Immune Disorders and Susceptibility to Neoplasms

The leading hypothesis that proper immune surveillance prevents the growth of neoplastic cells first emerged at the end of the 19th century, soon after it was recognized that immunity plays an important role in the defense against infection. Subsequent studies by several investigators based on this hypothesis led to the recognition that immunologic surveillance is a common link between allograft acceptance and malignancies in organ transplant recipients. While the degree of immunodeficiency dictates the occurrence of allograft acceptance, it also dictates the occurrence of malignancies. Over the last 2 decades, there has been a rapid increase in our understanding of the immune system and susceptibility to cancers. It is now clear from the epidemiological studies that the incidence of cancer is significantly higher in populations that are immunocompromised or suffer immune dysregulation. Predominant among these populations are human immunodeficiency virus (HIV)-infected individuals, organ transplant recipients, and persons with genetic immunodeficiency. However, individuals with these conditions do not become susceptible to several common human cancers such as breast, prostate, lung, colon, ovarian, and cervical cancer. Instead, there is a many-fold increase in cancers associated with oncogenic viral infections due to these patients' incompetent immune systems, which cannot suppress the latent infections or fight new infections. Although several malignancies show a rising trend in immunocompromised individuals compared with the general population, two malignancies, Kaposi's sarcoma (KS) and B-cell non-Hodgkin's lymphoma (NHL), etiologically linked to human herpesvirus type 8 (HHV-8) and Epstein-Barr virus (EBV) infections, respectively, have a remarkably high incidence in immunocompromised hosts. This brief overview focuses on our current understanding of the pathogenesis of these two malignancies.