I recently helped publish this paper below on tumorigenesis in the larvae. The latter half of the paper provides evidence that PcG proteins are malfunctioning in the tumorous state (these proteins have major regulatory influence on the epigenome) and could be a good starting point for exploring the molecular mechanisms behind the methylome.
http://www.ncbi.nlm.nih.gov/pubmed/25719210
For a more direct look at chromatin state you can use these ATAC-seq/FAIRE-seq datasets here:
Drosophila uses DNA methylation only in its very early embryonic stages, and hence there would be no correlations for tumor specific DNA methylation in this system. Yes, PCG protein are involved in Drosophila gene silencing during tumorigenesis (as pointed out by Ryan) as are NURF complexes (papers by Carl Wu http://www.ncbi.nlm.nih.gov/pubmed/12502740), but as Matthias mentions, there is no clear correlation between CpG DNA methylation and histone methylation in Drosophila yet. We do see plenty of Polycomb changes as seen in Mammalian systems predisposing to Cancer (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220885/pdf/nihms331000.pdf), but whether that is the same pathyway in drosophila or not is still not completely clear.
Agree with Matthias. Very little evidence supporting DNA methylation in flies. If at all present, levels are low, see http://www.ncbi.nlm.nih.gov/pubmed/23641003 and other papers by Lyko.
To be precise, the NURF tumours are melanotic tumours. These are better described as inflammatory aggregates or nodules. However, problematic though it may be, this is the term used in the Drosophila community to describe these structures. Melanotic tumours are distinct from the neoplastic overgrowths seen in scrib mutants