Publication: Apoptosis in adenoma and early adenocarcinoma of the colon
Authors
Yamamoto, T. ; Igarashi, N. ; Kato, Y. ; Kobayashi, M. ; Kawakami, M.
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
Twenty-six specimens of tubular adenoma
and 7 specimens of adenocarcinoma in adenoma of the
colon were examined to evaluate apoptosis between
adenoma and early adenocarcinoma. Cell proliferation
and cell death seemed to be balanced in adenoma with
mild and moderate atypia, but unbalanced in adenoma
with severe atypia and cancer. Apoptosis was considered
to be suppressed at cancer in some cases. However, a
number of apoptosis increased at cancer in other cases.
Necrosis was seen only in cancer areas. The ratio of cells
simultaneously stained by anti-Ki-67 antibody (MIB-1)
and terminal deoxynucleotidyl transferase-mediated
deoxyuridine triphosphate-nick end labeling (TUNEL)
tended to be high from adenoma with moderate atypia to
cancer, suggesting the unstableness of DNA. It is
possible that cancer cells having highly unstable DNA
easily underwent apoptosis as well as necrosis,
accidentally. The p53 protein was positive only in cancer
areas of three cases. One of these three cases showed
decreased apoptosis in a cancer area, but the other two
cases showed increased apoptosis. Furthermore, certain
numbers of cancer cells were double-stained by p53
immunohistochemistry and TUNEL. These results
suggest that the p53 protein may contribute to suppress
apoptosis in the last stage of carcinogenesis of the
colonic adenocarcinoma, but other factors including
extrinsic stimulation may cause apoptosis despite the mutation of p53 protein.
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.