Infection, inflammation and neoplasia: an interdisciplinary challenge

Abstract

During the past two to three decades there has been an exciting revolution in our understanding of the multistage carcinogenic process and of the molecular genetics of cancer. The general principle of multifactor interactions is central to our understanding of cancer causation. The paradigm that persistent infections and chronic inflammation contributes via cytokine- and chemokine-mediated disbalanced immune response to carcinogenesis becomes more and more attractive in cancer research. Besides genetic factors, the epigenetics of impaired cell signaling and signal transduction by proinflammatory cytokines and chemokines are important potentiators of carcinogenesis. The activation of the nuclear factor kappaB, for example, a hallmark of inflammatory responses that is frequently detected in tumors, might constitute a missing link between inflammation and cancer. It will be a challenge for future therapeutic and preventive cancer research to detect potential targets in chronic inflammatory disease which are essential links to promote inflammation-associated cancer.