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. 2022 Mar 10;5:219. doi: 10.1038/s42003-022-03161-x

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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. 7 — Schematic drawing shows distribution of CD200^low MEP cells (blue) in alveoli and CD200^high MEP cells (red) in terminal ducts and ducts. CD200^low MEP progenitors are multipotent since they can generate K14⁺/K19⁻ MEP cells (green), K14⁺/K19⁺ luminal progenitor cells (yellow) as well as K14⁻/K19⁺ luminal cells of alveoli and ducts (orange). Upon oncogenic activation as shown here by overexpression of PIK3CA^H1047R, CD200^low MEP progenitors can give rise to biphasic lesions with luminal hyperplasia.