Fig. 4: Clinic and biological characteristics of the 1,120 C1-CLL patients according to the presence of the g.3A>C U1 mutation.
From: Disease-specific U1 spliceosomal RNA mutations in mature B-cell neoplasms
a Bar plots showing the distribution of U1 g.3A>C mutated CLL among samples analyzed before and after the initiation of therapy. b Bar plots showing the distribution of U1 g.3A>C mutated tumors according to diagnosis (MBL vs CLL), Binet stages, IGHV gene SHM status, and epigenetic subtypes. m-CLL, memory-like CLL; i-CLL, intermediate CLL; n-CLL, naïve like CLL. c Stereotyped subsets in U1 wild-type and mutated CLL. d Oncoprint showing the co-occurrence of g.3A>C and g.9C>T U1 mutations with known CLL driver alterations and clinic-biological variables. The total number of previously recognized driver alterations (Num. drivers) is shown. The bar plot on the right represents the q value of the two-sided Fisher’s exact tests applied to study the co-occurrence/independence of g.3A>C (left) and g.9C>T (right) U1 mutations with the known driver alterations. e Distribution of known driver alterations in CLL with or without the g.3A>C mutation stratified based on their IGHV gene SHM status.
