Diffuse large B-cell lymphoma with a novel translocation involving BCL6

Iqbal, Jabed; Gupta, Shiphali; Chen, Q.H.; Brody, Judith; Koduru, Prasad

doi:10.1016/j.cancergencyto.2007.06.003

Cited by 4 publications

(3 citation statements)

References 15 publications

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“…Chromosomal translocations of BCL2 or c-MYC and mutations in EZH2 are more common in the GCB subtype (6, 10-12), whereas alterations in BLIMP1/PRDM1 (13-15) and various mutations leading to activation of the NF -κ B pathway (16-20) are associated with the ABC subtype. Common to both GCB and ABC subtypes are BCL6 translocations (21, 22) and mutations in CREBBP and EP300 (23). Additional recurrent mutations in DLBCL have been identified recently (23-27), although the functional consequence of these mutations in lymphomagenesis has not been studied experimentally.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Bromodomain Proteins for the Treatment of Human Diffuse Large B-cell Lymphoma

Trabucco

Gerstein

Evens

et al. 2015

Clinical Cancer Research

130

100

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Purpose Approximately 50% of patients with diffuse large B-cell lymphoma (DLBCL) enter long-term remission after standard chemotherapy. DLBCL patients who do not respond to chemotherapy have few treatment options. There remains a critical need to identify effective and targeted therapeutics for DLBCL. Experimental Design Recent studies have highlighted the incidence of increased c-MYC protein in DLBCL and the correlation between high levels of c-MYC protein and poor survival prognosis of DLBCL patients, suggesting that c-MYC is a compelling target for DLBCL therapy. The small molecule JQ1 suppresses c-MYC expression through inhibition of the bromodomain and extra-terminal (BET) family of bromodomain proteins. We investigated whether JQ1 can inhibit proliferation of DLBCL cells in culture and xenograft models in vivo. Results We show that JQ1 at nanomolar concentrations efficiently inhibited proliferation of human DLBCL cells in a dose-dependent manner regardless of their molecular subtypes, suggesting a broad effect of JQ1 in DLBCL. The initial G1 arrest induced by JQ1 treatment in DLBCL cells was followed by either apoptosis or senescence. The expression of c-MYC was suppressed as a result of JQ1 treatment from the natural, chromosomally-translocated or amplified loci. Furthermore, JQ1 treatment significantly suppressed growth of DLBCL cells engrafted in mice and improved survival of engrafted mice. Conclusion Our results demonstrate that inhibition of the BET family of bromodomain proteins by JQ1 has potential clinical utility in the treatment of DLBCL.

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Section: Introductionmentioning

confidence: 99%

Inhibition of Bromodomain Proteins for the Treatment of Human Diffuse Large B-cell Lymphoma

Trabucco

Gerstein

Evens

et al. 2015

Clinical Cancer Research

130

100

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“…Identification and classification of chromosomal aberrations of hematologic disorders is an important strategy for the diagnosis, prognosis and stratification of individualized treatment. Many kinds of structural aberrations, such as gain, deletion, translocation and other types, have been reported in DLBCL [1,[4][5][6][7][8][9][10][11]. However, few large case-control studies of DLBCL describing chromosomal aberrations are available.…”

Section: Introductionmentioning

confidence: 99%

Chromosome abnormalities in diffuse large B‐cell lymphomas: analysis of 231 Chinese patients

Zhao

Fan

Lin

et al. 2012

Hematological Oncology

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Genome instability is a hallmark of cancer. Diffuse large B-cell lymphoma (DLBCL) is the most common form of non-Hodgkin lymphoma with high levels of chromosomal aberrations. The purpose of this study was to characterize chromosomal aberrations in Chinese DLBCL patients and to compare chromosomal abnormalities between germinal centre B-cell-like (GCB) and non-GCB subgroups. Fluorescence in situ hybridization, G-band cytogenetics and immunohistochemistry were performed in 231 cases of de novo DLBCL. We demonstrated that the rate of abnormal and complex karyotypes was 89.1% (139/156) and 92.8% (129/139), respectively. We found a total of 490 structural chromosomal aberrations, including 96 frequent and recurring structural alterations. Most importantly, we identified several rare or novel chromosomal alterations: eight gains (5, 13, 14q, 17, 19p, 20, 21p, Y), one loss (21) and three recurrent translocations [t(7;15)(q22;q22), t(3;20)(p24;q13.1), t(2;3)(q21;q25)]. Moreover, the frequent recurrent genomic imbalance between GCB and non-GCB subgroups was different. Finally, we discovered two cases of concurrent IGH-BCL6 and MYC rearrangements. The rate of abnormal karyotypes in DLBCL patients of Chinese descent was similar to that of Western countries, but some common karyotypes were different, as were the abnormal karyotypes of GCB and non-GCB subgroups. Our discovery of rare and novel abnormal karyotypes may represent unique chromosomal alterations in Chinese DLBCL patients.

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“…DLBCL tumours present with complex chromosomal aberrations (Dave, Nelson et al 2002;Iqbal, Gupta et al 2007). These include in 35% of cases a translocation of the proto-oncogene BCL6.…”

Section: Dlbcl Are Characterised By a Complex Karyotype Involving The...mentioning

confidence: 99%

Identification and functional characterisation of oncogenic pathway signatures in malignant lymphoma

Schrader¹

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By this I declare that I independently authored the presented thesis:"Identification and functional characterisation of oncogenic pathway signatures in malignant Lymphoma"and that I did not use other auxiliary means than indicated. Paragraphs that are taken from other publications, by wording or by sense, are marked in every case with a specification of the literary source.Furthermore I declare that I carried out the scientific experiments following the principles of Good Scientific Practice according to the valid "Richtlinien der Georg-August-Universität Göttingen zur Sicherung guter wissenschaftlicher Praxis".

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Diffuse large B-cell lymphoma with a novel translocation involving BCL6

Cited by 4 publications

References 15 publications

Inhibition of Bromodomain Proteins for the Treatment of Human Diffuse Large B-cell Lymphoma

Inhibition of Bromodomain Proteins for the Treatment of Human Diffuse Large B-cell Lymphoma

Chromosome abnormalities in diffuse large B‐cell lymphomas: analysis of 231 Chinese patients

Identification and functional characterisation of oncogenic pathway signatures in malignant lymphoma

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