Editorial
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Clin Oncol. Feb 10, 2012; 3(2): 15-23
Published online Feb 10, 2012. doi: 10.5306/wjco.v3.i2.15
Intersecting pathways in inflammation and cancer: Hepatocellular carcinoma as a paradigm
Philip Y Wai, Paul C Kuo
Philip Y Wai, Paul C Kuo, Department of Surgery, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153, United States
Author contributions: Both Wai PY and Kuo PC contributed to the writing of this manuscript.
Correspondence to: Paul C Kuo, MD, MS, MBA, Department of Surgery, Loyola University Medical Center, 2160 S. First Avenue, EMS Building, Maywood, IL 60153, United States. pkuo@lumc.edu
Telephone: +708-3272705 Fax: +708-3272582
Received: November 2, 2011
Revised: January 29, 2012
Accepted: February 6, 2012
Published online: February 10, 2012
Abstract

Viral infection and chemical carcinogens trigger somatic changes resulting in activation of oncogenes during tumor initiation in the development of cancer. However, a critical interaction resides in the synergism between these somatic changes and an inflamed tumor microenvironment where myeloid and hematopoietic cells are subverted to enhance tumor progression. The causative molecular mechanisms leading to the development of hepatocellular cancer remain incompletely understood but appear to result from multiple factors related to direct hepatocyte injury and the ensuing inflammatory changes mediated by the host response to tissue injury, DNA damage, repair of cellular damage, and chronic, repetitive injury. In this review, the molecular and cellular changes that regulate inflammation and tissue repair will be compared to the activated local tumor microenvironment. Cell-cell signaling within this microenvironment that enhances tumor progression and inhibits anti-tumor immunity will be discussed

Keywords: Hepatocellular cancer; Inflammation; Tumor microenvironment