CREBBP along with p300 are considered general chromatin modifiers in that their acetyltransferase activities regulate transcription at a majority of genes in the cell. In fact, H3K27ac and p300 ChIPseq is often used alongside methylation marks to annotate most active enhancers or promoters in a cell type. That being said, any disruption to global transcriptional regulation through a variety of mutations could tip the balance against or in favor of cancerous behavior. In addition to direct changes to transcriptional regulation it's often forgotten that CREBBP and P300 acetylate other targets besides histones. Therefore, mutations may also affect signaling transduction pathways to promote cancerous phenotypes.

In general though, you're right it's context specific. Nature of mutation, cell fate/history, and the extracellular niche all play a role. The common themes in cancer genes

Thanks for the insight Ryan M Boileau . I guess in case of some of these genes it is all about balance, and any kind of distortion from equilibrium could affect cell proliferation/apoptosis.

There is a nice review on the subject that I found and the link is:

http://nmr.uhnres.utoronto.ca/ikura/publication/books/transcriptional%20epigenetic%20regulator.pdf