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. 2022 May 4;6:31. doi: 10.1038/s41698-022-00272-w

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© The Author(s) 2022

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Primary tumors are composed of different subclones. Some subclones are sensitive to selective pressures, including chemotherapy, androgen deprivation therapy, or immunotherapy, while some subclones are resistant to anticancer therapies. Outgrowth of resistant subclones, phenotype switch, or emergence of a new tumor phenotype are strongly related for resistance to anticancer therapies. As a result, the tumor heterogeneity plays a fundamental role in cancer progression to metastasis.