ArticleGenes & diseases2017
Epithelial-mesenchymal transition as strategic microenvironment mimicry for cancer cell survival and immune escape?
Article in Genes & diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Establishment of a canine lens epithelial cell line.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2021Article
- NR2F2 plays a major role in insulin-induced epithelial-mesenchymal transition in breast cancer cells.BMC cancer · 2020Article
- Differential distribution of immune cells in breast invasive carcinoma vs. breast carcinomaInternational journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is the phenotypic transition of epithelial cells to mesenchymal cells characterized by loss of epithelial markers, loss of intercellular adherence and acquirement of mesenchymal cell markers and increased locomotive ability. EMT is widely considered to be a gene regulated process necessary for cancer metastasis. Yet it is a highly controversial issue. We here propose that EMT is an environmentally induced cell behavior. It is the mimicry of their living environment. It is a survival strategy, a way of immune escape. We also propose here that the epithelial cell markers may functionally act as tumor antigens since in the mesenchymal surroundings there are no other structures bearing the same antigens as epithelial cells.
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Registered trials
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