There is very few current literature on how chemotherapy affects the DNA damage response and DNA repair, in the context of tumor resistance.
Is there an explanation for this?
While your question is an interesting one, it is slightly problematic because it misrepresents the phenomenon. Radiation does not cause greater amount of double strand breaks (DSBs) compared to some DNA damaging chemotherapy agents but perhaps does so faster. For instance, temozolomide or mitomycin also induce DSBs but only after the cells cycle and the replication fork encounters the chemical DNA adduct. This stalled replication fork is what causes the DSBs. In case of radiation however, the high energy is what causes random and instant breaks in the DNA structure thus causing instant DSBs. Essentially, a lot of chemotherapeutic agents induce DSBs by placing a chemical adduct into the DNA structure which causes the replication fork to break. Replication takes time. Radiation does not need replication or cells to cycle in order to induce the breaks because it just cuts it---depending on the dose of radiation used. This is of course a very general and lay answer and you will need to read on specific types of chemotherapeutics to understand differences between radiation induced DSBs and chemotherapy induced DSBs. There is a wealth of literature on this subject when it comes to emergence of chemoresistance in glioblastoma. You could perhaps check that out. Hope this helps.
If I remember correctly radiation cause DSB by both direct and indirect mechanism in the same time. So that's why in shorter time you can observe more DNA damages. Most chemotherapeutic agnets only can damage DNA by direct mechanism.
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