ArticleProceedings of the National Academy of Sciences of the United States of America2010
Tumor formation initiated by nondividing epidermal cells via an inflammatory infiltrate.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
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Who cites it
47 citing papers in PubMed, 74 citations in OpenAlex.
- Stimulator of interferon gene facilitates recruitment of effector CD8 T cells that drive neurofibromatosis type 1 nerve tumor initiation and maintenance.Science advances · 2024Article
- Myc-dependent dedifferentiation of Gata6Nature cell biology · 2023Article
- Advances in cutaneous squamous cell carcinoma.Nature reviews. Cancer · 2023Review
- Immune-Epithelial Cross Talk in Regeneration and Repair.Annual review of immunology · 2023Review
- Fibrotic enzymes modulate wound-induced skin tumorigenesis.EMBO reports · 2021Article
- Adamantinomatous craniopharyngioma as a model to understand paracrine and senescence-induced tumourigenesis.Cellular and molecular life sciences : CMLS · 2021Review
- Arachidonic and eicosapentaenoic acids induce oxidative stress to suppress proliferation of human glioma cells.Archives of medical science : AMS · 2020Article
- Mutant Lef1 controls Gata6 in sebaceous gland development and cancer.The EMBO journal · 2019Article
- Loss of GRHL3 leads to TARC/CCL17-mediated keratinocyte proliferation in the epidermis.Cell death & disease · 2018Article
- Homeostasis, regeneration and tumour formation in the mammalian epidermis.The International journal of developmental biology · 2018Review
- Stimulation of hair follicle stem cell proliferation through an IL-1 dependent activation of γδT-cells.eLife · 2017Article
- Stem cell senescence drives age-attenuated induction of pituitary tumours in mouse models of paediatric craniopharyngioma.Nature communications · 2017Article
- Activin promotes skin carcinogenesis by attraction and reprogramming of macrophages.EMBO molecular medicine · 2017Article
- The role of barrier genes in epidermal malignancy.Oncogene · 2016Review
- Protease-activated Receptor-2 (PAR-2)-mediated Nf-κB Activation Suppresses Inflammation-associated Tumor Suppressor MicroRNAs in Oral Squamous Cell Carcinoma.The Journal of biological chemistry · 2016Article
- Macrophage Infiltration and Alternative Activation during Wound Healing Promote MEK1-Induced Skin Carcinogenesis.Cancer research · 2016Article
- Concise Review: Paracrine Role of Stem Cells in Pituitary Tumors: A Focus on Adamantinomatous Craniopharyngioma.Stem cells (Dayton, Ohio) · 2016Review
- Asymmetric stem-cell division ensures sustained keratinocyte hyperproliferation in psoriatic skin lesions.International journal of molecular medicine · 2016Article
- Compartmentalized Epidermal Activation of β-Catenin Differentially Affects Lineage Reprogramming and Underlies Tumor Heterogeneity.Cell reports · 2016Article
- IL-1 in Colon Inflammation, Colon Carcinogenesis and Invasiveness of Colon Cancer.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
In mammalian epidermis, integrin expression is normally confined to the basal proliferative layer that contains stem cells. However, in epidermal hyperproliferative disorders and tumors, integrins are also expressed by suprabasal cells, with concomitant up-regulation of Erk mitogen-activated protein kinase (MAPK) signaling. In transgenic mice, expression of activated MAPK kinase 1 (MEK1) in the suprabasal, nondividing, differentiated cell layers (InvEE transgenics) results in epidermal hyperproliferation and skin inflammation. We now demonstrate that wounding induces benign tumors (papillomas and keratoacanthomas) in InvEE mice. By generating chimeras between InvEE mice and mice that lack the MEK1 transgene, we demonstrate that differentiating, nondividing cells that express MEK1 stimulate adjacent transgene-negative cells to divide and become incorporated into the tumor mass. Dexamethasone treatment inhibits tumor formation, suggesting that inflammation is involved. InvEE skin and tumors express high levels of IL1α; treatment with an IL1 receptor antagonist delays tumor onset and reduces incidence. Depletion of γδ T cells and macrophages also reduces tumor incidence. Because a hallmark of cancer is uncontrolled proliferation, it is widely assumed that tumors arise only from dividing cells. In contrast, our studies show that differentiated epidermal cells can initiate tumor formation without reacquiring the ability to divide and that they do so by triggering an inflammatory infiltrate.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.