Aberrant somatic hypermutation and expression of activation‐induced cytidine deaminase mRNA in mediastinal large B‐cell lymphoma

“…3 The involvement of aberrant SHM in PMLBCL has been suggested by a recent report based on a limited number of cases. 4 These observations prompted our comprehensive analysis aimed at exploring the involvement of aberrant SHM of PIM-1, PAX-5, RhoH/TTF and c-MYC in a sizeable panel of PMLBCL and at comparing the mutational spectrum with that of systemic DLBCL.…”

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confidence: 99%

Aberrant somatic hypermutation in primary mediastinal large B-cell lymphoma

et al. 2005

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“…In fact, despite some overlapping features, [37][38][39][40][41] NLPHL and cHL represent distinct diseases that clearly differ from DLBCL in terms of biologic properties, morphologic appearance, clinical course, and response to therapy. 1,42 The most probable explanation is that genetic alterations in addition to aberrant SHM may eventually concur in the pathogenesis of HL.…”

Section: Discussionmentioning

confidence: 99%

Aberrant somatic hypermutation in tumor cells of nodular-lymphocyte-predominant and classic Hodgkin lymphoma

Liso

Capello

Marafioti

et al. 2006

Blood

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Aberrant somatic hypermutation (SHM) has been identified as a mechanism for genomewide instability in diffuse large B-cell lymphoma (DLBCL). To assess whether aberrant SHM plays a role in the molecular pathogenesis of Hodgkin lymphoma (HL), we investigated microdissected neoplastic cells of nodular lymphocyte-predominant HL (NLPHL; n ‫؍‬ 10) and classic HL (cHL; n ‫؍‬ 9) for the presence of mutations in the 5 sequences of 4 previously identified aberrant SHM targets (PIM1, PAX5, RhoH/TTF, c-MYC). Mutations in one or more genes were detected in 80% of NLPHLs and 55% of cHLs, with 50% and 30% of patients carrying mutations in 2 or more genes, respectively. The most frequently involved protooncogene was PAX5, mutated in 7 of 9 patients with NLPHL and 2 of 9 patients with cHL. In total, 34 mutations were detected in NLPHL (frequency, 1.04/1000 bp) and 35 were detected in patients with cHL (frequency, 1.92/1000 bp). Mutations were of somatic origin because they were absent in control T cells and shared most of the features of the immunoglobulin variable (IGV) gene-associated SHM mechanism-ie, single nucleotide substitutions (n ‫؍‬ 63) with rare deletions/insertions (n ‫؍‬ 6) and a predominance of transitions over transversions with preferential targeting motifs. Our finding that NLPHL and cHL are targeted by aberrant SHM, as is DLBCL, suggests that these lymphomas may share common molecular pathogenetic events.

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“…Previous studies demonstrated the expression of AID in different lymphoma types using reverse transcriptase-polymerase chain reaction technology, western blot, and recently, also immunohistochemistry, examining cell lines and tissue samples of lymph nodes. [15][16][17][18][19][20][21] In the present study, we investigated the expression of AID in bone marrow infiltrates in different types of malignant lymphomas. A set of bone marrow trephines with infiltration of Hodgkin lymphoma (HL) and nonHodgkin lymphomas (NHL) of B cell and T-cell type was selected and the expression of AID was assessed immunohistochemically.…”

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confidence: 99%

Expression of Activation-induced Cytidine Deaminase in Malignant Lymphomas Infiltrating the Bone Marrow

Engels

Jungnickel

Tobollik

et al. 2008

Applied Immunohistochemistry &Amp; Molecular Morphology

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Somatic hypermutation of immunoglobulin genes and class switch recombination are pivotal processes in the germinal center (GC) reaction and have been implicated in the development of malignant B-cell lymphoma. Both processes require the enzyme activation-induced cytidine deaminase (AID). Expression of AID is largely restricted to GC B cells and B cells that undergo class switch recombination outside the GC. AID is also expressed in many B-cell lymphomas. This study investigates the expression of AID of malignant lymphomas infiltrating the bone marrow. Bone marrow trephines (n=130) with infiltration of Hodgkin lymphoma and non-Hodgkin lymphoma of B cell and T-cell type and trephines with reactive lymphoid follicles (n=16) were analyzed immunohistochemically for AID protein. AID is expressed in bone marrow infiltrates of malignant lymphomas. AID was generally detected in lymphomas of GC origin. Tumor cells of hairy cell leukemia are mostly AID. There is apparently no different expression of AID found in bone marrow infiltrates of malignant lymphomas compared with a control group with nodal malignant lymphoma infiltrates (n=105). These results suggest that the expression pattern of AID in lymphoma infiltrates in the bone marrow reflects that of extramedullary lymphoma infiltrates.

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Aberrant somatic hypermutation and expression of activation‐induced cytidine deaminase mRNA in mediastinal large B‐cell lymphoma

Cited by 28 publications

References 11 publications

Aberrant somatic hypermutation in primary mediastinal large B-cell lymphoma

Aberrant somatic hypermutation in primary mediastinal large B-cell lymphoma

Aberrant somatic hypermutation in tumor cells of nodular-lymphocyte-predominant and classic Hodgkin lymphoma

Expression of Activation-induced Cytidine Deaminase in Malignant Lymphomas Infiltrating the Bone Marrow

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