Journal of Leukocyte Biology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published online as doi:10.1189/jlb.1105646 on July 24, 2006

Published online before print July 24, 2006
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.1105646v1
80/4/685    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nelson, D.
Right arrow Articles by Ganss, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nelson, D.
Right arrow Articles by Ganss, R.
(Journal of Leukocyte Biology. 2006;80:685-690.)
© 2006 by Society for Leukocyte Biology

Tumor growth or regression: powered by inflammation

Delia Nelson* and Ruth Ganss{dagger},1

* School of Biomedical Sciences, Curtin University, Sydney, Western Australia; and
{dagger} Centre for Medical Research, Western Australian Institute for Medical Research, University of Western Australia, Perth, Australia

1 Correspondence: Western Australian Institute for Medical Research (WAIMR), Rear, 50 Murray Street, Perth WA 6000, Australia. E-mail: ganss{at}waimr.uwa.edu.au

ABSTRACT

Malignant cells thrive in a highly specialized, stromal environment, which harbors support cells, blood vessels, and diverse leukocyte populations. There is increasing evidence that "by default", intratumoral inflammation fosters angiogenic and vasculogenic processes and simultaneously creates an immunosuppressive micromilieu. This self-amplifying loop of proangiogenic inflammation represents a serious obstacle for adaptive anticancer immune responses. However, angiogenesis is a highly dynamic process, which can be reversed in the "right" inflammatory context; this in turn facilitates immune effector cell entry and tumor rejection. Thus, we propose that a shift from proangiogenic to antiangiogenic inflammation creates a tumor environment permissive for immune destruction. This is a new concept, which integrates antiangiogenic and immune therapeutic treatment modalities.

Key Words: multistep tumorigenesis • angiogenesis • stroma • chemokines • stem cells




This article has been cited by other articles:


Home page
 Cancer Res.Home page
W. Peng, H. Y. Wang, Y. Miyahara, G. Peng, and R.-F. Wang
Tumor-Associated Galectin-3 Modulates the Function of Tumor-Reactive T Cells
Cancer Res., September 1, 2008; 68(17): 7228 - 7236.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the Society for Leukocyte Biology.