Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1995-11-30
pubmed:abstractText
Long-Evans (Eker) rats carry a mutation that predisposes them to develop spontaneous renal cell tumors of two morphologic patterns: solid chromophilic masses or cystic lesions lined by eosinophilic cells. Previous studies have suggested that these tumors arise from the proximal tubules. In the present study, lectin-binding characteristics and cytokeratin expression of various stages of hereditary rat renal epithelial neoplasia were examined to localize the portion of the nephron from which tumors arise. Lectin-binding histochemistry has been used as a marker of cell surface glycoprotein expression, thought to be important in the differentiation of benign from malignant epithelial lesions and in the determination of their cell of origin. The presence or absence of keratin intermediate filaments in the rat nephron has been used to identify nephron segments. The polyclonal antibody to high- and low-molecular-weight cytokeratin stained the cells of the collecting ducts but not the proximal or distal tubules. Binding to the proximal tubules by the lectins Conavalia ensiformis (Con A), Dolichas biflorus, Ricinus communis (RCA-1), and Triticum vulgare and to the distal tubules by Con A, RCA-1, Arachis hypogaea (PNA) with and without neuraminidase, and the antibody for cytokeratins was demonstrated. The lectin binding and cytokeratin staining patterns of rat hereditary renal cell carcinoma, adenoma and the preneoplastic lesions of atypical tubules and hyperplasias suggest that cystic adenomas arise from the distal nephron, principally the collecting duct, whereas the solid atypical tubules, hyperplasias, and adenomas arise from the proximal nephron, principally the proximal tubule.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0300-9858
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
379-86
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7483212-Adenoma, pubmed-meshheading:7483212-Animals, pubmed-meshheading:7483212-Carcinoma, Renal Cell, pubmed-meshheading:7483212-Concanavalin A, pubmed-meshheading:7483212-Histocytochemistry, pubmed-meshheading:7483212-Hyperplasia, pubmed-meshheading:7483212-Immunohistochemistry, pubmed-meshheading:7483212-Keratins, pubmed-meshheading:7483212-Kidney Neoplasms, pubmed-meshheading:7483212-Kidney Tubules, Distal, pubmed-meshheading:7483212-Kidney Tubules, Proximal, pubmed-meshheading:7483212-Lectins, pubmed-meshheading:7483212-Male, pubmed-meshheading:7483212-Plant Lectins, pubmed-meshheading:7483212-Precancerous Conditions, pubmed-meshheading:7483212-Rats, pubmed-meshheading:7483212-Rodent Diseases, pubmed-meshheading:7483212-Tumor Markers, Biological, pubmed-meshheading:7483212-Wheat Germ Agglutinins
pubmed:year
1995
pubmed:articleTitle
Preneoplastic and neoplastic lesions of rat hereditary renal cell tumors express markers of proximal and distal nephron.
pubmed:affiliation
Department of Experimental Pathology and Toxicology, Chemical Industry Institute of Toxicology, Research Triangle Park, NC, USA.
pubmed:publicationType
Journal Article