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Genomic imbalances in BCL1/JH t(11;14)(q13;q32) positive multiple myeloma

ABSTRACT: The aim of this study is to determine copy number variations in the multiple myeloma patients, which were positive for BCL1/JH t(11;14)(q13;q32) translocation. Identification of common chromosomal aberrations representing the t(11;14)(q13;q32) subtype is possible by comparing the microarray data across all the samples under studied. Eight multiple myeloma samples were analyzed. Each sample was compared against normal control (match with patient's race and gender), which was pooled from ten healthy individuals.

ORGANISM(S): Homo sapiens

SUBMITTER: Ivyna Bong

PROVIDER: E-GEOD-33757 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genomic imbalances in BCL1/JH t(11;14)(q13;q32) positive multiple myeloma

Project description:The aim of this study is to determine copy number variations in the multiple myeloma patients, which were positive for BCL1/JH t(11;14)(q13;q32) translocation. Identification of common chromosomal aberrations representing the t(11;14)(q13;q32) subtype is possible by comparing the microarray data across all the samples under studied.

2012-12-31 | GSE33757 | GEO

CCND2 rearrangements are the most frequent genetic events in Cyclin D1-negative mantle cell lymphoma [Agilent]

Project description:Cyclin D1-negative mantle cell lymphomas (MCL) are not well characterized, in part due to the difficulties in their recognition. SOX11 has been recently identified as a reliable biomarker of MCL, also expressed in the cyclin D1-negative variant. We investigated 40 lymphomas with MCL morphology and immunophenotype, negative for cyclin D1 expression/t(11;14)(q13;q32) but SOX11-positive. These tumors presented clinically with generalized lymphadenopathy, advanced stage, and had a poor outcome (5-year overall survival 48%). Chromosomal rearrangements of the CCND2 locus were detected in 55% of the cases, with an IG gene as partner in 18/22 cases, in particular with light chains (10 IGK@, 5 IGL@). No mutations in the phosphorylation motifs of CCND1, CCND2 and CCND3 were detected. The global genomic profile and the high complexity of the 32 cyclin D1-negative SOX11-positive MCL analyzed by copy number arrays were similar to the conventional cyclin D1/SOX11-positive MCL. 17p deletions and high Ki67 expression conferred a significantly worse outcome to the patients. This comprehensive characterization of a large series of cyclin D1-negative MCL indicates that these tumors are clinically and biologically similar to the conventional cyclin D1-positive MCL and provides a basis for the proper identification and clinical management of these patients. Copy number analysis of Agilent 1*1M arrays was performed for 27 MCL, with sex-matched control DNAs and without duplicates or dye-swapt.

2012-12-19 | E-GEOD-42917 | biostudies-arrayexpress

Homo sapiens

Project description:Genomic imbalances in BCL1/JH t(11 14)(q13 q32) positive multiple myeloma

| PRJNA148397 | ENA

Identification of copy number variations by array comparative genomic hybridization in multi-ethnic multiple myeloma patients

Project description:The aim of this study is to identify copy number variations in multiple myeloma patients from the 3 major ethnic groups (Malays, Chinese and Indians) in Malaysia. Identification of common chromosomal aberrations and their degree of penetrance is possible by comparing the microarray data across all the samples under studied. 63 multiple myeloma samples were analyzed. Each sample was compared against normal control (match with patient's race and gender), which was pooled from ten healthy individuals.

2015-12-31 | E-GEOD-44745 | biostudies-arrayexpress

The Gene Expression Study (GEP) was based on a 6 MCL cell line models.

Project description:The aggressive clinical behavior of mantle cell lymphoma (MCL) is attributed to specific genetic and molecular mechanisms involved in its pathogenesis, mainly the t(11;14)(q13;q32) traslocation and cyclin D1 (CCND1) overexpression. Nevertheless, evidence of a certain degree of heterogeneity has been disclosed by gene expression profile (GEP) and (immuno)genetic/immunohistochemistry studies. AIM: To use a GEP approach in MCL cell line models.

2017-12-31 | GSE89615 | GEO

The Gene Expression Study (GEP) was based on a cohort of 27 MCL cases enrolled in the Fondazione Italiana Linfomi (FIL)-MCL-0208 randomized Italian clinical trial.

Project description:The aggressive clinical behavior of mantle cell lymphoma (MCL) is attributed to specific genetic and molecular mechanisms involved in its pathogenesis, mainly the t(11;14)(q13;q32) traslocation and cyclin D1 (CCND1) overexpression. Nevertheless, evidence of a certain degree of clinical/biological heterogeneity has been disclosed by gene expression profile (GEP) and (immuno)genetic/immunohistochemistry studies. AIM: To use a GEP approach to identify MCL subsets with peculiar clinical/biological features in the context of of MCL patients treated homogeneously with an autologous transplantation-based program.

2017-12-31 | GSE89447 | GEO

RNA-sequencing in MCL cell lines after silencing cyclin D1

Project description:Mantle cell lymphoma (MCL) is an aggressive B-cell neoplasm characterized by the t(11;14)(q13;q32) translocation leading to cyclin D1 overexpression. Cyclin D1 is a major cell cycle regulator and also has a role in transcription, but the effect of the latter in tumorigenesis remains largely unknown. Here, we investigated the transcriptional role of cyclin D1 in MCL and its impact on the pathogenesis of this neoplasm. Integrating genome-wide expression analysis of cyclin D1-silenced and overexpressing cells with cyclin D1 chromatin binding profiles, we identified a cyclin D1-activated transcriptional program in MCL cells.

2021-06-30 | GSE144106 | GEO

Expression data from JVM13 cells with cyclin D1 exogenous overexpression

2021-06-30 | GSE144095 | GEO

Copy number analysis of plasma cells from AL amyloidosis patients

Project description:Immunoglobulin light chain (AL) amyloidosis is characterized by deposition of abnormal amyloid fibrils in multiple organs impairing their function. CD138-purified plasma cells producing these fibrils are investigated regarding chromosomal alterations by interphase fluorescence in situ hybridization (iFISH) using a multiple myeloma specific probe set for the IgH translocations as well as recurrent numerical aberrations. Aberrations genuine to AL amyloidosis cannot be detected due to the inherent limitation of this probe panel to known loci. We analyzed 118 AL amyloidosis patients by high-density copy number array to quantitatively detect genome-wide chromosomal imbalances. Most prevalent gains affected chromosomes 1q (37%), 9 (24%), 11q (24%), and 19 (16%). The most frequent deletion was monosomy 13 (28%) followed by partial deletions on 14q (21%), 16q (14%), and 13q (12%). The results were analyzed with respect to cytogenetic subgroups. In 88% of patients with translocation t(11;14) and concomitant gain of 11q22.3/11q23 detected by iFISH, the latter aberration was not due to trisomy of chromosome 11 but part of the unbalanced translocation der(14)t(11;14)(q13;q32) with breakpoint in the CCND1/MYEOV gene region. Partial loss of chromosomes 14q and 16q were significantly associated to patients with gain 1q. Our iFISH probe set is highly concordant with copy number results as it detects the most common cytogenetic aberrations present in AL amyloidosis. Beyond that, the probe panel is also the method of choice to detect translocations involving the IgH locus. In contrast to the results of our iFISH panel the frequency of hyperdiploidy detected by copy number array analysis is higher.

2017-03-29 | GSE89616 | GEO

Follicular lymphoma in situ and partial involvement by follicular lymphoma are clona lesions that carry the t(14;18) and lack genetic secondary alterations

Project description:Follicular lymphoma (FL) is characterized by the t(14;18)(q32;q21), frequent numerical chromosomal alterations, and recurrent somatic mutations. However, no genetic studies are available for FL in situ (FLIS), a putative precursor lesion of FL. In this study, we analyzed cases of FLIS without manifest (m)FL, partial involvement by FL (PFL), and paired cases of FLIS and mFL to detect possible early chromosomal imbalances, as well as DNA-methylation patterns of genomic regions of selected genes. We demonstrated that paired FLIS and mFL cases are always clonally related. FLIS and PFL have no or few secondary chromosomal imbalances detectable by copy number arrays and a lower level of gene methylation as compared to mFL. Additionally, EZH2 Tyr641 mutations were detected in a subset of both FLIS and PFL cases. In conclusion, this study provides evidence that FLIS represents a FL precursor lesion of long-lived clonal B-cells carrying the t(14;18) with no or few secondary genetic changes. The earliest secondary genetic alterations detected in FLIS are the EZH2 Tyr641 mutation and low levels of CNAs, as evidence of clonal evolution. Our data suggest that there may be more than one distinct lesion driving the progression from FLIS to manifest lymphoma. DNA from cases, 20 tumor samples (10 in situ Follicular lymphoma, 4 Partial infiltration folliculary lymphoma and 6 manifest FL) were analyzed with Agilent-014693 Human Genome CGH Microarray 244A platform for copy number alterations study. For cases 9-14 paired samples of in situ follicular lymphoma and manifest follicular lymphoma were analyzed. Agilent-014693 Human Genome CGH Microarray 244A arrays were performed according to the manufacturer's directions on DNA extracted from lymph nodes that were hybridized against a normal DNA (pool) of the same gender.

2013-11-12 | E-GEOD-48548 | biostudies-arrayexpress

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