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- relationship between signalling footprints and pathway expression
- overlap
- which signal activates transcription of which pathway?
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which pathways are more posttranslationally controlled, which more by expression? (would need phospho for this, but could probably do drug/survival response) -
is the effect the same for cell lines and primary tumors? - for each cancer type, where do pathway expression/footprints correlate more? less?
- should do a pancan and tissue-specific correlation plot here (resp<->resp and resp<->expr)
- TCGA pathway activation + enrichment of variants that activate those
- e.g., we find
PI3K_variantTP53_R282Wand enrichment of this variant in some cancers (BRCA)- does the same cancer need to have PI3K activated?
- does p53 bind more PI3K-responsive genes with modified motif?
- e.g., we find
- tcga_pathway_per_mutation: use GISTIC scores as regression coeffs? (= include +/-1)