Table 2.
Approach | Major Findings Early Stage |
Major Findings Late Stage |
---|---|---|
Genomics | Low mutation rate High copy number and structural aberrations ETS-TMPRSS2 fusion PTEN deletion SPOP mutation FOXA1 mutation |
AR amplification and mutation TP53 mutation RB1 deletion PIK3CA amplification |
Epigenomics | Identification of DNA hypermethylation subtype associated with disease recurrence | Hypomethylation around AR gene Changes in H3K27 acetylation Changes in H3K9 di- and trimethylation Upregulation of lncRNA HOTAIR |
Cistromics | AR cistrome rearrangement ETS factor-driven AR cistrome reprogramming Enrichment of FOXA1 and HOXB13 cistromes |
Novel AR-V7 cistrome Changes in ZFX and SOX2 cistromes |
Transcriptomics | Identification of subtypes predictive of recurrence and metastasis Changes linked to ETS fusion Changes linked to SPOP or FOXA1 mutation |
Emergence of AR-V7 and other AR splice variants Expression upregulation of steroid synthesis genes |
Proteomics | Ubiquitylome changes linked to SPOP mutation | Abundance of cell cycle and DNA damage response pathway proteins Role of FOXA1 and HOXB13 interactomes |
Metabolomics | Changes in lipid and nucleotide metabolism Changes in TCA cycle, polyamine synthesis and hexoamine biosynthesis pathway |