Fig. 1

Circadian reprogramming in diverse cancer types. a Schematic diagram depicting the project design and the identification of putative loss-of-function and gain-of-function clock genes. Somatic copy number alteration (SCNA) and transcript expression of 32 clock genes are investigated in 21 cancer types. A total of 19 or 12 genes are recurrently lost or gained respectively. Of these SCNA events, 11 or two genes are also downregulated or upregulated in tumours, representing Clock^Loss and Clock^Gain gene sets respectively. Both gene sets are prognostic in seven cancer cohorts. Pie slices indicate the number of patients within each cancer type. Crosstalk between circadian genes and tumour hypoxia is investigated. b The proportion of samples with deep and shallow somatic alterations are represented using stacked bar graphs. The number of samples within each cancer type is represented by the width of the stacked bars. c Somatic losses and differential expression profiles of 19 clock genes that are recurrently deleted in at least seven cancer types. d Somatic gains and differential expression profiles of 12 clock genes that are recurrently amplified in at least seven cancer types. Bar charts on the far right represent the number of cancers with at least 20% of samples affected by copy number alteration. Heatmaps on the far left depict the cohort fraction in which a given gene is deleted or amplified. Cancer types are ordered using Euclidean distance metric. Heatmaps in the centre represent differential expression values between tumour and non-tumour samples. Clock^Loss and Clock^Gain genes are highlighted in red. Cancer abbreviations are listed in Additional file 2