High Frequency of t(14;18)-Translocation Breakpoints Outside of Major Breakpoint and Minor Cluster Regions in Follicular Lymphomas

Albinger-Hegyi, Andrea; Hochreutener, Bernhard; Abdou, Marie-Therese; Hegyi, Ivan; Dours-Zimmermann, Marı́a T.; Kurrer, Michael; Heitz, Philipp U.; Zimmermann, Dieter R.

doi:10.1016/s0002-9440(10)64905-x

Cited by 104 publications

(75 citation statements)

References 22 publications

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“…Bcl2/IGH is the most frequent gene alteration and is regarded as the hallmark genetic change in FL. As Albinger-Heygi et al 21 pointed out, detection rates were significantly lower in Europe (41-61%) and in the Far East (32-39%), using both cytogenetic and molecular Southern blot techniques, in comparison with the USA. More recent analyses, however, suggest that the variation in the incidence of t (14;18) in FL across studies may be technical rather than real.…”

Section: Discussionmentioning

confidence: 95%

Low-grade follicular lymphoma with t(14;18) presents a homogeneous disease entity otherwise the rest comprises minor groups of heterogeneous disease entities with Bcl2 amplification, Bcl6 translocation or other gene aberrances

et al. 2005

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JapanFollicular lymphomas (FL) are morphologically classified into grades 1, 2, 3a and 3b by the World Health Organization. Bcl2, Bcl6 and CD10 are phenotypic markers of FL while the Bcl2 t(14;18) and Bcl6 t(3q27) gene translocations are common genetic changes. However, to date, there has been no integrated analysis based on phenotype, grade and genotype from large numbers of FL cases. We graded 261 cases of FL and determined their phenotypes and gene alterations. According to the antigen markers and gene alterations of 147 cases, we classified FL into typical and the others types. The typical group, which includes 69% cases of FL, is characterized by low histological grade (grade 1, 2), coexpression of BCL2 and CD10 and Bcl2 gene translocation. The rest comprises a small part of low-grade FL without Bcl2 gene translocation and high-grade (grade 3a, 3b) FL. These FLs include some heterogeneous disease entities. They are characterized by high histological grade (87%), no definite expression of BCL2 or CD10 and several kinds of gene aberrances including Bcl2 translocation, Bcl6 translocation, Bcl2 amplification or other unknown gene abnormality. Our findings indicate that typical FL presents a homogeneous disease entity whereas the rest comprises heterogeneous diseases entities.

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Section: Discussionmentioning

confidence: 95%

Low-grade follicular lymphoma with t(14;18) presents a homogeneous disease entity otherwise the rest comprises minor groups of heterogeneous disease entities with Bcl2 amplification, Bcl6 translocation or other gene aberrances

et al. 2005

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“…33 Detection of the BCL2/JH gene rearrangements involving the major breakpoint region (MBR), the intermediate cluster region (ICR), or the minor cluster region (MCR) of the BCL2 gene was performed as described previously. [34][35][36] PCR assays were performed in a 25 ml reaction volume containing 400 ng DNA template, 20 pmol each primer, 1 U GoTaq DNA polymerase (Promega, Madison, WI, USA), 2 mM MgCl 2 , and 200 mM each dNTP. The optimized PCR conditions were 10 min at 931C for initial denaturation, then 35 cycles of 1 min of denaturation at 931C, 1 min of annealing following a gradient in annealing temperatures from 55 to 601C for MBR, from 58 to 621C for ICR, and from 59 to 611C for MCR, and 1 min of extension at 721C.…”

Section: Bcl2/jh Gene Rearrangements Detection By Pcrmentioning

confidence: 99%

Presence of simian virus 40 in diffuse large B-cell lymphomas in Tunisia correlates with germinal center B-cell immunophenotype, t(14;18) translocation, and P53 accumulation

et al. 2008

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Previously we have reported the presence of simian virus 40 DNA in 56% of diffuse large B-cell lymphomas in Tunisia. Here, we investigated the relationship between the status of simian virus 40 and t(14;18) translocation, germinal center status, and P53 and BCL2 expression to assess the clinical and biological relevance of simian virus 40 presence in diffuse large B-cell lymphomas. Therefore, we evaluated by immunohistochemistry the expression patterns of CD10, BCL6, MUM1, BCL2, and P53 in 86 diffuse large B-cell lymphomas (48 simian virus 40-positive and 38 simian virus 40-negative cases). The t(14;18) translocation was investigated by polymerase chain reaction. Immunostaining patterns for CD10, BCL6, and MUM1 were used to subclassify diffuse large B-cell lymphoma cases as germinal center or non-germinal center phenotypes. Germinal center phenotype, t(14;18), P53, and BCL2 expression were found in 71, 30, 55, and 65% of cases, respectively. Interestingly, germinal center phenotype, t(14;18), and P53 accumulation were found to be more frequent in simian virus 40-positive cases than in simian virus 40-negative ones (81, 44, 69 vs 58, 13, 37%; P ¼ 0.018, 0.002, and 0.003, respectively). However, there were no correlations between the presence of simian virus 40 and the expression of CD10, BCL6, MUM1 and BCL2, patient's age and gender, clinical stage, or the International Prognosis Index. Multivariate logistic regression analyses revealed that the germinal center phenotype, P53 accumulation, and t(14;18) were independent factors for simian virus 40 association (P ¼ 0.029, 0.006, and 0.014, respectively). There were no significant differences in overall survival regarding P53, BCL2, or t(14;18) status. However, patients with germinal center phenotype or low International Prognosis Index scores displayed a significantly better survival than those with non-germinal center phenotype or high International Prognosis Index scores (P ¼ 0.003 and 0.0001, respectively). These two prognosis factors remain independent in multivariate analyses (P ¼ 0.001 and o0.0001, respectively). Interestingly, among patients with germinal center phenotype, simian virus 40-positive subgroup displayed a significantly shorter survival than simian virus 40-negative subgroup (P ¼ 0.034). In summary, these findings support a role of simian virus 40 in the pathogenesis of diffuse large B-cell lymphomas. On other hand, they suggest that a significant proportion of diffuse large B-cell lymphoma cases with germinal center phenotype may result from early transformation by simian virus 40, mainly those harboring the t(14;18).

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“…2A). (3,10,11,13) Within the 150 bp, there are three peaks of breakage, each about 15 to 20 bp in size (Fig. 2B).…”

Section: Lymphoid Translocations: An Overviewmentioning

confidence: 99%

DNA structures at chromosomal translocation sites

Raghavan

Lieber

2006

BioEssays

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SummaryIt has been unclear why certain defined DNA regions are consistently sites of chromosomal translocations. Some of these are simply sequences of recognition by endogenous recombination enzymes, but most are not. Recent progress indicates that some of the most common fragile sites in human neoplasm assume non-B DNA structures, namely deviations from the Watson-Crick helix. Because of the single strandedness within these non-B structures, they are vulnerable to structure-specific nucleases. Here we summarize these findings and integrate them with other recent data for non-B structures at sites of consistent constitutional chromosomal translocations.

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High Frequency of t(14;18)-Translocation Breakpoints Outside of Major Breakpoint and Minor Cluster Regions in Follicular Lymphomas

Cited by 104 publications

References 22 publications

Low-grade follicular lymphoma with t(14;18) presents a homogeneous disease entity otherwise the rest comprises minor groups of heterogeneous disease entities with Bcl2 amplification, Bcl6 translocation or other gene aberrances

Low-grade follicular lymphoma with t(14;18) presents a homogeneous disease entity otherwise the rest comprises minor groups of heterogeneous disease entities with Bcl2 amplification, Bcl6 translocation or other gene aberrances

Presence of simian virus 40 in diffuse large B-cell lymphomas in Tunisia correlates with germinal center B-cell immunophenotype, t(14;18) translocation, and P53 accumulation

DNA structures at chromosomal translocation sites

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