The Pathologic Spectrum of Aids- Related Non-Hodgkin’s Lymphomas

Carbone, Antonino; Tirelli, Umberto; Gloghini, Annunziata; Falini, Brunangelo; Dalla‐Favera, Riccardo; Gaïdano, Gianluca

doi:10.1007/978-1-4615-4797-6_25

Cited by 6 publications

(9 citation statements)

References 34 publications

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“…According to the site of involvement, the present spectrum of AIDS-NHL includes 'extranodal/nodal lymphomas' and 'primary central nervous system lymphomas'; (ii) unusual lymphomas occurring more specifically in HIVpositive patients. These lymphomas include two rare entities, namely 'PEL' and 'plasmablastic lymphoma of the oral cavity (PBL; Delecluse et al, 1997;Carbone et al, 1999a;Knowles & Pirog, 2001;Raphael et al, 2001;Carbone, 2002); (iii) lymphomas also occurring in other immunodeficiency states (Table II).…”

Section: Pel and Other Hiv-associated Lymphomasmentioning

confidence: 99%

“…The lymphoma cells have abundant cytoplasm and eccentrically placed nuclei with a single prominent nucleolus (Delecluse et al, 1997;Carbone et al, 1999a;Knowles & Pirog, 2001;Raphael et al, 2001;Carbone, 2002). Their immunophenotype is characterised by a weak or absent expression of the most commonly used lymphoid markers.…”

Section: Pel and Other Hiv-associated Lymphomasmentioning

confidence: 99%

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KSHV/HHV8‐associated lymphomas

2007

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SummaryThis review looks at the current state of knowledge on primary effusion lymphoma (PEL) and other Kaposi sarcoma herpesvirus (KSHV)/human herpesvirus 8 (HHV8)‐associated lymphomas. In 1995, KSHV DNA sequences were identified within a distinct subgroup of acquired immunodeficiency syndrome‐related non‐Hodgkin lymphomas localized in body cavities and presenting as pleural, peritoneal and pericardial lymphomatous effusions. Subsequently, the spectrum of KSHV/HHV8‐associated lymphomas has been expanded by the identification of cases of extracavitary solid lymphomas without serous effusions. Despite the diversification in the clinical presentation of KSHV/HHV8‐associated lymphomas, the majority of the cases reported demonstrated similar morphology, immunophenotype and KSHV/HHV8 viral status. KSHV/HHV8 infection is also in multicentric Castleman disease‐associated plasmablastic lymphoma. The exact oncogenic mechanisms of KSHV/HHV8 are not clearly defined. The prognosis for KSHV/HHV8‐associated lymphomas is poor. Novel approaches for therapy, outside traditional chemotherapy with CHOP (cyclophosphamide, doxorubicin, prednisone, vincristine), have been suggested. These include the addition of antiviral therapy as well as inhibition of specific cellular targets.

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Section: Pel and Other Hiv-associated Lymphomasmentioning

confidence: 99%

Section: Pel and Other Hiv-associated Lymphomasmentioning

confidence: 99%

KSHV/HHV8‐associated lymphomas

2007

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“…As assayed by immunohistochemistry, BCL-6 protein expression is high in germinal-center B cells, a subset of germinal-center T cells, and a small number of CD4 T cells scattered throughout peripheral lymphoid tissues (33)(34)(35)(36). BCL-6 protein is not expressed at high levels in most other cell types of the body.…”

Section: Discussionmentioning

confidence: 99%

T helper type 2 inflammatory disease in the absence of interleukin 4 and transcription factor STAT6

Dent

Hu‐Li

Paul

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

135

102

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An important signaling pathway for the differentiation of T helper type 2 (TH2) cells from uncommitted CD4 T cell precursors is activation of the STAT6 transcription factor by interleukin 4 (IL-4). The protooncogene BCL-6 is also involved in TH2 differentiation, as BCL-6 ؊͞؊ mice develop an inf lammation of the heart and lungs associated with an overproduction of TH2 cells. Surprisingly, IL-4 ؊͞؊ BCL-6 ؊͞؊ and STAT6 ؊͞؊ BCL-6 ؊͞؊ double-mutant mice developed the same TH2-type inf lammation of the heart and lungs as is characteristic of BCL-6 ؊͞؊ mice. Furthermore, a TH2 cytokine response developed in STAT6 ؊͞؊ BCL-6 ؊͞؊ and IL-4 ؊͞؊ BCL-6 ؊͞؊ mice after immunization with a conventional antigen in adjuvant. In contrast to these in vivo findings, STAT6 was required for the in vitro differentiation of BCL-6 ؊͞؊ T cells into TH2 cells. BCL-6, a transcriptional repressor that can bind to the same DNA binding motifs as STAT transcription factors, seems to regulate TH2 responses in vivo by a pathway independent of IL-4 and STAT6.

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“…AIDS diffuse large B cell lymphoma accounts for 70% of systemic lymphomas and is the second most common type of cancer after Kaposi's sarcoma in AIDS patients (25,26). Systemic AIDS diffuse large B cell lymphoma are further classified into two subclasses (6,7,(27)(28)(29). AIDS large noncleaved-cell lymphoma is postulated to originate from germinal center B cells and often exhibits dysregulated expression of the BCL-6 protooncogene because of chromosomal translocations or promoter mutations.…”

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TCL1 oncogene expression in AIDS-related lymphomas and lymphoid tissues

Teitell

Damore

Sulur

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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AIDS-related non-Hodgkin's lymphoma (AIDS NHL) comprises a diverse and heterogeneous group of high-grade B cell tumors. Certain classes of AIDS NHL are associated with alterations in oncogenes or tumor-suppressor genes or infections by oncogenic herpesviruses. However, the clinically significant class of AIDS NHL designated immunoblastic lymphoma plasmacytoid (AIDS IBLP) lacks any consistent genetic alterations. We identified the TCL1 oncogene from a set of AIDS IBLP-associated cDNA fragments generated by subtractive hybridization with non-AIDS IBLP. Aberrant TCL1 expression has been implicated in T cell leukemia/lymphoma development, and its expression also has been seen in many established B cell tumor lines. However, TCL1 expression has not been reported in AIDS NHL. We find that TCL1 is expressed in the majority of AIDS IBLP tumors examined. AIDS-related non-Hodgkin's lymphoma (AIDS NHL) occurs in up to 10% of HIV-infected individuals who have moderate to severe immunodeficiency (1-3). These lymphomas are biologically and genetically heterogeneous, are derived from germinal center or postgerminal center B cells, and are classified according to body location and histologic criteria (reviewed in refs. 4-7). Certain AIDS NHL classes are associated with specific oncogenic lesions or viral involvement. For example, AIDS-related Burkitt's lymphoma usually contain activating c-MYC translocations, whereas AIDS-related primary-effusion lymphoma consistently contain human herpesvirus-8 (8-24). AIDS diffuse large B cell lymphoma accounts for 70% of systemic lymphomas and is the second most common type of cancer after Kaposi's sarcoma in AIDS patients (25,26). Systemic AIDS diffuse large B cell lymphoma are further classified into two subclasses (6,7,(27)(28)(29). AIDS large noncleaved-cell lymphoma is postulated to originate from germinal center B cells and often exhibits dysregulated expression of the BCL-6 protooncogene because of chromosomal translocations or promoter mutations. AIDS immunoblastic lymphoma plasmacytoid (AIDS IBLP) is thought to derive from postgerminal center B cells and is not associated with any predominant genetic alteration (30, 31). AIDS IBLP are monoclonal tumors that usually contain Epstein-Barr virus, indicating that they are not simply Epstein-Barr virusdriven polyclonal proliferations. The lack of any consistently associated oncogene involvement in AIDS IBLP strongly suggests that these tumors arise through novel patterns of dysregulated gene expression (7,15,32).We sought to identify differentially expressed genes in AIDS IBLP patient samples versus non-AIDS lymphoma samples by using suppression subtractive hybridizations (SSH) (33,34). Large cell lymphomas with immunoblastic/plasmacytoid features consistent with postgerminal center derivations (IBLP) were selected for these subtractions from HIV-infected or uninfected patient samples. The TCL1 oncogene was identified among multiple differentially expressed genes isolated from AIDS IBLP in these studies.TCL1 is developmentally reg...

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The Pathologic Spectrum of Aids- Related Non-Hodgkin’s Lymphomas

Cited by 6 publications

References 34 publications

KSHV/HHV8‐associated lymphomas

KSHV/HHV8‐associated lymphomas

T helper type 2 inflammatory disease in the absence of interleukin 4 and transcription factor STAT6

TCL1 oncogene expression in AIDS-related lymphomas and lymphoid tissues

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