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. 2021 Oct 19;61(1):169–175. doi: 10.1007/s00411-021-00948-0

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Simplified 2D scheme of DNA double chain with a proto-oncogenes (light gray) scattered all over the chain; b randomly distributed hits (lesions) in the DNA (red stars): when not repaired (or repaired wrongly) they can cause c mutations in oncogenes (dark gray), which can finally result in d the cancer transformation of the whole DNA chain (black) when mutated oncogenes reach the summarized effective volume threshold V_T. See Table 1 for description of corresponding parameters (color figure online)