Can non-driver mutations disrupt the function of proteins and further affect a cellular pathway?

Can non-driver mutations disrupt the function of proteins and further affect a cellular pathway?

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Hi all,

I had found compelling evidence that a cellular pathway is disrupted during cancer. Then I tried to analyze the genetic status of proteins involved in that pathway (which mutations occur in their genes?!) I analyzed for multiple cancer types. After analysis of the VCF files of about 100 patients, I found that a lot of mutations occur in those genes, but just a handful of those mutations have reported evidence in databases after annotation (e.g. likely pathogen, pathogen, etc.)

With these results, I do not know if my assumption about this pathway was wrong or not?

Despite these mutations that don’t have any clinical reports, is it possible to claim that this pathway is disrupted during cancer?

Is it possible to claim that non-driver mutations can disrupt the function of proteins and further affect a cellular pathway?

Can I still visualize these not-reported mutations by oncoplot or something like that?

Thanks for any help


driver


somatic


annotation


VCF


oncoplot

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