 mutation status, (B) FLT3-ITD mutation status within NPM1 mutated cases only, (C) IDH1 mutation status, and (D) IDH2 mutation status. Reported p-values utilized the cox model Wald test.
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Surface expression of CD14, CD64, and CD11b in cases by genetic mutation compared to a wild-type reference cohort within the subset of patients with centralized quantitative MFC performed (n = 144). * indicates p < 0.05, ** indicates p < 0.01, *** …
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Overall survival based on monocytic differentiation status censored at HCT for patients within specific mutation subgroups including (A) combined RAS pathway mutations (N/KRAS and PTPN11), and isolated mutations in (B) FLT3-ITD, (C) NRAS, (D) KRAS, (E) PTPN11, and (F) TP53. Patients with …
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Overall survival in the subgroup of patients not receiving allogeneic cell transplantation (HCT) based on (A) monocytic vs. non-monocytic differentiation, (B) monocytic differentiation and NPM1 mutation status, (C) in the subgroup of patients with RAS pathway and FLT3-ITD mutations (K/NRAS, PTPN11, FLT3-ITD) …
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Overall survival within the US cohort (n = 279) based on the presence of signaling pathway mutations including (A) NRAS, (B) KRAS, (C) PTPN11, (D) BRAF, (E) NF1, and (F) WT1. Reported p-values utilized the cox model Wald test.
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Patient and disease characteristics for Beat AML RNAseq cohort (N = 228)
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Overview of immunophenotypic expression profiling. (A) Flow cytometry was performed on diagnostic bone marrow specimens and fluorescence measurements, forward light scatter (FSC) and right-angle light scatter (SSC) characteristics were collected for 200,000 events. Leukemic populations were identified by CD45 v SSC gating, …
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
RNA expression of alternative anti-apoptotic proteins based on RNA-seq defined cell differentiation state. Samples from the top quartile of each state are displayed below.
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
(A) mutation frequency within the Beat AML cohort (n = 228). (B) Heatmap depicting the point-biserial correlation values for RNAseq defined cell state scores in relationship to specific genetic mutations. (C) Heatmap depicting the point-biserial correlation values for RNA expression of primitive …
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Overall survival in patients classified as monocytic vs. non-monocytic in (A) patients classified as mPRS higher-benefit (wild-type for FLT3, N/KRAS and TP53), (B) with mutated IDH1/2 and wild-type for N/KRAS, PTPN11, FLT3-ITD, and TP53, and (C) wild-type for NPM1, FLT3-ITD, IDH1/2, K/NRAS, …
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Abstract Resistance to venetoclax (VEN)-based therapy in acute myeloid leukemia (AML) includes genetic (i.e., mutations in N/KRAS, FLT3-ITD, TP53) and phenotypic (i.e., monocytic differentiation) features. Whether monocytic differentiation contributes to clinical VEN resistance secondary to a genetic bias remains unknown. This multimodal, …
Curtis Andrew Lachowiez, Maël Heiblig, Gaspar Aspas Requena, Emmanuelle Tavernier et autres
Overall survival in patients classified as monocytic vs. non-monocytic in (A) patients classified as mPRS higher-benefit (wild-type for FLT3, N/KRAS and TP53), (B) with mutated IDH1/2 and wild-type for N/KRAS, PTPN11, FLT3-ITD, and TP53, and (C) wild-type for NPM1, FLT3-ITD, IDH1/2, K/NRAS, …
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