|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0015127,
umls-concept:C0017262,
umls-concept:C0022567,
umls-concept:C0185117,
umls-concept:C0205183,
umls-concept:C0205263,
umls-concept:C0205282,
umls-concept:C0243072,
umls-concept:C0600210,
umls-concept:C1314792,
umls-concept:C1523298,
umls-concept:C1565860,
umls-concept:C1704256,
umls-concept:C1705323,
umls-concept:C2911684
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|
pubmed:issue |
2
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|
pubmed:dateCreated |
2010-4-26
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|
pubmed:abstractText |
Transforming growth factor beta (TGF-beta) acts as a tumor promoter by inducing epithelial-mesenchymal transition (EMT), which leads to a motile phenotype, enabling invasion and metastasis of cancer cells. Cancer-related inflammation, mediated by prostaglandins, has been proposed as a critical mechanism in conversion of benign cells to malignant.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
|
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1873-569X
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pubmed:author |
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pubmed:copyrightInfo |
2010 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:volume |
58
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
97-104
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pubmed:meshHeading |
pubmed-meshheading:20399617-Cell Line, Tumor,
pubmed-meshheading:20399617-Cell Movement,
pubmed-meshheading:20399617-Cell Proliferation,
pubmed-meshheading:20399617-Chemotaxis,
pubmed-meshheading:20399617-Epithelium,
pubmed-meshheading:20399617-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:20399617-Humans,
pubmed-meshheading:20399617-Immunohistochemistry,
pubmed-meshheading:20399617-Keratinocytes,
pubmed-meshheading:20399617-Mesoderm,
pubmed-meshheading:20399617-Models, Biological,
pubmed-meshheading:20399617-Neoplasm Metastasis,
pubmed-meshheading:20399617-Transforming Growth Factor beta,
pubmed-meshheading:20399617-Transforming Growth Factor beta1,
pubmed-meshheading:20399617-Wound Healing
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pubmed:year |
2010
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pubmed:articleTitle |
TGF-beta1 causes epithelial-mesenchymal transition in HaCaT derivatives, but induces expression of COX-2 and migration only in benign, not in malignant keratinocytes.
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pubmed:affiliation |
Haartman Institute, POB 21, FI-00014 University of Helsinki, Finland. kati.rasanen@helsinki.fi
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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