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J Gastroenterol Hepatol. 2007 Nov;22(11):1877-81.

Further studies on the arrest of cell proliferation in tumor cells at the invading front of colonic adenocarcinoma.

Author information

1
Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and University Hospital, Stockholm, Sweden. carlos.rubio@ki.se

Abstract

BACKGROUND AND AIM:

The author has previously reported that neoplastic glands at the leading invading edge of colorectal carcinomas often display flat tumor cells and cellular gaps called glandular pores. The aim of this study was to audit cell proliferation and p53 mutation in flat tumor cells and in tumor cells at the tip of glandular pores at the leading invading front of colonic carcinomas.

METHODS:

Sections from 40 colonic adenocarcinomas were immunostained with the proliferation marker Ki67 and with p53 protein. Expression was assessed at the leading invading front in consecutive neoplastic glands having flat tumor cells and epithelial pores and in neoplastic glands showing neither flat tumor cells nor glandular pores.

RESULTS:

Flat tumor cells in neoplastic glands usually showed no Ki67 expression but overexpressed p53 mutation. In neoplastic glands with pores 40% of the tumor cells at the tip of the pores showed no Ki67, but they overexpressed p53 mutation.

CONCLUSIONS:

The results showed, for the first time, that p53-positive flat neoplastic colonic cells arrest their proliferation at the invading front. It is possible that these p53-positive/Ki67-negative neoplastic cells were temporarily removed from the cell cycle (G0). This paradoxical biological behavior of tumor cells might be connected with the formation of glandular pores and appears to indicate that arrest of cell proliferation at the advancing tumor front in colonic carcinomas occurs independently of p53 mutation. The possible existence of two independent molecular systems at the advancing tumor edge of colonic carcinomas, one supervising cell proliferation and the other zealously transferring the p53 mutation to daughter cells, is suggested.

[Indexed for MEDLINE]

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