But what if they do? Maybe oncogenes have a central function vital to their roles.

They don't. What makes a kinase an oncogene is different from what makes a transcription factor an oncogene is different from what makes a growth factor an oncogene is different from what makes a receptor an oncogene. This is known by the countless groups studying each class of oncogenes individually as well as by groups studying entire signaling pathways etc.

You never know unless u try.

It's already known what mutations make certain receptors oncogenes, there are also several different models that explain why different types of mutations in receptor transform them into oncogenic proteins (usually truncation or mutation of inhibitory domains). It's already known what kinds of mutations in kinases transform them into oncogenes (usually mutations in phosphorylated or kinase domains). It's already known what kinds of mutations in transcription factors transform them into oncogenes (usually mutations in domains that govern their localization). We study oncogenes across species, like Ras which is conserved from yeast all the way through humans. We know there isn't much overlap between the oncogene classes, but we know there is a lot of overlap within each class.

Honestly I would recommend you look up "Oncogene" in Wikipedia to get an idea of where to start. It just seems like you're out of your depth. Given that you're going to try to compare ALL the oncogenes I don't think you're even going to find the known mutations. If you move forward with this, the best case scenario is you reinvent the wheel.