Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1981-10-29
pubmed:abstractText
Tumor cell membrane glycoproteins may be involved in the induction of tumor immunity or in the escape of tumors from immunologic defense mechanisms. Previous investigations have suggested a role for blood group antigens and their precursors, in the generation of the immune response to neoplasia. In this study, 44 benign and malignant breast lesions were examined for the presence of a carbohydrate precursor antigen (T-antigen) of the human blood group system MN. T-antigen was demonstrated using an immunohistochemical technique to detect tissue binding of a plant lectin (PNA) with specificity for T-antigen. Of the 22 benign breast lesions examined, 19 showed T-antigen present along the luminal cytoplasmic membrane and occasionally on intraluminal secretions. T-antigen, as demonstrated by lectin binding, was confined to this region in all benign lesions except one, which also showed cytoplasmic positivity. Malignant breast lesions showed a pattern of T-antigen expression markedly different from that of benign breast tissues. Of 22 breast carcinomas, 17 showed diffuse cytoplasmic T-antigen. Five carcinomas showed no evidence of T-antigen by this technique. These malignancies tended to be the most poorly differentiated when judged by histologic criteria. A possible role for T-antigen in the modulation of the immune response to breast carcinoma is suggested.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0008-543X
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2872-7
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Carcinoma-associated cytostructural antigenic alterations: detection by lectin binding.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.