Review
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World J Gastrointest Surg. Mar 27, 2012; 4(3): 62-72
Published online Mar 27, 2012. doi: 10.4240/wjgs.v4.i3.62
Inflammation and cancer
Noemí Eiró, Francisco J Vizoso
Noemí Eiró, Francisco J Vizoso, Research Unit, Fundación Hospital de Jove, 33290 Gijón, Asturias, Spain
Author contributions: Both authors made substantial contributions to the conception and design, acquisition, analysis and interpretation of data, drafting the article and revising it critically for important intellectual content; and both gave final approval of the version to be published.
Correspondence to: Francisco J Vizoso, MD, PhD, Head, Research Unit, Fundación Hospital de Jove, 33290 Gijón, Asturias, Spain. investigacion@hospitaldejove.com
Telephone: +34-985-320050 Fax: +34-985-315710
Received: October 20, 2010
Revised: November 17, 2011
Accepted: November 25, 2011
Published online: March 27, 2012
Abstract

There is evidence supporting the hypothesis that inflammation participates in providing conditions that lead to cancer. An unresolved inflammation due to any failure in the precise control of the immune response can continue to perturb the cellular microenvironment, thereby leading to alterations in cancer-related genes and posttranslational modification in crucial cellular proteins involved in the cell cycle, DNA repair and apoptosis. In addition, there are data indicating that inflammatory cells and immunomodulatory mediators present in the tumor microenvironment influence tumor progression and metastasis. Historically, tumor-infiltrating leukocytes have been considered to be manifestations of an intrinsic defence mechanism against developing tumors. However, increasing evidence indicates that leukocyte infiltration can promote tumor phenotypes, such as angiogenesis, growth and invasion. This may be due to inflammatory cells that probably can influence cancer promotion by secreting cytokines, growth factors, chemokines and proteases, which stimulate proliferation and invasiveness of cancer cells. Consequently, events and molecules implicated in this cross talk between the tumor microenvironment and inflammatory process may emerge as attractive targets in anticancer therapeutic interventions with significant clinical impact.

Keywords: Inflammation; Cancer; Cytokines; Proliferation; Cancer progression; Metastasis