For example, all the genes involved in the cell cycle could form the module "cell cycle".
Using Luminal A as a reference, the least aggressive subtype with the lowest β-diversity, we see that only the first non-core module, cell cycle, shows an increase in β-diversity for all non-Luminal A subtypes.
The first of the non-core modules, cell cycle, shows higher heterogeneity in all subtypes except in Luminal A. This module highlights the clinical difficulty of targeting the cell cycle with cytotoxic agents due to most tumor's high heterogeneity.
To facilitate discussion, representative names were assigned to each module based on GO terms: Module 1, heme biosynthesis; Module 2, respiration and energy generation; Module 3, cell wall organization; Module 4, cell cycle; Module 5, transport; Module 6, pyridoxine biosynthesis; Module 7, RNA processing; and Module 8, undefined function, because no GO term enrichment was found.
Additional modules were involved in molecular functions (three modules), signalling pathways (two modules each), cell cycle, development, DNA repair and protein localization (one module each).
Moreover, network analysis suggests another, tumor-specific module of cell cycle regulators formed by p107, p130, p15INK4b, and Wee1 (Figure 5).
Notably, this applies to a compact module of cell cycle regulators, namely survivin, cyclin B1, Cdk1, Plk1, and Bub1, whose expression increased about 2-fold in tumor versus transgenic cells according to measured fold changes.
Function of the Gwl → pEndos ⊣ PP2A-B55 module in cell cycle transitions.
Another example is the module "BP: cell cycle arrest" in "CC: cytoplasm".
This smaller landscape contains modules of cell cycle genes, glycolysis genes and genes encoding mitochondrial proteins, mirroring some of the main modules in the Always Correlated parent landscape and highlighting those modules built of only the most extreme correlation coefficients.
