Clinical and genetic characteristics of CK AML cohort. (A) Clinical characteristics of CK and non-CK AML cohorts. (B) Patient survival comparing CK AML (n = 68) vs non-CK AML (n = 347). All patients with available survival data are represented, including those not treated with intensive chemotherapy. (C) Primary structure of TP53 and positions of mutations. (D) Mutations identified in CK AML. Each column represents a patient sample. CK AML samples are grouped according to their TP53 alteration status: altered (mutated and/or abnormal FISH) or not altered (no mutation and no deletion by FISH). Bar graph on the left indicates mutation frequency, and column on the right provides the enrichment for a mutation in CK vs non-CK cohorts. (E) TP53 isoform expression in CK AML. (F) Analysis of mutations in genes involved in the RAS pathway. CK samples with NF1 expression below the first percentile of control AML, designated by the dotted line, were considered to have low NF1 expression. P values are based on 2-tailed Fisher's exact test or on Wilcoxon rank-sum test. FAB, French-American-British; FL, full-length; ITD, internal tandem duplication; MPN, myeloproliferative neoplasm; NA, not applicable; NC, not classified; PTD, partial tandem duplication; RPKM, reads per kilobase million; TAD, transactivating domain; T-AML, therapy-related acute myeloid leukemia; WBC, white blood cell counts.