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. 2022 Oct 26;13:6360. doi: 10.1038/s41467-022-33870-0

Fig. 5. Co-existence of MYC amplification and SCNAs from the PI3K and RAS pathways in lung squamous and triple-negative p53-mutant breast cancers.

Fig. 5

Frequency plots showing the distribution of chromosomal amplifications/homozygous losses (continuous line) or gains/heterozygous losses (shade) across the genome in both MYC-amplified/gain (pink for amplifications/gains and blue for losses) and MYC diploid tumours (gray) in the Breast TCGA cohort (a triple-negative invasive ductal p53-mutant tumours only), Breast Metabric cohort (b triple-negative invasive ductal p53-mutant tumours only) and Lung Squamous TCGA cohort c. The location of a list of functional cancer genes selected in ref. 49 is indicated on top. Cancer genes are colour-coded in green if they belong to the PI3K or RAS pathways based on the Reactome definition. The boxplots (right panel) show, for both PI3K/RAS and other cancer genes, the difference between the frequency of cancer genes SCNAs in tumours with and without MYC amplification or gain. The p-value of the one-sided permutation test of equality of means is indicated. A list of known driver genes is also presented across all plots – the genes are highlighted in yellow if they are recognised GISTIC drivers in each specific tumour. For all boxplots (a, b and c), the central box was defined by the quantiles 0.25, 0.5 and 0.75 of the data, and the maximum whisker size equals 1.5 times of the interquartile range (inference without multiplicity correction).