Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1522282 (EMT)
 2,868 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A highly desirable use of delayed contact dermal hypersensitivity data from animal tests is an accurate prediction of the relative potency of positive agents in humans. Because of the manner in which all such animal tests are performed, the wide variety of exposure conditions and concentrations (which are generally more severe than human exposure conditions) have traditionally made prediction of potency (and therefore the extent of hazard) in humans either impossible or extremely crude. A numerical/graphical method has been developed to adjust results from suitable animal studies of all sorts for exposure conditions and allow for ranking of agents for potency and classification of relative hazards. Results from four animal test systems (MEST, EMT, GPMT and Buehler) are compared with results from human studies to show that all four test systems can generate data that are usable for a relative hazard classification process, though they may vary in their performance characteristics as screens.
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PMID:A scheme for the prediction and ranking of relative potencies of dermal sensitizers based on data from several systems. 323 Feb 47

The loss of imprinting of MEST has been linked to certain types of cancer by promoter switching. However, MEST-mediated regulation of tumorigenicity and metastasis are yet to be understood. Herein, we reported that MEST is a key regulator of IL-6/JAK/STAT3/Twist-1 signal pathway-mediated tumor metastasis. Enhanced MEST expression is significantly associated with pathogenesis of breast cancer patients. Also, MEST induces metastatic potential of breast cancer through induction of the EMT-TFs-mediated EMT program. Moreover, MEST leads to Twist-1 induction by STAT3 activation and subsequently enables the induction of activation of the EMT program via the induction of STAT3 nuclear translocation. Furthermore, the c-terminal region of MEST was essential for STAT3 activation via the induction of JAK2/STAT3 complex formation. Finally, MEST is required for metastasis in an experimental metastasis model. These observations suggest that MEST is a promising target for intervention to prevent tumor metastasis.
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PMID:MEST induces Twist-1-mediated EMT through STAT3 activation in breast cancers. 3090 2