A Daemen

A Mantovani

A Sutton

AH Sillars-Hardebol

B Starcher

BM Mian

BM Wittig

C Campregher

C Rubie

CH Shih

Claus Mayer

D Wang

DA Notterman

DG DeNardo

DM Mosser

Emad M. El-Omar

ER Fearon

G Lorusso

Georgina L. Hold

GG Vaday

Gillian Norrie

Graeme I. Murray

H Kamohara

H Kita

IT Vermeer

J Galon

J Hwang

J Jablonska

J Sabates-Bellver

JA Baron

Janice E. Drew

John Thomson

Keith N. Stewart

KJ Livak

KN Son

LM Coussens

M Inada

M Kumarakulasingham

M Munder

Mairi H. McLean

Mairi Hope

MB Grisham

MD Gunn

MH McLean

MJ Thun

MR Dinapoli

N Jeffery

N. Ashley G. Mowat

Nicky Fyfe

PK Baier

R Benamouzig

R Duncan

RS Sandler

S Mori

T Ishiko

TT MacDonald

U Forssmann

Wael El-Rifai

Y Ichikawa

Y Kitadai

Y Wen

YM Lin

Z Sun

ZQ Tang

PLoS ONE

English

PubMed

Crossref

Colorectal cancer (CRC) is a major cause of mortality and morbidity worldwide. Inflammatory activity within the stroma of invasive colorectal tumours is known to be a key predictor of disease activity with type, density and location of immune cells impacting on patient prognosis. To date, there has been no report of inflammatory phenotype within pre-malignant human colonic adenomas. Assessing the stromal microenvironment and particularly, inflammatory activity within colorectal neoplastic lesions is central to understanding early colorectal carcinogenesis. Inflammatory cell infiltrate was assessed by immunohistochemistry in paired colonic adenoma and adjacent normal colonic mucosa samples, and adenomas exhibiting increasing degrees of epithelial cell dysplasia. Macrophage phenotype was assessed using double stain immunohistochemistry incorporating expression of an intracellular enzyme of function. A targeted array of inflammatory cytokine and receptor genes, validated by RT-PCR, was used to assess inflammatory gene expression. Inflammatory cell infiltrates are a key feature of sporadic adenomatous colonic polyps with increased macrophage, neutrophil and T cell (specifically helper and activated subsets) infiltration in adenomatous colonic polyps, that increases in association with characteristics of high malignant potential, namely, increasing degree of cell dysplasia and adenoma size. Macrophages within adenomas express iNOS, suggestive of a pro-inflammatory phenotype. Several inflammatory cytokine genes (CXCL1, CXCL2, CXCL3, CCL20, IL8, CCL23, CCL19, CCL21, CCL5) are dysregulated in adenomas. This study has provided evidence of increased inflammation within pre-malignant colonic adenomas. This may allow potential mechanistic pathways in the initiation and promotion of early colorectal carcinogenesis to be identified

Mairi H McLean

Graeme I Murray

Keith N Stewart

Georgina L Hold

N Ashley G Mowat

Janice E Drew

Emad M El-Omar

Directory of Open Access Journals

The inflammatory microenvironment in colorectal neoplasia.

Colorectal cancer (CRC) is a major cause of mortality and morbidity worldwide. Inflammatory activity within the stroma of invasive colorectal tumours is known to be a key predictor of disease activity with type, density and location of immune cells impacting on patient prognosis. To date, there has been no report of inflammatory phenotype within pre-malignant human colonic adenomas. Assessing the stromal microenvironment and particularly, inflammatory activity within colorectal neoplastic lesions is central to understanding early colorectal carcinogenesis. Inflammatory cell infiltrate was assessed by immunohistochemistry in paired colonic adenoma and adjacent normal colonic mucosa samples, and adenomas exhibiting increasing degrees of epithelial cell dysplasia. Macrophage phenotype was assessed using double stain immunohistochemistry incorporating expression of an intracellular enzyme of function. A targeted array of inflammatory cytokine and receptor genes, validated by RT-PCR, was used to assess inflammatory gene expression. Inflammatory cell infiltrates are a key feature of sporadic adenomatous colonic polyps with increased macrophage, neutrophil and T cell (specifically helper and activated subsets) infiltration in adenomatous colonic polyps, that increases in association with characteristics of high malignant potential, namely, increasing degree of cell dysplasia and adenoma size. Macrophages within adenomas express iNOS, suggestive of a pro-inflammatory phenotype. Several inflammatory cytokine genes (CXCL1, CXCL2, CXCL3, CCL20, IL8, CCL23, CCL19, CCL21, CCL5) are dysregulated in adenomas. This study has provided evidence of increased inflammation within pre-malignant colonic adenomas. This may allow potential mechanistic pathways in the initiation and promotion of early colorectal carcinogenesis to be identified.</p

McLean, Mairi H.

Murray, Graeme I.

Stewart, Keith N.

Norrie, Gillian

Mayer, Claus

Hold, Georgina L.

Thomson, John

Fyfe, Nicky

Hope, Mairi

Mowat, N. Ashley G.

Drew, Janice E.

El-Omar, Emad M.

Discovery Research Portal

The inflammatory microenvironment in colorectal Neoplasia

E. A. Nikipelova

O. I. Kit

A. V. Shaposhnikov

E. V. Zlatnik

I. A. Novikova

Е. А. Никипелова

О. И. Кит

А. В. Шапошников

Е. Ю. Златник

И. А. Новикова

Malignant tumours (E-Jounal) / Злокачественные опухоли

КОЛОКАНЦЕРОГЕНЕЗ: ОНКОИММУНОЛОГИЯ ЛОКАЛЬНЫХ ИЗМЕНЕНИЙ

McLean, Mairi H

Murray, Graeme I

Stewart, Keith N

Hold, Georgina L

Mowat, N Ashley G

Drew, Janice E

El-Omar, Emad M

The Open University

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The inflammatory microenvironment in colorectal neoplasia

The Inflammatory Microenvironment in Colorectal Neoplasia

http://dx.plos.org/10.1371/journal.pone.0015366

The inflammatory microenvironment in colorectal neoplasia

Abstract

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Directory of Open Access Journals

Discovery Research Portal

Malignant tumours (E-Jounal) / Злокачественные опухоли

The Open University

Crossref

Discovery Research Portal

Discovery Research Portal