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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1991-8-9
pubmed:abstractText
HLA-A,B,C and HLA-DR molecules are involved in cognate LFA-3 (CD58) in antigen-independent T-cell/target-cell interaction. T-cell-mediated host-versus-tumor response might therefore depend on the presence of both types of molecules on the surface of the target cell. To investigate whether presence or absence of these molecules in colorectal carcinoma influences the recurrence rate, 149 patients who underwent curative surgery were surveyed for a maximum of 65 months (mean, 48 months). As determined by immunohistochemistry, aberrant reduction of HLA-A,B,C determinants was observed in 34.9 and a complete loss in 8.7% of the tumor specimens. An induction of HLA-DR molecules was found in 55.0 and of the HLA-DR-associated invariant chain (Ii) in 81.9%. An abnormal reduction of LFA-3 was detected in 43.6%, while a complete loss of this structure was observed in 6.7%. Reduction/loss of HLA-A,B,C was correlated with reduction/loss of LFA-3 (p = 0.03). In contrast to the prognostic role of tumor stage and grade, the presence vs. absence of all these structures was not correlated with the recurrence rate. We conclude that, although encoded on different chromosomes, an abnormal reduction/loss of HLA-A,B,C and LFA-3 might be the consequence of one transacting down-regulating signal. However, the resulting deviant immunophenotypes do not profoundly influence survival and growth potential of residual tumor cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0898-6924
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
155-62
pubmed:dateRevised
2007-7-23
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Frequency of abnormal expression of HLA-A,B,C and HLA-DR molecules, invariant chain, and LFA-3 (CD58) in colorectal carcinoma and its impact on tumor recurrence.
pubmed:affiliation
Institute of Pathology, University of Heidelberg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't