Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

The emerging concept of antigen-driven lymphomas: epidemiology and treatment implications

Fisher, Susan G; Fisher, Richard I

doi: 10.1097/01.cco.0000239878.31463.0b
Lymphoma
Buy

Purpose of review Dramatic increases in the incidence of lymphomas worldwide have stimulated considerable efforts to identify factors that contribute to the etiology of this heterogeneous group of malignancies. The treatment and, ultimately, the prevention of lymphoma depend on our understanding of the complex interaction of exogenous agents with the molecular milieu which initiates and sustains a lymphoid malignancy. This review discusses the current evidence for the role of foreign or self antigens in the initiation of lymphomagenesis.

Recent findings Recent data have demonstrated an increased risk of lymphoma among individuals with chronic inflammatory conditions, persistent infections or immunodeficient states. Common to these clinical conditions is antigenic stimulation leading to an inflammatory cascade of cellular and cytokine reactions that may tax the host immune response, provoke tissue injury and eventually result in lymphoid neoplasia.

Summary Efforts to detect and suppress chronic, antigen-driven inflammation have suggested that neoplastic progression may often be interrupted and controlled. Elucidation of the etiologic mechanisms critical to the survival of these malignancies would provide promising alternatives for the prevention and treatment of some lymphomas.

Division of Epidemiology, Department of Community & Preventive Medicine and James P. Wilmot Cancer Center, University of Rochester, Rochester, New York, USA

Correspondence to Susan G. Fisher, PhD, Director, Division of Epidemiology, Department of Community & Preventive Medicine, University of Rochester, Box 644, 601 Elmwood Avenue, Rochester, NY 14642, USA Tel: +1 585 273 2849; fax: +1 585 461 4532; e-mail: Susan_Fisher@urmc.rochester.edu

© 2006 Lippincott Williams & Wilkins, Inc.