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Genome-wide copy number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma [gene expression]

ABSTRACT: We studied 277 lymphoma samples (198 FL and 79 transformed FL [tFL]) using a single-nucleotide polymorphism array to identify the secondary chromosomal abnormalities that drive the development of FL and its transformation to diffuse large B-cell lymphoma. This dataset is corresponding Gene expression data that is available for a subset of the tFL cases for Series GSE67385.

ORGANISM(S): Homo sapiens

PROVIDER: GSE81183 | GEO | 2016/05/07

SECONDARY ACCESSION(S): PRJNA320842

REPOSITORIES: GEO

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Genome-wide copy number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma [SNP arrays]

2015-03-30 | GSE67385 | GEO

Genome-wide copy number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma

Project description:We studied 277 lymphoma samples (198 FL and 79 transformed FL [tFL]) using a single-nucleotide polymorphism array to identify the secondary chromosomal abnormalities that drive the development of FL and its transformation to diffuse large B-cell lymphoma. Affymetrix 250K NspI SNP arrays were performed according to the manufacturer's directions on DNA extracted from frozen follicular lymphoma or transformed follicular lymphoma tumor specimens

2015-03-30 | E-GEOD-67385 | biostudies-arrayexpress

Affymetrix SNP array data for follicular lymphoma (FL) and transformed follicular lymphoma (tFL) samples

Project description:Follicular lymphoma is the most common indolent non-Hodgkin's lymphoma involving germinal centre B cells, with a subset of patients undergoing transformation to a diffuse large B-cell lymphoma (DLBCL) morphology for which the clinical outcomes are poor. To elucidate the differences in copy number profiles between FL and tFL groups, we performed Affymetrix SNP 6.0 Array analysis on 31 paired FL-tFL cases. We wanted to identify and compare recurrent somatic copy number alterations (CNAs) between the two groups (FL vs. tFL). In addition, the concordance and discordance in the copy neutral loss of heterozygosity (cnLOH) between the two groups were also investigated to identify recurrent target gene regions. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from follicular lymphoma (FL), transformed follicular lymphoma (tFL) and matching germline (GL) sample (if available). Copy number analysis of Affymetrix SNP 6.0 Array were performed on 91 DNA samples, consisting of 31 patients. Among the 31 patients, 19 had matching germline samples, while 12 had no germline samples. The Log R Ratio (LRR) values and the B Allele Frequency (BAF) values were subsequently calculated to search for copy number aberrations and copy neutral (CN)-LOH in the FL and tFL samples. Paired and unpaired analyses were performed accordingly.

2013-10-01 | E-GEOD-42525 | biostudies-arrayexpress

Affymetrix SNP array data for follicular lymphoma (FL) and transformed follicular lymphoma (tFL) samples

2013-10-01 | GSE42525 | GEO

Multi-omics profiling of longitudinal samples reveals early genomic changes in follicular lymphoma

Project description:Follicular lymphoma (FL) is the most common indolent type of B-cell non-Hodgkin lymphoma. Advances in treatment have improved overall survival, but early relapse or transformation to aggressive disease is associated with inferior outcome. To identify early genetic events and track tumor clonal evolution, we performed multi-omics analysis of 94 longitudinal biopsies from 44 FL patients; 22 with transformation (tFL) and 22 with relapse without transformation (nFL). Deep whole-exome sequencing confirmed recurrent mutations in genes encoding epigenetic regulators (CREBBP, KMT2D, EZH2, EP300), with similar mutational landscape in nFL and tFL patients. Calculation of genomic distances between longitudinal samples revealed complex evolutionary patterns in both subgroups. CREBBP and KMT2D mutations were identified as genetic events that occur early in the disease course, and cases with CREBBP KAT domain mutations had low risk of transformation. Gains in chromosomes 12 and 18 (TCF4), and loss in 6q were identified as early and stable copy number alterations. Identification of such early and stable genetic events may provide opportunities for early disease detection and disease monitoring. Integrative analysis revealed that tumors with EZH2 mutations exhibited reduced gene expression of numerous histone genes, including histone linker genes. This might contribute to the epigenetic dysregulation in FL.

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siRNA smart pool silencing of master regulators of Follicular Lymphoma transformation to DLBCL

Project description:Follicular lymphoma (FL) is the most common indolent subtype of non-Hodgkin’s lymphoma, with relatively long overall survival rate ranging from 6 to 10 years from time of diagnosis. However, 20-60% of FL patients undergo transformation to aggressive diffuse large B cell lymphoma (DLBCL), with a reduced median survival of about 1.2 years. The specific functional and genetic determinants of FL transformation are still elusive and only a relatively small fraction of the cases is accounted for by established, recurrent alterations in TP53, MYC and BCL6, inactivation of CDKN2A and CDKN2B, or amplification of REL. We addressed this deficiency by performing systematic analysis of a B cell specific regulatory model with FL transformation signatures, using the Master Regulator Inference algorithm (MARINa). We show that the candidate master regulators inferred by the algorithm in FL induce synthetic lethality in DLBCL cells and lead to identification of specific compound combinations inducing synergistic loss of viability in transformed DLBCL cells

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Gene expression profiling in follicular lymphoma (FL) samples and paired transformed follicular lymphoma (tFL) (n=6 samples)

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siRNA smart pool silencing of master regulators of Follicular Lymphoma transformation to DLBCL

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2015-11-11 | E-GEOD-66714 | biostudies-arrayexpress

Abberant Cathepsin S Activity Modulates the Immune Microenvironment in Follicular Lymphoma

Project description:Tumor cells can induce their own advantageous microenvironment. Here, we describe aberrant cathepsin S (CTSS) activity to modulate T-cell activation in follicular lymphoma (FL). In donor-derived FLs following bone marrow transplantation, we identified independent acquisition of CTSS mutations at Y132 in the donor´s and recipient's tumors. In a larger cohort, 6% of FL (20/312) harbored CTSS mutations, mostly Y132D, another 14% had CTSS amplification (40/280). Y132D leads to accelerated conversion from pro-CTSS to active CTSS and increased substrate cleavage, including CD74, which regulates MHC-II restricted antigen-presentation. In co-culture experiments, CTSS mutant lymphoma cells induced increased antigen-specific CD4+ T-cell activation. Moreover, antigen-processing was the top upregulated pathway in CTSS mutant primary FL biopsies. Thus, aberrant CTSS activity is a promising target in lymphoma.

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