I have a question about cancer. How is it, that in a cancerogenous cell, once a specific gene changes, subsequent DNAs in cells end up exponentially acquiring more and more mutations?

Can, these mutations, for instance starting from a given, be computed?

Is there key genes, responsible for subsequent sequences of mutations in subsequent cell divisions, that are the subjects of what is targeted with drugs (to, fix, in this way, at a manageable level, the problem (and it's it possible to develop drugs that discover and target the responsible genes, ...?

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    $\begingroup$ This doesn't seem to be related to bioinformatics, it's more of a general biology question. You might want to ask on Biology instead. One key thing you might want to consider is that in many cases, the mutation that causes cancer does so by affecting the DNA error correcting mechanisms of the cell. A classic culprit is P53. $\endgroup$
    – terdon
    Commented Sep 4, 2022 at 10:08
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    $\begingroup$ Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer. $\endgroup$
    – Community
    Commented Sep 4, 2022 at 19:22
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    $\begingroup$ The preliminary answer to approach your question are 'driver mutations' and its a specialist area of oncology. You need both the correct tissue, control tissue and funky bioinformatics regarding extracting minority alleles amongst the 'contaminants' in context to identify the mutations 'driving' the cancer. The Broad Institute have worked on this problem for a long time. Your main question appears to be that given a 'driver mutation' what happens next. The question appears to be about biology of oncogenesis and its a different forum (Biology SE) in my opinion but is way outside my area. $\endgroup$
    – M__
    Commented Sep 4, 2022 at 22:20

1 Answer 1


Your assumptions are correct. There are genes that amplify mutation rate, once they get mutated/dysregulated.

Mutations in cancer are classified into different types. Each type has its own signature, which can be tracked back to its origin, since the sequence pattern is characteristic for e.g. specific enzymes or failed DNA repair.

One such mutation type is caused by e.g. APOBEC3. This enzyme usually mutates viral DNA. But cancer found a way to have APOBEC3 mutate its own genome. This increases the genetic variability of cancerous tissues and might allow them to gain new survival benefits. Jakobsdottir et al. 2022

Another enzyme that cancer is using to mutate itself is AID.

I don‘t think that drugs are used against APOBEC or AID. However, their relevance as a potential target for therapy is actively discussed (Olson 2018).


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