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. Author manuscript; available in PMC: 2021 May 1.
Published in final edited form as: Nat Rev Endocrinol. 2020 Mar 3;16(5):276–283. doi: 10.1038/s41574-020-0329-9

Fig. 3 |. Analysis of the frequency of mutations in insulin–PI3K signalling.

Fig. 3 |

Histogram of the frequency of mutations for the 32 The Cancer Genome Atlas (TCGA) pan-cancer data sets from cBioPortal75,76 showing that the distribution of mutations in genes (PIK3CA, PIK3R1, AKT1, AKT2, AKT3, PTEN and INSR) encoding elements of the insulin–phosphoinositide 3-kinase (PI3K) cascade are not uniform across tumour types. These data highlight the frequency with which this pathway is altered in human cancer and support the idea that different tumour types might be differentially sensitive to genetic modulations of this pathway as the result of the tissues from which they arise or the specific environment of that tissue. Looking across the data set, which covers sequencing from 32 studies, demonstrates the high frequency with which components of this signalling cascade are altered, particularly p110α (encoded by PIK3CA, p110α is a catalytic subunit of PI3K) and phosphatase and tensin homologue (the phosphatase that catalyses the reverse reaction). In total, 38% of the cases in the TCGA pan-cancer studies had mutations in these seven genes.