AIDS-related lymphoproliferative disease

University of California, San Francisco, San Francisco, California, United States
Blood (Impact Factor: 10.45). 02/2006; 107(1):13-20. DOI: 10.1182/blood-2004-11-4278
Source: PubMed


Not long after the recognition of HIV as the causative agent of AIDS, it was evident that individuals infected with HIV developed lymphoma at a greater rate than the population at large. Approximately two thirds of AIDS-related lymphoma (ARL) cases are categorized as diffuse large B-cell type, with Burkitt lymphomas comprising 25% and other histologies a much smaller proportion. Typically, these individuals have presented with advanced extranodal disease and CD4+ lymphocyte counts of less than 200/mm3. Recent clinical trials have demonstrated a better outcome with chemotherapy for ARL since the introduction of combination antiretroviral treatment, termed highly active antiretroviral therapy (HAART). For patients with relapses, solid evidence points to the safety and utility of hematopoietic-cell transplantation as a salvage modality. Coinfection with other viruses such as Epstein-Barr virus and Kaposi sarcoma-associated herpesvirus have led to the genesis of previously rare or unrecognized lymphoma subtypes such as plasmablastic and primary effusion lymphomas. The immunosuppressive impact of treatment for patients with ARL receiving chemotherapy with HAART appears transient and opportunistic infections have become less problematic than prior to HAART. Significant progress has been made in the understanding and management of ARL but outcomes still remain inferior compared to those achieved in HIV- individuals.

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    • "Histological subtypes commonly seen display a B-cell origin such as Burkitt, centroblastic, plasmablastic , or primary effusion lymphoma [1]. Nevertheless, several cases of T-cell NHL have been described [1] [7]. "
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    ABSTRACT: Cases of anaplastic large-cell lymphoma (ALCL) of T phenotype are sparse in the setting of HIV patients. We report herein a case of T-ALCL, with an advanced stage, pulmonary involvement, high HIV viral load, and low CD4 level. Anaplastic lymphoma kinase (ALK) protein expression was negative. Anthracyclin-based chemotherapy was unsuccessful. The literature review was performed focusing on incidence, clinical characteristics, prognosis, and physiopathology of ALCL in HIV patients. More data are needed to improve the knowledge of such cases and to define a better treatment approach.
    Full-text · Article · Dec 2012
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    • "Since the introduction of HAART, the overall incidence of ARL has been reduced approximately 50%; however, it still occurs at a rate much higher than in non-HIV infected individuals, suggesting a viral component is involved in the development of ARL [1]. The primary difference between lymphoma in non-HIV infected individuals and ARL is that ARLs are uniformly high grade and widely metastatic, with death occurring in as little as two weeks after diagnosis [2]. HIV-related lymphomas are predominately of B-cell origin and often involve extranodal sites, especially the liver and GI tract [3], with about 80% of ARLs arising in the periphery while the remaining occur in the central nervous system (CNS) [4]. "
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    ABSTRACT: Despite highly active antiretroviral therapy (HAART), AIDS related lymphoma (ARL) occurs at a significantly higher rate in patients infected with the Human Immunodeficiency Virus (HIV) than in the general population. HIV-infected macrophages are a known viral reservoir and have been shown to have lymphomagenic potential in SCID mice; therefore, there is an interest in determining if a viral component to lymphomagenesis also exists. We sequenced HIV-1 envelope gp120 clones obtained post mortem from several tumor and non-tumor tissues of two patients who died with AIDS-related Non-Hodgkin's lymphoma (ARL-NH). Similar results were found in both patients: 1) high-resolution phylogenetic analysis showed a significant degree of compartmentalization between lymphoma and non-lymphoma viral sub-populations while viral sub-populations from lymph nodes appeared to be intermixed within sequences from tumor and non-tumor tissues, 2) a 100-fold increase in the effective HIV population size in tumor versus non-tumor tissues was associated with the emergence of lymphadenopathy and aggressive metastatic ARL, and 3) HIV gene flow among lymph nodes, normal and metastatic tissues was non-random. The different population dynamics between the viruses found in tumors versus the non-tumor associated viruses suggest that there is a significant relationship between HIV evolution and lymphoma pathogenesis. Moreover, the study indicates that HIV could be used as an effective marker to study the origin and dissemination of lymphomas in vivo.
    Full-text · Article · Dec 2009 · PLoS ONE
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    • "The pathogenesis of HIV-NHL is a multistep process involving factors provided by the host, as well as alterations intrinsic to the tumour clone (Carbone et al, 2001b, 2009; Capello et al, 2008; Moir & Fauci, 2009). Screening of known genetic lesions has revealed that the molecular pathogenesis of HIV-NHL is characterized by molecular heterogeneity and involves distinct pathogenetic pathways that preferentially associate with specific clinico-pathological entities (Carbone et al, 2001a, 2009; Jenner et al, 2003; Klein et al, 2003; Nair et al, 2006; Navarro & Kaplan, 2006). "
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    ABSTRACT: Non-Hodgkin lymphomas (NHL) represent a frequent complication of human immunodeficiency virus (HIV) infection. To elucidate HIV-NHL pathogenesis, we performed a genome-wide DNA profiling based on a single nucleotide polymorphism-based microarray comparative genomic hybridization in 57 HIV-lymphomas and, for comparison, in 105 immunocompetent diffuse large B-cell lymphomas (IC-DLBCL). Genomic complexity varied across HIV-NHL subtypes. HIV-Burkitt lymphoma showed a significantly lower number of lesions than HIV-DLBCL (P = 0.032), whereas the median number of copy number changes was significantly higher in Epstein-Barr virus negative (EBV-) HIV-DLBCL (42.5, range 8-153) compared to EBV+ cases (22; range 3-41; P = 0.029). Compared to IC-DLBCL, HIV-DLBCL displayed a distinct genomic profile with no gains of 18q and specific genetic lesions. Fragile sites-associated genes, including FHIT (FRA3B), WWOX (FRA16D), DCC (FRA18B) and PARK2 (FRA6E) were frequently inactivated in HIV-NHL by interstitial deletions, and a significantly higher prevalence of FHIT alterations was observed in HIV-DLBCL compared to IC-DLBCL. The same genes involved by fragile site deletions were also frequently affected by aberrant methylation of regulative regions.
    Full-text · Article · Oct 2009 · British Journal of Haematology
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