There's this database of genetic/drug interactions, which I think is pretty much exactly what you're looking for.
Probably your best approach is to classify your drugs into a couple different categories of action. Some drugs will have to be in several categories at once(I'm lookin at you anthracyclines) Dose-dependent mutagens(cisplatin), growth-dependent mutagens(fluorouracil), topoisomerase inhibitors, tyrosine kinase inhibitors, microtubule inhibitors, retinoid signaling, immune adjuvants, and then 'misc'.
Alkylating agents and platinum-containing drugs like cisplatin directly damage DNA, while there are other drugs(methotrexate,fluorouracil) destroy or damage DNA by pretending to be nucleotides and breaking things that way.
Anthracyclines bind into DNA strands damaging it, directly create free radicals, disable topoisomerase II, and displace histones.
There are the topoisomerase inhibitors which prevent cell growth by preventing DNA from being unwound for replication.
There is a fairly diverse(chemically) class of 'mitotic inhibitors' that screw up microtubule formation or proper microtubule dissolution, any of which prevents mitosis.
Sunitinib blocks tyrosine kinases, which are involved in blood vessel formation(and nerve formation and some other things). Other tyrosine kinase inhibitors are more specific to vascular endothelial growth factor(VEGF) receptors, but most tyrosine kinases target more or less specifically VEGFR and related receptors. Some are antibodies, some are just small molecules that bind TKRs.
There are a few retinoid-related drugs most of which influence the vitamin A pathways, like tretinoin, bexarotene, etc. Dual use in skin creams.
Immunoadjuvants are designed to activate the immune system to aid in tumor cell destruction. Interferon-alpha, imidazoquinoline, et cetera.
In the miscellaneous category: Bortezomib, a short peptide that interferes with proper protein degradation. L-asparaginase slows all protein production by destroying asparagine, an amino acid. Some blood cancers respond to corticosteroids, and some ovarian/testicular cancers are treated with sex hormone inhibitors. Nearly any blood-borne poison works as a chemotherapy agent due to the EPR effect, so heavy metals or radioactive isotopes also are sometimes used. Arsenic trioxide, for instance, is just arsenic.
It's also worth looking at the steroids that are given along with cancer treatment(dexamethasone) to mitigate side effects. As regulatory hormones, there's going to be a hefty impact on genetic regulation from regular steroid injections. If nothing else it's a confounding effect you'll need to control for.
The preparations/solvents of chemotherapy agents can also be significant. Cremophor was used to suspend some anticancer drugs, but recent developments imply that might be on its way out.
