Genome wide DNA‐profiling of HIV‐related B‐cell lymphomas

Capello, Daniela; Scandurra, Marta; Poretti, Giulia; Rancoita, Paola Maria Vittoria; Mian, Michael; Gloghini, Annunziata; Deambrogi, Clara; Martini, Maurizio; Rossi, Davide; Greiner, Timothy C.; Chan, Wing C.; Ponzoni, Maurilio; Moreno, Santiago Montes; Piris, Miguel Á.; Canzonieri, Vincenzo; Spina, Michele; Tirelli, Umberto; Inghirami, Giorgio; Rinaldi, Andrea; Zucca, Emanuele; Favera, Riccardo Dalla; Cavalli, Franco; Larocca, Luigi Maria; Kwee, Ivo; Carbone, Antonino; Gaïdano, Gianluca; Bertoni, Francesco

doi:10.1111/j.1365-2141.2009.07943.x

Cited by 69 publications

(86 citation statements)

References 49 publications

(72 reference statements)

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“…Although our analysis is restricted to single loci, our results fit with the presence of a lower number of genomic alterations in EBV-positive diffuse large B-cell lymphoma found by comparative genomic hybridization analysis in cases associated with other sources of immunosuppression (human immunodeficiency virus and post-transplant setting) by other groups. [49][50][51][52] Thus, our results are in line with the concept that both immunosuppression and EBV oncogenic effects in concert may reduce the need of additional chromosomal alterations frequently found in conventional EBV-negative diffuse large B-cell lymphoma.…”

Section: Discussionsupporting

confidence: 77%

EBV-positive diffuse large B-cell lymphoma of the elderly is an aggressive post-germinal center B-cell neoplasm characterized by prominent nuclear factor-kB activation

et al. 2012

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Here, we report a retrospective series of 47 EBV-positive diffuse large B-cell lymphoma associated with advanced age. Histopathology allowed to the identification of different histological patterns: cases with polymorphic diffuse large B-cell lymphoma (29 cases), Hodgkin-like (8 cases) and polymorphic lymphoproliferative disorder-like (9 cases) patterns. One case was purely monomorphic diffuse large B-cell lymphoma. We show that this lymphoma type is a neoplasm with prominent classical and alternative nuclear factor-kB pathway activation in neoplastic cells (79% of the cases showed nuclear staining for p105/p50, 74% for p100/p52 and 63% for both proteins), with higher frequency than that observed in a control series of EBV-negative diffuse large B-cell lymphoma (v 2 o0.001). Most cases showed an activated phenotype (95% non-germinal center (Hans algorithm); 78% activated B cell (Choi algorithm)). Clonality testing demonstrated IgH and/or K/Kde/L monoclonal rearrangements in 64% of cases and clonal T-cell populations in 24% of cases. C-MYC (1 case), BCL6 (2 cases) or IgH (3 cases) translocations were detected by FISH in 18% cases. These tumors had a poor overall survival and progression-free survival (the estimated 2-year overall survival was 40±10% and the estimated 2-year progression-free survival was 36±9%). Thus, alternative therapies, based on the tumor biology, need to be tested in patients with EBV-positive diffuse large B-cell lymphoma of the elderly. Modern Pathology (2012) 25, 968-982;

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Section: Discussionsupporting

confidence: 77%

EBV-positive diffuse large B-cell lymphoma of the elderly is an aggressive post-germinal center B-cell neoplasm characterized by prominent nuclear factor-kB activation

et al. 2012

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“…In the immunodeficiency-related DLBCL, the presence of Epstein-Barr virus infection is associated with a lower number of genomic aberrations. 28,29 Although RS arises in the preexisting immunodeficiency associated with CLL, 1 Epstein-Barr virus infection does not play a major role in RS 2,3 and is an unlikely explanation for our data. Epigenetic changes, such as specific methylation patterns, 30 or still-unidentified somatic mutations, might explain the observed relative low genomic complexity in RS vs DLBCL.…”

Section: Discussionmentioning

confidence: 72%

Two main genetic pathways lead to the transformation of chronic lymphocytic leukemia to Richter syndrome

Chigrinova

Rinaldi

Kwee

et al. 2013

Blood

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Key Points• Richter syndrome has genomic complexity intermediate between chronic lymphocytic leukemia and diffuse large B-cell lymphoma.• Inactivation of TP53 and of CDKN2A is a main mechanism in the transformation to Richter syndrome.Richter syndrome (RS) occurs in up to 15% of patients with chronic lymphocytic leukemia (CLL). Although RS, usually represented by the histologic transformation to a diffuse large B-cell lymphoma (DLBCL), is associated with a very poor outcome, especially when clonally related to the preexisting CLL, the mechanisms leading to RS have not been clarified. To better understand the pathogenesis of RS, we analyzed a series of cases including 59 RS, 28 CLL phase of RS, 315 CLL, and 127 de novo DLBCL. RS demonstrated a genomic complexity intermediate between CLL and DLBCL. Cell-cycle deregulation via inactivation of TP53 and of CDKN2A was a main mechanism in the histologic transformation from CLL phase, being present in approximately one half of the cases, and affected the outcome of the RS patients. A second major subgroup was characterized by the presence of trisomy 12 and comprised one third of the cases. Although RS shared some of the lesions seen in de novo DLBCL, its genomic profile was clearly separate. The CLL phase preceding RS had not a generalized increase in genomic complexity compared with untransformed CLL, but it presented clear differences in the frequency of specific genetic lesions. (Blood. 2013;122(15):2673-2682

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“…A SNP array analysis of HIV-related BL found recurrent gain of 1q (18%) and loss of 17p including TP53 (27%) but not gain of 13q (Capello et al, 2009). Scholtysik et al (2010) reported gains on 1q localized to minimum common regions (MCRs) at 1q21.1 (26%) and 1q31.3 (33%).…”

Section: Array Cgh and Snp Arraysmentioning

confidence: 99%

Risk factors and treatment of childhood and adolescent Burkitt lymphoma/leukaemia

2012

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SummaryBurkitt lymphoma/leukaemia is the most common (40%) form of non-Hodgkin lymphoma that occurs in children and adolescents. The prognosis of advanced (disseminated) Burkitt lymphoma/leukaemia in children and adolescents three decades ago had a 5-year event-free survival (EFS) of <40%, and required combination chemotherapy and radiation therapy over a 1-2 year period. Currently, the prognosis for the same advanced stage has a 5-year EFS of 85-90% with <6 months of chemotherapy only. Radiation therapy has been eliminated for children and adolescents with Burkitt lymphoma/leukaemia except in emergencies, such as superior vena cava syndrome and acute neurological impairment or in patients with relapse/progression. Current risk factors in the prognosis of childhood and adolescent Burkitt lymphoma/leukaemia include: lactate dehydrogenase level 29 the upper normal limit at diagnosis, bone marrow and central nervous system involvement, poor response to cyclophosphamide, vincristine and prednisone reduction therapy and poor risk cytogenetics. New and novel therapeutic approaches include monoclonal antibody (anti-CD20) therapy, targeted cellular immune therapy and small molecule inhibitors. Future strategies should include improved staging and risk classification, reduction of cytotoxic chemotherapy, the investigation of targeted therapy, an increased understanding of the underlying biology of Burkitt lymphoma/leukaemia, strategies for prevention and approaches to reduce acute and chronic toxicities.

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Genome wide DNA‐profiling of HIV‐related B‐cell lymphomas

Cited by 69 publications

References 49 publications

EBV-positive diffuse large B-cell lymphoma of the elderly is an aggressive post-germinal center B-cell neoplasm characterized by prominent nuclear factor-kB activation

EBV-positive diffuse large B-cell lymphoma of the elderly is an aggressive post-germinal center B-cell neoplasm characterized by prominent nuclear factor-kB activation

Two main genetic pathways lead to the transformation of chronic lymphocytic leukemia to Richter syndrome

Risk factors and treatment of childhood and adolescent Burkitt lymphoma/leukaemia

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