Skip Navigation



Journal of the National Cancer Institute Advance Access published online on October 30, 2007
JNCI Journal of the National Cancer Institute, doi:10.1093/jnci/djm187
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
99/21/1583    most recent
djm187v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Hoelzinger, D. B.
Right arrow Articles by Berens, M. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hoelzinger, D. B.
Right arrow Articles by Berens, M. E.
Related Collections
Right arrowRelated Article in JNCI
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press.

REVIEW

Autocrine Factors That Sustain Glioma Invasion and Paracrine Biology in the Brain Microenvironment

Dominique B. Hoelzinger, Tim Demuth, Michael E. Berens

Affiliation of authors: Cancer and Cell Biology Division, Translational Genomics Research Institute, Phoenix, AZ

Correspondence to: Michael E. Berens, PhD, Cancer and Cell Biology Division, Translational Genomics Research Institute, 445 North Fifth Street, Phoenix, AZ 85004 (e-mail: mberens{at}tgen.org).

Invasion is a defining hallmark of glioblastoma multiforme, just as metastasis characterizes other high-grade tumors. Glial tumors invariably recur due to the regrowth of invasive cells, which are unaffected by standard treatment modalities. Drivers of glioma invasion include autocrine signals propagated by secreted factors that signal through receptors on the tumor. These secreted factors are able to diffuse through the peritumoral stroma, thereby influencing parenchymal cells that surround the tumor mass. Here we describe various autocrine motility factors that are expressed by invasive glioma cells and explore the effects that they may have on normal cells present in the path of invasion. Conversely, normal brain parenchymal cells secrete ligands that can stimulate receptors on invasive glioma cells and potentially facilitate glioma invasion or create a permissive microenvironment for malignant progression. Parallel observations have been made for solid tumors of epithelial origin, in which parenchymal and stromal cells either support or suppress tumor invasion. Most autocrine and paracrine interactions involved in glioma invasion constitute known signaling systems in stages of central nervous system development that involve the migration of precursor cells that populate the developing brain. Key paracrine interactions between glioma cells and the brain microenvironment can influence glioma pathobiology and therefore contribute to its poor prognosis. Current therapies for glioma that could have an impact on paracrine communication between tumors and normal cells are discussed. We suggest that cells in the normal brain parenchyma be considered as potential targets for adjuvant therapies to control glioma growth because such cells are less likely to develop resistance than glioma cells.

Manuscript received April 10, 2007; revised August 13, 2007; accepted September 4, 2007.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related Article in JNCI

IN THIS ISSUE
J Natl Cancer Inst 2007 99: 1561. [Extract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
 Mol. Cell. ProteomicsHome page
U. Rajcevic, K. Petersen, J. C. Knol, M. Loos, S. Bougnaud, O. Klychnikov, K. W. Li, T. V. Pham, J. Wang, H. Miletic, et al.
iTRAQ-based Proteomics Profiling Reveals Increased Metabolic Activity and Cellular Cross-talk in Angiogenic Compared with Invasive Glioblastoma Phenotype
Mol. Cell. Proteomics, November 1, 2009; 8(11): 2595 - 2612.
[Abstract] [Full Text] [PDF]

Home page
 Neuro Oncol DukeHome page
Y. Piao, L. Lu, and J. de Groot
AMPA receptors promote perivascular glioma invasion via {beta}1 integrin-dependent adhesion to the extracellular matrix
Neuro-oncol, January 1, 2009; 11(3): 260 - 273.
[Abstract] [Full Text] [PDF]

Home page
 Am Soc Clin Oncol Ed BookHome page
L. Miele, N. Takebe, and S. P. Ivy
The Cancer Stem Cell Hypothesis, Embryonic Signaling Pathways, and Therapeutics: Targeting an Elusive Concept
ASCO Educational Book, January 1, 2009; 2009(1): 145 - 156.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
A. M. Guo, J. Sheng, G. M. Scicli, A. S. Arbab, N. L. Lehman, P. A. Edwards, J. R. Falck, R. J. Roman, and A. G. Scicli
Expression of CYP4A1 in U251 Human Glioma Cell Induces Hyperproliferative Phenotype in Vitro and Rapidly Growing Tumors in Vivo
J. Pharmacol. Exp. Ther., October 1, 2008; 327(1): 10 - 19.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Biol. CellHome page
C. Beadle, M. C. Assanah, P. Monzo, R. Vallee, S. S. Rosenfeld, and P. Canoll
The Role of Myosin II in Glioma Invasion of the Brain
Mol. Biol. Cell, August 1, 2008; 19(8): 3357 - 3368.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.