ArticleOncotarget2016
Lgr5+ stem cells and their progeny in mouse epidermis under regimens of exogenous skin carcinogenesis, and their absence in ensuing skin tumors.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Method to Study Skin Cancer: Two-Stage Chemically Induced Carcinogenesis in Mouse Skin.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Anorectal Remodeling in the Transitional Zone with Increased Expression of LGR5, SOX9, SOX2, and Keratin 13 and 5 in a Dextran Sodium Sulfate-Induced Mouse Model of Ulcerative Colitis.International journal of molecular sciences · 2024Article
- The Use of Retinoids for the Prevention and Treatment of Skin Cancers: An Updated Review.International journal of molecular sciences · 2022Review
- Integrin α3β1 in hair bulge stem cells modulates CCN2 expression and promotes skin tumorigenesis.Life science alliance · 2020Article
- Method to Study Skin Cancer: Two-Stage Chemically Induced Carcinogenesis in Mouse Skin.Methods in molecular biology (Clifton, N.J.) · 2020Article
- IL-17R-EGFR axis links wound healing to tumorigenesis in Lrig1The Journal of experimental medicine · 2019Article
- Article
- Pathogenesis of Skin Carcinomas and a Stem Cell as Focal Origin.Frontiers in medicine · 2018Review
- Lgr6+ stem cells and their progeny in mouse epidermis under regimens of exogenous skin carcinogenesis, and their absence in ensuing skin tumors.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Actively proliferating Lgr5+ skin stem cells are found deep in the hair follicle (HF). These cells renew the HF and drive its expansion in anagen phase. Their long residence and continuous mitotic activity make them prime candidates to transform into skin tumor-initiating cells. This was investigated by subjecting Lgr5-EGFP-Ires-CreERT2/R26R-LacZ mice (haired and hairless) to chemical and UV carcinogenic regimens. In the course of these regimens Lgr5+ cells (EGFP+) remained exclusively located in HFs, and in deep-seated cysts of hairless skin. In haired mice, progeny of Lgr5+ stem cells (LacZ+ after a pulse of tamoxifen) appeared in the interfollicular epidermis upon UV-induced sunburn and in TPA-induced hyperplasia. In hairless mice the progeny remained located in deep-seated cysts and in HF remnants. Progeny in hairless skin was only detected interfollicularly at a late stage, in between outgrowing tumors. Lgr5+ stem cells were absent in the ultimate tumor masses, and no tumor appeared to be a (clonal) expansion of Lgr5+ cells (52 tumors with tamoxifen at the start of carcinogenesis, 42 tumors with tamoxifen late during tumor outgrowth). In contrast to CD34/K15+ quiescent bulge stem cells, actively proliferating Lgr5+ stem cells do therefore not appear to be tumor drivers in experimental skin carcinogenesis.
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