Figure 1.
CBFB-MYH11 fusion transcript subtype predicts relapse in AML. (A) CBFB-MYH11 fusion transcripts within our cohort with line weights that correspond to the associated prevalence. (B) Kaplan-Meier estimates for the probability of EFS, OS, and RR in patients with CBFB-MYH11 AML stratified based on fusion transcript (E5-E33 vs all others). (C) Oncoplot with associated somatic driver mutations based on fusion transcript status. KIT mutations are more prevalent in E5-E33 CBFB-MYH11 AMLs compared with others (Fisher’s exact test, P value = .0003). (D) Kaplan-Meier estimates for the probability of EFS, OS, and RR in patients with CBFB-MYH11 AML stratified based on fusion transcript and E17 KIT mutation status. (E) Age distribution comparing Schwind et al (adults) and patients from our cohort (pediatrics).

CBFB-MYH11 fusion transcript subtype predicts relapse in AML. (A) CBFB-MYH11 fusion transcripts within our cohort with line weights that correspond to the associated prevalence. (B) Kaplan-Meier estimates for the probability of EFS, OS, and RR in patients with CBFB-MYH11 AML stratified based on fusion transcript (E5-E33 vs all others). (C) Oncoplot with associated somatic driver mutations based on fusion transcript status. KIT mutations are more prevalent in E5-E33 CBFB-MYH11 AMLs compared with others (Fisher’s exact test, P value = .0003). (D) Kaplan-Meier estimates for the probability of EFS, OS, and RR in patients with CBFB-MYH11 AML stratified based on fusion transcript and E17 KIT mutation status. (E) Age distribution comparing Schwind et al (adults) and patients from our cohort (pediatrics).

Close Modal
This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal