If you have human samples of responders to a drug (n=27) and non-responders to this drug (n=38)
And have enough money to perform whole genome sequencing with depth of 50x coverage for tumours and 30x coverage for normal samples, with 94% of the known genome being sequenced to at least 8× coverage
Would chose to do WES or WGS?
In any case, please can you tell me your reasons in term of advantages?
The answer very much depends on the mechanism of action of your drug. If your drug is an ALK inhibitor, you absolutely need the ability to detect ALK fusions. WES is good at finding point mutations in coding sequence, but is terrible at finding fusion genes. In the case of ALK, you'd be looking at WGS, an ALK fusion assay, or a capture panel that includes the introns of ALK.
WGS gives you a much more extensive of the rearrangement landscape of your cancer. ~70% of driver mutations involve some sort of genomic rearrangement. A lot of these are detectable in WES (e.g. loss of function caused by a SNV and CN loss will be reported in WES as a homozygous SNV), but many of these aren't.
If you're not looking at SVs, then WGS is a waste of money.
Shameless plug: our GRIDSS/PURPLE/LINX pipeline gives the most comprehensive picture of the somatic genomic rearrangements landscape of any pipeline that I'm aware of. It has some really nice features including driver prediction and can even identifiy and classify complex multi-breakpoint driver fusions. See our preprints here and here for more details.