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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-4-24
pubmed:abstractText
Missing in metastasis (MIM) gene encodes a putative metastasis suppressor. However, the role of MIM in tumorigenesis and metastasis has not yet been established. Western blot analysis using a MIM specific antibody demonstrated that MIM protein is present at varying levels in a variety of normal cells as well as tumor cell lines. Immunohistochemical staining of adult mouse tissues revealed abundant MIM immunoreactivity in uroepithelial cells in the bladder, neuron Purkinje cells in the cerebellum, and megakaryocytes in the bone marrow and spleen in addition. MIM immunoreactivity also was found in human normal bladder transitional epithelial cells. However, the reactivity was not seen in 69 percent of human primary transitional cell carcinoma specimens. Over 51 percent of the tumors at low grade display MIM staining similarly to the normal cells, whereas only 16.7 percent of the tumors at high-grade with poor differentiation show faint or mild staining. Furthermore, full-length MIM protein is highly expressed in SV-HUC-L an immortalized normal transitional epithelial cell line, moderately expressed in T24 and poorly expressed in J82 and TCCSUP transitional cell carcinoma cells. This finding indicates that downegulation of MIM expression may correlate with the transition of tumor cells from distinct epithelium-like morphology to less differentiated carcinomas.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0735-7907
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
79-86
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Downregulation of missing in metastasis gene (MIM) is associated with the progression of bladder transitional carcinomas.
pubmed:affiliation
Department of Pathology, University of Maryland, Marlene Stewart Greenebaum Cancer Center, Baltimore, Maryland 21201, USA.
pubmed:publicationType
Journal Article