Molecular resemblance of an AIDS-associated lymphoma and endemic Burkitt lymphomas: implications for their pathogenesis.

Haluska, Frank G.; Russo, Giandomenico; Kant, Jeffrey A.; Andreef, M; Croce, C. M.

doi:10.1073/pnas.86.22.8907

Cited by 48 publications

(6 citation statements)

References 26 publications

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“…All cases of AIDS-BLL (n ¼ 2) and AIDS-DLCL (n ¼ 2) which carried c-MYC alterations were found to harbour gross rearrangements of the gene which were detectable by Southern blot analysis. Overall, the relative distribution of rearrangements and first exon-first intron border mutations of c-MYC observed are consistent with those observed in studies of other AIDS-NHL panels (Haluska et al, 1989;Ballerini et al, 1993;Bhatia et al, 1994).…”

Section: Genetic Lesions Of C-mycsupporting

confidence: 87%

Genetic heterogeneity of AIDS‐related small non‐cleaved cell lymphoma

Gaïdano

Pastore

Gloghini³

et al. 1997

Br J Haematol

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AIDS‐related small noncleaved cell lymphoma (AIDS‐SNCCL) includes Burkitt's lymphoma (BL) and high‐grade B‐cell Burkitt‐like lymphoma (BLL). Due to the marked polymorphism of AIDS‐related non‐Hodgkin's lymphomas (AIDS‐NHL), the morphologic distinction between these two types of lymphomas is frequently controversial, although it may bear clinical relevance. Although the molecular features of AIDS‐BL have been clarified to a certain extent, the genetic peculiarities of AIDS‐BLL have not been investigated in detail. In this study we have compared morphologic and genetic features of AIDS‐BL and AIDS‐BLL in a blind coded fashion. Molecular studies were focused on the genetic lesions known to be implicated in AIDS‐NHL, including alterations of c‐MYC, BCL‐6, p53, deletions of 6q, as well as infection by EBV and HHV‐8. Alterations of c‐MYC occurred in 10/10 AIDS‐BL, whereas they were restricted to 2/10 AIDS‐BLL (P < 0.01). Mutations of p53 were present in 5/10 AIDS‐BL, whereas they were consistently absent among AIDS‐BLL (n = 10; P < 0.05). Infection by EBV occurred in 30% of both AIDS‐BL and AIDS‐BLL. Rearrangements of BCL‐6, deletions of 6q and infection by HHV‐8 scored consistently negative in both AIDS‐BL and AIDS‐BLL. Based on the genetic lesions tested, the molecular profile of AIDS‐BLL appears to be closer to that of AIDS‐related diffuse large cell lymphoma (AIDS‐DLCL) than to that of AIDS‐BL. In contrast to AIDS‐BLL, however, AIDS‐DLCL carried rearrangements of BCL‐6 in a fraction of cases (2/9). This study, the largest of its kind reported so far, suggests that AIDS‐BL and AIDS‐BLL have a different molecular pathogenesis and that characterization of genetic lesions may help to distinguish between these two lymphomas.

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Section: Genetic Lesions Of C-mycsupporting

confidence: 87%

Genetic heterogeneity of AIDS‐related small non‐cleaved cell lymphoma

Gaïdano

Pastore

Gloghini³

et al. 1997

Br J Haematol

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“…Up to 12% of HIVseropositive individuals in the U.S. develop clinically aggressive B-cell non-Hodgkin lymphomas (37). A frequent role for c-myc activation in the pathogenesis of these lymphomas is documented by rearrangements of this protooncogene in many specimens (38)(39)(40). Both EBV expression and c-myc deregulation occur in at least 30%o of these tumors.…”

Section: Methodsmentioning

confidence: 99%

Human immunodeficiency virus induction of malignant transformation in human B lymphocytes.

Laurence

Astrin

1991

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

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“…EBV infection appears to be the only genetic lesion associated with a significant fraction of these tumors, particularly with the subset displaying plasmacytoid features; p53 lesions have not been found N ~oss~l.3. [14][15][16][17][18][19][20][21][22][23][24][25][26] On the other hand, the pathogenesis of AIDS-Blood, Vol 84, No 2 (July 15). 1994 pp 397-402 study, we have tested a panel of 40 AIDS-NHL for structural alterations of BCL-6, a putative proto-oncogene that is frequently altered in DLCL in the immunocompetent host.…”

mentioning

confidence: 99%

“…These observations have prompted our analysis of BCL-6 re-cases.l-3. [14][15][16][17][18][19][20][21][22][23][24][25][26] arrangements in a panel of AIDS-NHL representative of both the SNCCL and DLCL subtypes. We wished to define the frequency of BCL-6 involvement in AIDS-NHL and to correlate its presence with other genetic lesions that have been described in the pathogenesis of AIDS-NHL.…”

mentioning

confidence: 99%

Rearrangements of the BCL-6 gene in acquired immunodeficiency syndrome- associated non-Hodgkin's lymphoma: association with diffuse large-cell subtype

Gaïdano

Coco

et al. 1994

Blood

108

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Acquired immunodeficiency syndrome (AIDS)-associated non-Hodgkin's lymphomas (AIDS-NHL), a major source of morbidity and mortality among AIDS patients, are derived from B cells and can be classified into two main histologic categories, small noncleaved cell lymphoma (SNCCL) and diffuse large-cell lymphoma (DLCL). DLCL includes two histologic subsets, ie, large noncleaved cell lymphoma (LNCCL) and large cell- immunoblastic plasmacytoid lymphoma (LC-IBPL). Several studies have shown that AIDS-SNCCL is associated with the clonal accumulation of multiple genetic lesions, including Epstein-Barr virus (EBV) infection, activation of the c-MYC and RAS oncogenes, as well as inactivation of the p53 tumor suppressor gene at variable frequencies. On the contrary, the molecular pathogenesis of AIDS-DLCL is largely obscure, because no genetic lesion other than EBV infection has been specifically identified in this group. In this study, we have tested a panel of 40 AIDS-NHL for structural alterations of BCL-6, a putative proto-oncogene that is frequently altered in DLCL in the immunocompetent host. Our results show that rearrangements of BCL-6 are present in 20% of AIDS- DLCL (5 of 24), including 2 of 8 LNCCL and 3 of 16 LC-IBPL, but in no case of AIDS-SNCCL. BCL-6 rearrangements were detected both in the presence and in the absence of EBV infection of the tumor clone, but in no case were associated with activation of c-MYC or mutations of p53. These data identify a novel genetic lesion in AIDS-DLCL and corroborate the notion that lymphomagenesis in AIDS follows two distinct molecular pathways that are associated with the development of histologically distinct types of AIDS-NHL.

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Molecular resemblance of an AIDS-associated lymphoma and endemic Burkitt lymphomas: implications for their pathogenesis.

Cited by 48 publications

References 26 publications

Genetic heterogeneity of AIDS‐related small non‐cleaved cell lymphoma

Genetic heterogeneity of AIDS‐related small non‐cleaved cell lymphoma

Human immunodeficiency virus induction of malignant transformation in human B lymphocytes.

Rearrangements of the BCL-6 gene in acquired immunodeficiency syndrome- associated non-Hodgkin's lymphoma: association with diffuse large-cell subtype

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