Publication: Development and progression of malignancy in human colon tissues are correlated with expression of specific ca2+-binding S100 proteins
Loading...
Date
2001
Authors
Bronckart, Y. ; Decaestecker, C. ; Nagy, N. ; Harper, L. ; Schafer, B.W. ; Salmon, I. ; Pochet, R. ; Kiss, R. ; Heizman, C.W.
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
The expression levels of seven different S100
proteins (S100A1, S100A2, S100A3, S100A4, S100A5,
S100A6, and S100B) were characterized by
immunohistochemistry in the epithelial versus
connective tissues of a series of 35 colon specimens,
including 6 normal samples, 5 adenomas with low-grade
dysplasia, 5 adenomas with high-grade dysplasia, and 19
cancers. The results showed that S100A2, S100A3, and
SlOOB proteins could not (or only marginally) be
detected in colon tissues. On the other hand, the
expression of S100A6 increased in epithelial tissues
directly proportional to the increase of malignancy. The
percentage of epithelial (or connective tissue) cells
expressing S100A4 significantly decreased as the
malignancy grade increased. The expression level of
SlOOAl proteins was somewhat higher in the connective
tissues of normal cases and adenomas with low-grade
dysplasia than in adenomas with high-grade dysplasia
and cancers. This pattern of expression was not observed
in epithelial tissues. While the node-positive cancers did
not express S100A1, about half of the node-negative
specimens did. The expression levels of S100A5 were
similar in different epithelial tissues. However, in the
connective tissues the expression levels decreased
inversely proportional to the increase in pathological
grading of the specimens. Therefore, the present study
implicates several S100 proteins as useful tools for
histochemical typing of colon cancer malignancy
development.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.