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. Author manuscript; available in PMC: 2014 Feb 14.
Published in final edited form as: Cell. 2013 Feb 14;152(4):714–726. doi: 10.1016/j.cell.2013.01.019

Figure 6. Presence of subclonal drivers mutations adversely impacts clinical outcome.

Figure 6

(A) Analysis of genetic evolution and clonal heterogeneity in 149 CLL samples. Top panel - total number (red) and the number of subclonal (blue) mutations per sample. Bottom panel - co-occurring CLL or cancer drivers (sSNVs in highly conserved sites in Cancer Gene Census genes) detected in the 149 samples. Color spectrum (light yellow to black) corresponds to estimated cancer cell fraction (CCF); white boxes - not detected; grey – CCF not estimated (genes on the X chromosome and indels other than in NOTCH1). (B-C) Subclonal drivers are associated with adverse clinical outcome. (B) CLL samples containing a detectable subclonal driver (n=68) exhibited shorter FFS_Sample compared to samples with absent subclonal drivers (n=81) (also see Figure S5). (C) Subclonal drivers were associated with shorter FFS_Rx in 67 samples which were treated after sampling. (D) A Cox multivariable regression model designed to test for prognostic factors contributing to shorter FFS_Rx showed that presence of a subclonal driver was an independent predictor of outcome.