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About the Authors:
Susan M. Varnum
Affiliation: Department of Cell Biology and Biochemistry, Pacific Northwest National Laboratory, Richland, Washington, United States of America
Bobbie-Jo M. Webb-Robertson
Affiliation: Department of Computational Biology and Bioinformatics, Pacific Northwest National Laboratory, Richland, Washington, United States of America
Nancy A. Hessol
Affiliation: Department of Clinical Pharmacy, University of California at San Francisco, San Francisco, California, United States of America
Richard D. Smith
Affiliation: Department of Biological Sciences Division, Pacific Northwest National Laboratory, Richland, Washington, United States of America
Richard C. Zangar
* E-mail: [email protected]
Affiliation: Department of Cell Biology and Biochemistry, Pacific Northwest National Laboratory, Richland, Washington, United States of America
Introduction
In the presence of human immunodeficiency virus (HIV) infection, non-Hodgkin's lymphoma (NHL) and Kaposi sarcoma (KS) were the first malignancies used to define acquired immune deficiency syndrome (AIDS). People with HIV infection are also at increased risk of a number of other cancers [1]. As people with HIV infection live longer due to highly active antiretroviral therapy (HAART), the incidence of these non-AIDS-defining cancers has increased among HIV-infected individuals. One of the most common of these malignancies is Hodgkin's lymphoma (HL), and it has been estimated that people with HIV/AIDS have a 5.6- to 14.7-fold increased risk of developing HL compared to the general population [1]–[3].
HL is a solid tumor that is comprised of no more than 2% of the cancerous B lymphocytes. Instead, these lymphocytes secrete a wide range of cytokines that attract numerous normal leukocytes that then comprise the large majority of the tumor [4]. Thus, HL is largely seen as an uncontrolled inflammatory disease [4]. In people with immunosuppression, HL is believed to result from the Epstein-Barr virus (EBV). EBV is present in nearly all adults, but typically only causes HL when the immune system is suppressed, such as with HIV infection [4].
The increase in non-AIDS-defining cancers has created a greater need for the early detection of these malignancies in this susceptible population. It seems likely that HIV-infected individuals would benefit from a routine, non-invasive screen for HL, but no such screen exists. Rather, HL patients are identified after they become symptomatic [5]. Chemotherapy and radiation therapy have been shown to be very effective at causing HL remission, but morbidity and mortality associated...