Translocation (18;22)(q21;q11) in B-cell lymphomas: a report of 4 cases and review of the literature

Lin, Pei; Jetly, Rechna; Lennon, Patrick A.; Abruzzo, Lynne V.; Prajapati, Sapana; Medeiros, L. Jeffrey

doi:10.1016/j.humpath.2008.04.007

Cited by 16 publications

(12 citation statements)

References 27 publications

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“…Similarly, rearrangements of BCL6 (3q27), seen in 20% of our cases, have also been described in follicular lymphoma, DLBCL, nodular lymphocyte predominant Hodgkin lymphoma, and rarely other types of B-NHL [10]. Other aberrations (1q, 22q11 and 12q), though less frequently observed, have also been documented in different B-NHL [31][32][33]. A notable exception in our series was a failure to detect t(14;18).…”

Section: Discussionsupporting

confidence: 81%

Cytogenetic abnormalities in reactive lymphoid hyperplasia: byproducts of the germinal centre reaction or indicators of lymphoma?

Sevilla

Murty

Sun

et al. 2011

Hematological Oncology

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Non-random karyotypic abnormalities associated with non-Hodgkin lymphomas (NHLs) have been described in cases of reactive lymphoid hyperplasia (RLH). However, the frequency and types of cytogenetic aberrations detected and their clinical relevance are unknown. To address these questions, we undertook a retrospective analysis of a large series of RLH diagnosed at our institute over 8 years. Cytogenetic abnormalities were identified in 20 of 116 (17%) cases with informative karyotypes, comprising 14 (70%) structural and 11 (55%) numerical changes. Clonal (n = 14, 70%) and non-clonal (n = 6, 30%) abnormalities were observed. Aberrations of chromosome 14 were the most frequent (n = 8, 42%, 7 represented IgH translocations), followed by chromosome 3 (n = 4, 3 represented BCL6 translocations), and chromosome 12 (n = 4). Abnormal karyotypes were most often associated with florid follicular hyperplasia. Isolated lymphoid organ (lymph node, tonsil or spleen) enlargement (12/20, 60%) was more common, no specific etiology was identified in 10/20 (50%) cases and only 1 of 18 patients with clinical follow-up (range 2-107 months, median 60 months) developed lymphoma. In our experience, cytogenetic abnormalities involving loci associated with B-cell NHL are not infrequently detected in RLH. Their occurrence portends low risk for lymphomagenesis, however longer follow-up is prudent to further evaluate the natural history of such cases.

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Section: Discussionsupporting

confidence: 81%

Cytogenetic abnormalities in reactive lymphoid hyperplasia: byproducts of the germinal centre reaction or indicators of lymphoma?

Sevilla

Murty

Sun

et al. 2011

Hematological Oncology

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“…These are found in typical CLL (sometimes during Richter's transformation) and in CLL/PL (29,30,32). Atypical cytological characteristics (increased number of lymphoid cells with irregular nuclear contour, plasmacytoid features or PLs) and̸or immunophenotypic profile (lack of CD23 and intermediate̸strong CD20 expression) is reported and hypothesized to be linked to trisomy 12 (29,33,34).…”

Section: T(14;18)(q32;q21) and Variants (Igh/bcl2mentioning

confidence: 98%

“…All 3 translocations, t(14;18) (q32;q21), t(2;18)(p11;q21.3) and t(18;22) (q21.3;q11), and their molecular consequences, IGH/BCL2, IGK/BCL2 and IGL/BCL2, have been reported (28,29). These translocations are present at diagnosis or arise during evolution and are usually associated with additional karyotypic changes, more particularly with trisomy 12 (30)(31)(32).…”

Section: T(14;18)(q32;q21) and Variants (Igh/bcl2mentioning

confidence: 99%

“…Atypical cytological characteristics (increased number of lymphoid cells with irregular nuclear contour, plasmacytoid features or PLs) and̸or immunophenotypic profile (lack of CD23 and intermediate̸strong CD20 expression) is reported and hypothesized to be linked to trisomy 12 (29,33,34). IG/BCL2 fusion is significantly associated with mutated IGHV status (30-32), which led Baseggio et al (30) to conclude at a post-germinal center cellular origin.…”

Section: T(14;18)(q32;q21) and Variants (Igh/bcl2mentioning

confidence: 99%

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Immunoglobulin gene translocations in chronic lymphocytic leukemia: A report of 35 patients and review of the literature

Braekeleer

Tous

Guéganic

et al. 2016

Molecular and Clinical Oncology

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Abstract. Chronic lymphocytic leukemia (CLL) represents the most common hematological malignancy in Western countries, with a highly heterogeneous clinical course and prognosis. Translocations involving the immunoglobulin (IG) genes are regularly identified. From 2000 to 2014, we identified an IG gene translocation in 18 of the 396 patients investigated at diagnosis (4.6%) and in 17 of the 275 analyzed during follow-up (6.2%). A total of 4 patients in whom the IG translocation was identified at follow-up did not carry the translocation at diagnosis. The IG heavy locus (IGH) was involved in 27 translocations (77.1%), the IG κ locus (IGK) in 1 (2.9%) and the IG λ locus (IGL) in 7 (20.0%). The chromosome band partners of the IG translocations were 18q21 in 16 cases (45.7%), 11q13 and 19q13 in 4 cases each (11.4% each), 8q24 in 3 cases (8.6%), 7q21 in 2 cases (5.7%), whereas 6 other bands were involved once (2.9% each). At present, 35 partner chromosomal bands have been described, but the partner gene has solely been identified in 10 translocations. CLL associated with IG gene translocations is characterized by atypical cell morphology, including plasmacytoid characteristics, and the propensity of being enriched in prolymphocytes. The IG heavy chain variable region (IGHV) mutational status varies between translocations, those with unmutated IGHV presumably involving cells at an earlier stage of B-cell lineage. All the partner genes thus far identified are involved in the control of cell proliferation and/or apoptosis. The translocated partner gene becomes transcriptionally deregulated as a consequence of its transposition into the IG locus. With the exception of t(14;18)(q32;q21) and its variants, prognosis appears to be poor for the other translocations.Therefore, searching for translocations involving not only IGH, but also IGL and IGK, by banding and molecular cytogenetics is required. Furthermore, it is important to identify the partner gene to ensure the patients receive the optimal treatment.

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“…1 Significantly, clinical tests aimed at recurrent translocations/gene fusions involving Bcl-Abl, TMPRSS2-ERG, c-myc and bcl2 already impact clinical decisions. 1–4 …”

Section: Introductionmentioning

confidence: 99%

Mate Pair Sequencing of Whole-Genome-Amplified DNA Following Laser Capture Microdissection of Prostate Cancer

et al. 2012

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High-throughput next-generation sequencing provides a revolutionary platform to unravel the precise DNA aberrations concealed within subgroups of tumour cells. However, in many instances, the limited number of cells makes the application of this technology in tumour heterogeneity studies a challenge. In order to address these limitations, we present a novel methodology to partner laser capture microdissection (LCM) with sequencing platforms, through a whole-genome amplification (WGA) protocol performed in situ directly on LCM engrafted cells. We further adapted current Illumina mate pair (MP) sequencing protocols to the input of WGA DNA and used this technology to investigate large genomic rearrangements in adjacent Gleason Pattern 3 and 4 prostate tumours separately collected by LCM. Sequencing data predicted genome coverage and depths similar to unamplified genomic DNA, with limited repetition and bias predicted in WGA protocols. Mapping algorithms developed in our laboratory predicted high-confidence rearrangements and selected events each demonstrated the predicted fusion junctions upon validation. Rearrangements were additionally confirmed in unamplified tissue and evaluated in adjacent benign-appearing tissues. A detailed understanding of gene fusions that characterize cancer will be critical in the development of biomarkers to predict the clinical outcome. The described methodology provides a mechanism of efficiently defining these events in limited pure populations of tumour tissue, aiding in the derivation of genomic aberrations that initiate cancer and drive cancer progression.

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Translocation (18;22)(q21;q11) in B-cell lymphomas: a report of 4 cases and review of the literature

Cited by 16 publications

References 27 publications

Cytogenetic abnormalities in reactive lymphoid hyperplasia: byproducts of the germinal centre reaction or indicators of lymphoma?

Cytogenetic abnormalities in reactive lymphoid hyperplasia: byproducts of the germinal centre reaction or indicators of lymphoma?

Immunoglobulin gene translocations in chronic lymphocytic leukemia: A report of 35 patients and review of the literature

Mate Pair Sequencing of Whole-Genome-Amplified DNA Following Laser Capture Microdissection of Prostate Cancer

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