Characterization of 6q deletions in mature B cell lymphomas and childhood acute lymphoblastic leukemia

Thelander, Emma Flordal; Ichimura, Koichi; Corcoran, Martin; Barbany, Gisela; Nordgren, Ann; Heyman, Mats; Berglund, Mattias; Mungall, Andrew J.; Rosenquist, Richard; Collins, V. Peter; Grandér, Dan; Larsson, Catharina; Lagercrantz, Svetlana

doi:10.1080/10428190701817282

Cited by 53 publications

(33 citation statements)

References 28 publications

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“…7,10 The chromosomal region 6q21 is frequently deleted in various B-cell malignancies, including DLBCL, mantle cell lymphoma, acute lymphatic leukemia and immunoblastic lymphoma. 7,[31][32][33][34][35] This region has been suggested to harbor a tumor suppressor gene. In fact, 6q21 contains the PRDM1 gene encoding BLIMP1, which has recently been reported to function as tumor suppressor gene in PCNSL as well as in systemic DLBCL of the activated B-cell type.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma

et al. 2009

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To determine the pattern of genetic alterations in primary central nervous system lymphomas (PCNSL), 19 PCNSL were studied by high-density single-nucleotide polymorphism arrays. Recurrent losses involved 6p21.32, 6q21, 8q12-12.2, 9p21.3, 3p14.2, 4q35.2, 10q23.21 and 12p13.2, whereas gains involved 18q21-23, 19q13.31, 19q13.43 and the entire chromosomes X and 12. Partial uniparental disomies (pUPDs) were identified in 6p and 9p21.3. These genomic alterations affected the HLA locus, the CDKN2A/p16, CDKN2B/p15 and MTAP, as well as the PRDM1, FAS, MALT1, and BCL2 genes. Increased methylation values of the CDKN2A/p16 promoter region were detected in 75% (6/8) PCNSL. Gene expression profiling showed 4/21 (20%) minimal common regions of imbalances to be associated with a differential mRNA expression affecting the FAS, STAT6, CD27, ARHGEF6 and SEPT6 genes. Collectively, this study unraveled novel genomic imbalances and pUPD with a high resolution in PCNSL and identified target genes of potential relevance in the pathogenesis of this lymphoma entity.

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Section: Discussionmentioning

confidence: 99%

Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma

et al. 2009

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“…The other genes with the same role in CLL, such as CCNC, CD24, PRDM1 located at 6q21 (106.5 Mb)(ref. [41][42][43][44] ), were excluded from consideration in our patients because they are located outside of our established SCDR.…”

Section: Discussionmentioning

confidence: 99%

Array-based karyotyping in chronic lymphocytic leukemia (CLL) detects new unbalanced abnormalities that escape conventional cytogenetics and CLL FISH panel

Urbánková¹,

Papajík²,

Plachy³

et al. 2014

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Aims. Chronic lymphocytic leukemia (CLL) is the most common adult leukemia with a very heterogeneous course. Progress in molecular genetic characterization of CLL has confirmed the prognostic role of unbalanced chromosomal abnormalities currently defined by molecular cytogenetic methods: conventional karyotyping and FISH. However, a significant percentage of genomic abnormalities escapes routine investigation due to the limitations of these methods. It is presently clear that some of these aberrations have impact on prognosis and disease progression. Methods. We examined copy number changes in the tumor genomes of 50 CLL patients using bacterial artificial chromosome (BAC) and/or oligonucleotide array platforms. We compared the results of arrayCGH with those obtained by FISH and conventional cytogenetics and evaluated their clinical importance. Results. A total of 111 copy number changes were detected in 43 patients (86%) with clonal abnormalities present in at least 23% of the cells. Moreover, 14 patients (28%) were found to have 39 genomic changes that had not been detected by standard cytogenetic and/or FISH analyses. These included possibly prognostically important recurrent 2p and 8q24 gains. The most frequent unbalanced changes involved chromosomes 18, 7, 3, 9 and 17. We also determined the minimal deleted region on chromosome 6q in 7 cases by chromosome 6/7 specific array. Conclusions. The results showed that a subset of potentially significant genomic aberrations in CLL is being missed by the current routine techniques. Further, we clearly demonstrated the robustness, high sensitivity and specificity of the arrayCGH analysis as well as its potential for use in routine screening of CLL.

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“…The region encompassing the PRDM1 gene (6q21-q22.1) is frequently deleted in B cell lymphomas 51,52 . Inactivation of the PRDM1 gene was found in a subset of diffuse large B cell lymphoma (DLBCL) of the activated B-cell type (ABC) and is believed to contribute to lymphomagenesis by blocking post-GC B cell differentiation [53][54][55] .…”

Section: Blimp1 Is a Tumour Suppressor Genementioning

confidence: 99%

BLIMP1α, the master regulator of plasma cell differentiation is a tumor supressor gene in B cell lymphomas

Vrzalikova¹,

Woodman²,

Murray³

2012

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Aims. The aim of this review was to summarize recent knowledge of the structure and function of a transcriptional repressor, B lymphocyte induced maturation protein 1 (BLIMP1) and its participation in the pathogenesis of B lymphomas. Methods and results. This review summarizes the structure and function of BLIMP1, its major target genes and its role as a tumour suppressor in B cell lymphomas. We review our recent data implicating the loss of BLIMP1α as an important step in the pathogenesis of the Epstein-Barr virus (EBV) associated B cell lymphomas. Conclusions. BLIMP1 is a transcriptional repressor essential for the differentiation of germinal centre (GC) B cells to plasma cells. The loss of BLIMP1 in GC B cells could contribute to the pathogenesis of EBV-associated lymphomas by preventing plasma cell differentiation and viral replication.

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Characterization of 6q deletions in mature B cell lymphomas and childhood acute lymphoblastic leukemia

Cited by 53 publications

References 28 publications

Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma

Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma

Array-based karyotyping in chronic lymphocytic leukemia (CLL) detects new unbalanced abnormalities that escape conventional cytogenetics and CLL FISH panel

BLIMP1α, the master regulator of plasma cell differentiation is a tumor supressor gene in B cell lymphomas

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