Fig. 4: Enrichment of protein-altering SNVs in ‘long-tail’ genes reveal a shared landscape of common and rare driver genes.
From: Genome-wide mapping of somatic mutation rates uncovers drivers of cancer
a,b, Estimated mutation rates with 95% CIs of excess oncogenic SNVs in oncogenes (a) and pLoF variants in TSGs (b) that were not previously associated with a given cancer (x axis) in three large driver gene catalogs7,10,11. Stars indicate that the burden of oncogenic (pLoF) SNVs was significant in long-tail oncogenes (TSGs) in the cancer type (P values and number of SNVs per category are in Supplementary Tables 20 and 21). c,d, Oncogene–tumor pairs and TSG–tumor pairs with a significant burden of oncogenic or protein-truncating SNVs. Gene–tumor pairs previously reported by Dietlein et al.10, Bailey et al.11 or Martínez-Jiménez et al.7 are marked in gray. Pairs that are not present in those catalogs are marked in red, with color intensity indicating significance of association. Marker size is proportional to the estimated rate of excess mutations after accounting for cancer-specific neutral mutation rates. CNS, central nervous system; NSC, non-small-cell.
