Primary mediastinal (thymic) B-cell lymphoma is characterized by gains of chromosomal material including 9p and amplification of the REL gene

Joos, Stefan; Otano-Joos, MI; Ziegler, Sebastian; Brüderlein, Silke; Manoir, Stanislas du; Bentz, Martin; Möller, Peter; Lichter, Peter

doi:10.1182/blood.v87.4.1571.bloodjournal8741571

Cited by 301 publications

(92 citation statements)

References 31 publications

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“…In line with our results, polysomy of chromosome 12 was detected as the most common abnormality in B-cell malignancies studied by fluorescence in situ hybridization (59). In addition, previous CGH studies reported gains and/or amplifications on 12q as recurrent aberrations in various types of non-Hodgkin lymphomas, including extracerebral DLBCL (3,5,6,22,35,55). A molecular genetic study reported amplifications of the proto-oncogenes GLI1, CDK4 and MDM2 (all located at 12q13-q15) in 11-14% of extracerebral DLBCL (43).…”

Section: Discussionsupporting

confidence: 89%

“…We identified one tumor with a high-level amplification of sequences from 9p23-p24. Amplification on distal 9p was previously observed in primary mediastinal B-cell lymphomas (22). Further evidence for a lymphoma-associated proto-oncogene at distal 9p comes from cytogenetic studies, which reported translocation breakpoints at 9p23-p24 in malignant lymphomas (40).…”

Section: Discussionmentioning

confidence: 75%

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Characteristic Chromosomal Imbalances in Primary Central Nervous System Lymphomas of the Diffuse Large B‐Cell Type

Weber

Kaulich

et al. 2000

Brain Pathology

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We performed a genome wide screening for genomic alterations on a series of 19 sporadic primary central nervous system lymphomas (PCNSL) of the diffuse large B-cell type by comparative genomic hybridization (CGH). The tumors were additionally analyzed for amplification and rearrangement of the BCL2 gene at 18q21 as well as for mutation of the recently cloned BCL10 gene at 1p22. Eighteen tumors showed genomic imbalances on CGH analysis. On average, 2.1 losses and 4.7 gains were detected per tumor. The chromosome arm most frequently affected by losses of genomic material was 6q (47%) with a commonly deleted region mapping to 6q21-q22. The most frequent gains involved chromosome arms 12q (63%), 18q and 22q (37% each), as well as 1q, 9q, 11q, 12p, 16p and 17q (26% each). High-level amplifications were mapped to 9p23-p24 (1 tumor) and to 18q21-q23 (2 tumors). However, PCR-based analysis, Southern blot analysis and high-resolution matrix-CGH of the BCL2 gene revealed neither evidence for amplification nor for genetic rearrangement. Mutational analysis of BCL10 in 16 PCNSL identified four distinct sequence polymorphisms but no mutation. Taken together, our data do not support a role of BCL2 rearrangement/ amplification and BCL10 mutation in PCNSL but indicate a number of novel chromosomal regions that likely carry yet unknown tumor suppressor genes or proto-oncogenes involved in the pathogenesis of these tumors.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 75%

Characteristic Chromosomal Imbalances in Primary Central Nervous System Lymphomas of the Diffuse Large B‐Cell Type

Weber

Kaulich

et al. 2000

Brain Pathology

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“…With regard to these findings, gains in 2p16 were most frequent in patients who failed to achieve a CR. It is noteworthy that a gain in chromosome 2p has been identified as a recurrent alteration in 20% of patients DLBCL 12,[31][32][33][34][35][36][37] and is the most frequent CGH alteration in classic Hodgkin lymphoma (identified in 50% of patients). 38,39 The common recurrent region expands 4.2 Mb in 2p15-16.…”

Section: Discussionmentioning

confidence: 99%

Array comparative genomic hybridization identifies genetic regions associated with outcome in aggressive diffuse large B‐cell lymphomas

Robledo¹,

Garcı́a²,

Caballero³

et al. 2009

Cancer

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BACKGROUND: Diffuse large B‐cell lymphomas (DLBCLs) are the most common type of non‐Hodgkin lymphomas. With chemotherapy and progenitor stem cell transplantation, about 60% of patients with DLBCL are long‐term survivors. The International Prognostic Index identifies patients with different outcomes. However, biologic characteristics also may help to discriminate different treatments groups. METHODS: DNA copy number changes identified by array comparative genomic hybridization (array‐CGH) were studied in 40 patients who had DLBCL with a poor prognosis and who were treated uniformly with dose‐escalated cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) and intensification before high‐dose chemotherapy with autologous stem cell transplantation. RESULTS: In total, 722 copy number changes were observed (median, 5 copy number changes per patient; range, 0‐75 copy number changes per patient), with a predominance of gains. Gains on 2p16 were present only in patients who failed to achieve a complete response after escalated CHOP therapy (P < .05). In univariate analysis, gains on 2p16 and losses on 17p13 (the tumor protein p53 gene TP53 gene) were associated with a poor response to the therapy. Furthermore, age >60 years and losses on 10q23.31 (the phosphatase and tensin homolog gene PTEN) or on 17p13 were associated with short survival. In multivariate analysis, only advanced age and losses on 10q23.31 retained an adverse prognostic impact. CONCLUSIONS: Array‐CGH identified multiple regions with common copy number changes, some of which were associated with outcome in patients with DLBCL. Cancer 2009. © 2009 American Cancer Society.

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“…DNA microarrays have shown similarities between PMBL and cHL, suggesting that PMBL falls somewhere along the biological spectrum between NHL and cHL (Fig 4B;Rosenwald et al, 2003;Abramson & Shipp, 2005). In addition, several chromosomal aberrations found in PMBL, including gains in chromosome 9p [Janus kinase (JAK)-2] and 2p (c-Rel), are also amplified in cHL (Joos et al, 1996). PMBL is typically a malignancy of adolescents and young adults.…”

Section: Primary Mediastinal B-cell Lymphomamentioning

confidence: 99%

Adolescent non‐Hodgkin lymphoma and Hodgkin lymphoma: state of the science

et al. 2008

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SummaryLymphoma is the most common malignancy among adolescents, accounting for >25% of newly diagnosed cancers in the 15-19 year age group. Hodgkin lymphoma (HL) accounts for the majority (two-thirds) of cases, while the remainder of patients have one of four subtypes of non-Hodgkin lymphoma (NHL): diffuse large B-cell lymphoma (DLBCL) including primary mediastinal B-cell lymphoma (PMBL), Burkitt lymphoma (BL), lymphoblastic lymphoma (LL) or anaplastic large cell lymphoma (ALCL). Epidemiology, histology, treatment and outcome differ between HL and NHL, as well as among the various subtypes of NHL. Adolescent lymphoma is particularly interesting because it often shares features with both childhood and adult lymphoma. As medical oncologists and paediatric oncologists often follow divergent treatment plans, disagreements may arise between practitioners as to how best treat the adolescent group. Additional complicating factors associated with the adolescent years, such as lack of insurance, issues pertaining to body image, and concerns about fertility, can also hinder prompt, appropriate medical management. This review details the complexities associated with the diagnosis and treatment of adolescent lymphoma and updates the state of the science, with particular emphasis on epidemiology, diagnosis, and proper management of HL and the various subtypes of NHL.

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Primary mediastinal (thymic) B-cell lymphoma is characterized by gains of chromosomal material including 9p and amplification of the REL gene

Cited by 301 publications

References 31 publications

Characteristic Chromosomal Imbalances in Primary Central Nervous System Lymphomas of the Diffuse Large B‐Cell Type

Characteristic Chromosomal Imbalances in Primary Central Nervous System Lymphomas of the Diffuse Large B‐Cell Type

Array comparative genomic hybridization identifies genetic regions associated with outcome in aggressive diffuse large B‐cell lymphomas

Adolescent non‐Hodgkin lymphoma and Hodgkin lymphoma: state of the science

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