These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [Lymphoma genesis in the context of HIV infection].
    Author: Besson C, Raphaël M.
    Journal: Ann Med Interne (Paris); 2003 Dec; 154(8):523-8. PubMed ID: 15037828.
    Abstract:
    The incidence of lymphomas is high among HIV infected patients. These lymphomas are non-Hodgkin's lymphoma (NHL) in 70% of cases and Hodgkin's disease (HD) in 30% of cases. Their localization is often extra-nodal with early dissemination. B-cell high grade NHL predominates. The most frequent histological types are diffuse large B-cell lymphoma (30 to 40%) and Burkitt's lymphoma (40 to 50%). Other histological types are low-grade B-cell lymphoma, polymorphic B cell lymphoma and primary effusion lymphoma. Three main factors are predominant in HIV-related lymphomagenesis: cellular immunodeficiency, oncogene viruses (Epstein-Barr and HHV8) and molecular lesions. HIV-related cellular immunodeficiency leads to the increase of EBV infected B-cells and to the diminution of antitumor immunity. Clonal EBV genome is found in lymphoma cells in 30 to 70% of cases of HIV-related NHL. It expresses oncogenic proteins including LMP-1 which behaves like an activated CD40. It induces the expression of intra-cellular genes which stimulate cell growth and inhibit apoptosis. Cytogenetic and molecular lesions are not specific to HIV-related NHL or to histological subtypes. A better knowledge of these mechanisms should lead to the development of specific targeted treatments (antiviral, cytotoxic anti-EBV lymphocytes, cell cycle regulators).
    [Abstract] [Full Text] [Related] [New Search]