Molecular profile of Epstein–Barr virus infection in HHV-8-positive primary effusion lymphoma

Fassone, Lucia; Bhatia, Kishor; Mi, Gutiérrez; Capello, Daniela; Gloghini, Annunziata; Dolcetti, Riccardo; Vivenza, Daniela; Ascoli, Valeria; Coco, Francesco Lo; Pagani, Léonardo; Dotti, Gianpietro; Rambaldi, Alessandro; Raphaël, Martine; Tirelli, Umberto; Saglio, Giuseppe; Magrath, I. T.; Carbone, Antonino; Gaïdano, Gianluca

doi:10.1038/sj.leu.2401651

Cited by 61 publications

(46 citation statements)

References 44 publications

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“…34,35 Mutational analysis of the BCL-6 gene was performed by DNA direct sequencing of a unique PCR product encompassing 739 nucleotides (positions +404 to +1142) of the BCL-6 5′ noncoding regions. 13,36 The choice of this fragment was based on the fact that Ͼ95% of BCL-6 mutations detected in B-DLCL fall within this region.…”

Section: Analysis Of Bcl-6 Mutations and Rearrangementsmentioning

confidence: 99%

Point mutations of the BCL-6 gene: clinical and prognostic correlation in B-diffuse large cell lymphoma

et al. 2002

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Although point mutations of the 5′ noncoding regions of the BCL-6 proto-oncogene are frequently detected in B-diffuse large cell lymphoma (B-DLCL), a thorough analysis of the clinical correlation of these mutations has not been performed to date. In this study, BCL-6 mutations were examined by DNA direct sequencing in 103 patients with B-DLCL. BCL-6 mutations were found in 53/103 patients, including 38/76 treated with standard chemotherapy and 15/27 treated with autologous stem cell transplantation (ASCT) up front. The presence of BCL-6 mutations was correlated with clinical features at diagnosis and outcome. Mutated patients had a significantly higher LDH level (66% vs 38%, P Ͻ 0.05), and bulky disease (51% vs 32%, P = 0.05). In the whole series of patients BCL-6 mutations did not affect CR and OS. Patients with BCL-6 mutations tended to have a prolonged 5-years DFS and FFS compared to those without mutations (DFS 82% vs 63%, FFS 63% vs 49%). Among B-DLCL treated with standard chemotherapy, mutated patients showed a significantly improved 5-year DFS (85% vs 61%, P Ͻ 0.05) and, notably, the only four relapses observed among mutated patients occurred in less than 8 months. The multivariate regression analysis (P Ͻ 0.01) with DFS as endpoint confirmed the independent prognostic value of BCL-6 mutations. There was a trend for 5-year failurefree survival to be better for patients with BCL-6 mutations (63% vs 43%, P = 0.09). In the 27 patients treated with ASCT, BCL-6 mutations did not correlate with outcome. These results suggest that BCL-6 mutations may predict a higher chance of being free of disease in B-DLCL treated with standard chemotherapy. Larger series of patients need to be analyzed to evaluate the clinical relevance of BCL-6 mutations properly. Leukemia (2002) 16, 268-275.

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Section: Analysis Of Bcl-6 Mutations and Rearrangementsmentioning

confidence: 99%

Point mutations of the BCL-6 gene: clinical and prognostic correlation in B-diffuse large cell lymphoma

et al. 2002

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“…While PELs are almost universally KSHV positive, the majority of PELs have concomitant EBV infection (reviewed in Dourmishev et al, 2003;Drexler et al, 1998;Moore and Chang, 2001). EBV apparently establishes levels type II latency in PELs with low of LMP-1 expression (Callahan et al, 1999;Fassone et al, 2000;Horenstein et al, 1997;Lacoste et al, 2000).…”

Section: B Primary Effusion Lymphomamentioning

confidence: 99%

The Viral Etiology of AIDS‐Associated Malignancies

Angeletti

Zhang

Wood

2008

Advances in Pharmacology

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“…The hypothesis that certain strains of EBV are associated with malignant transformation or with certain tumor types has been an area of active investigation. EBV gene polymorphisms have been demonstrated in a variety of EBV-associated tumors, including endemic Burkitt's lymphoma, Hodgkin's disease, immune deficiency-related lymphomas, gastric carcinoma, and nasopharyngeal carcinoma, as well as in EBV-positive reactive tissues and cultured lymphoblastoid cell lines (Bhatia et al, 1996;Chang et al, 1999;Chen et al, 1998;Fassone et al, 2000;Greiner et al, 2000;Gutierrez et al, 1997;Habeshaw et al, 1999;MacKenzie et al, 1999;Sandvej et al, 2000;Wrightham et al, 1995). Although some earlier studies suggested association of particular EBV strains with certain malignancies (Bhatia et al, 1996;Gutierrez et al, 1997), many subsequent studies have not confirmed this and, instead, have concluded that EBV sequence differences reflect geographic variations rather than any oncogenic potential Chen et al, 1998;Fassone et al, 2000;Habeshaw et al, 1999;MacKenzie et al, 1999;Sandvej et al, 2000).…”

Section: E Pstein-barr Virus (Ebv) Is Found In Essentially Allmentioning

confidence: 99%

“…Laboratory Investigation • July 2002 • Volume 82 • Number 7 liferative disorder termed P-ala VI (Greiner et al, 2000) and a single case (1/11 studied) of primary effusion lymphoma termed P-alaЉ (Fassone et al, 2000). One of the Peruvian/Mexican-NL cases (NL4) of Gutierrez and coworkers was also similar, sharing the same five base substitutions but also had an additional mutation at codon 529 (Gutierrez et al, 1998).…”

Section: Ebna Polymorphisms In Us Nk/t-cell Lymphomamentioning

confidence: 99%

Epstein-Barr Virus Nuclear Antigen (EBNA)-1 Carboxy-Terminal and EBNA-4 Sequence Polymorphisms in Nasal Natural Killer/T-Cell Lymphoma in the United States

Gaal

Weiss

Chen

et al. 2002

Laboratory Investigation

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SUMMARY:Epstein-Barr virus (EBV) polymorphisms were examined in 12 cases of nasal natural killer (NK)/T-cell lymphoma diagnosed in the United States (U.S.-NL) with respect to the EBV-associated nuclear antigen (EBNA)-1 carboxy (C)-terminal region and the EBNA-4 region. A single dominant EBV strain was found in all cases. EBNA-1 sequences were remarkably homogeneous, showing either a P-ala (2/12) or P-ala variant (9/12) sequence. Other EBNA-1 subtypes known to be common in U.S.-reactive samples, such as P-thr or V-leu, were not identified. The final case had a base deletion with frame shift and premature stop codon. EBNA-1 C-terminal amino acid substitutions were common at codons 499 (10/12 cases), 502 (7/12), 524 (9/12), and 528 (6/12), all previously reported "hot spots." However, unlike previous reports of other EBV-associated neoplastic and reactive tissues, mutations were absent at residues 487 and 492. Mutations within HLA-A11-restricted immunogenic EBNA-4 epitopes 399 -408 and 416 -424 occurred in 3 of 12 cases but were not associated with HLA-A11 status. In summary, the exclusive finding of P-ala variant or P-ala EBNA-1 sequences in U.S.-NL cases differs from that reported in U.S.-reactive and non-U.S.-NL cases. Although the significance of this difference is not known for certain, it may be related to geographic and/or site-specific variations, rather than oncogenicity per se. (Lab Invest 2002, 82:957-962).

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Molecular profile of Epstein–Barr virus infection in HHV-8-positive primary effusion lymphoma

Cited by 61 publications

References 44 publications

Point mutations of the BCL-6 gene: clinical and prognostic correlation in B-diffuse large cell lymphoma

Point mutations of the BCL-6 gene: clinical and prognostic correlation in B-diffuse large cell lymphoma

The Viral Etiology of AIDS‐Associated Malignancies

Epstein-Barr Virus Nuclear Antigen (EBNA)-1 Carboxy-Terminal and EBNA-4 Sequence Polymorphisms in Nasal Natural Killer/T-Cell Lymphoma in the United States

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