Question ID: WS-32
Submitted by: Jill Koshiol
February 4, 2011
Question: What failures in immune surveillance lead to cancer development and to poorer prognosis given cancer? (Jill Koshiol; Eric Engels) Background: HIV-infected individuals are at increased risk for some cancers, in large part due to immunosuppression and the frequent presence of viral co-infections. Although use of highly active antiretroviral therapy (HAART) has led to declines in Kaposi sarcoma and non-Hodgkin lymphoma (NHL), other cancers that occur more often in HIV-infected populations have not decreased (e.g., cervical, anal, and lung cancers), and some (e.g., Hodgkin lymphoma) have increased. Perhaps surprisingly, HIV-infected persons do not have markedly high risk for other cancers that appear to be influenced by the immune system (e.g., melanoma). Finally, cancers occurring in HIV-infected individuals appear to be more aggressive than similar cancers arising in uninfected individuals. These differences in outcome may reflect interactions in the tumor microenvironment involving tumor cells and the host immune system. Feasibility: Detailed evaluation of tumor tissues from those cancers arising in HIV-infected persons compared to HIV-uninfected persons can yield important information on the etiology of cancers in the HIV-infected population, and by extension, the role of an intact immune system in preventing and controlling cancer in healthy individuals. Examination of these tissues can identify histologic characteristics (e.g., tumor infiltration by immune cell subsets) or molecular markers that could have etiologic or prognostic importance. Implications of success: By identifying differences in immune response between HIV-infected and HIV-uninfected persons, it may be possible to identify normal immune surveillance mechanisms that must be overcome in HIV-uninfected persons for the development of cancer but do not need to be circumvented in HIV-infected persons given the extensive immunosuppression due to HIV itself. Identification of these underlying molecular mechanisms may allow development of interventions to prevent progression to cancer in HIV-uninfected individuals and improvement of prognosis in HIV-infected individuals.
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