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Human SU-DHL-5 and TMD-8 B-lymphome cell line subclones

ABSTRACT: human SU-DHL-5 and TMD-8 B-lymphome cell line subclones

PROVIDER: PRJEB14876 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1544600_1.fastq.gz	Fastqsanger.gz
	ERR1544600_2.fastq.gz	Fastqsanger.gz
	ERR1544601_1.fastq.gz	Fastqsanger.gz
	ERR1544601_2.fastq.gz	Fastqsanger.gz
	ERR1544602_1.fastq.gz	Fastqsanger.gz

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human SU-DHL-5 and TMD-8 B-lymphome cell line subclones

Project description:Genetic heterogeneity though common in tumors has been rarely documented in cell lines. To examine how often B-lymphoma cell lines are comprised of subclones, we performed immunoglobulin (Ig) heavy chain hypermutation analysis. Revealing that subclones are not rare in B-cell lymphoma cell lines, 6/49 Ig hypermutated cell lines (12%) consisted of subclones with individual Ig mutations. Subclones were also identified in 2/284 leukemia/lymphoma cell lines exhibiting bimodal CD marker expression. We successfully isolated 10 subclones from four cell lines HG3, SU-DHL-5, TMD-8, U-2932). Whole exome sequencing was performed to molecularly characterize these subclones. We in detail describe the clonal structure of cell line HG3, derived from chronic lymphocytic leukemia. HG3 consists of three lineages each bearing clone-specific aberrations, gene expression and DNA methylation patterns. While donor patient leukemic cells were CD5+, two of three HG3 subclones had independently lost this marker. CD5 on HG3 cells was regulated by epigenetic/transcriptional mechanisms rather than by alternative splicing as reported hitherto. In conclusion, we show that the presence of subclones in cell lines carrying individual mutations and characterized by sets of differentially expressed genes is not uncommon. We show also that these subclones can be useful isogenic models for regulatory and functional studies.

2016-09-30 | E-MTAB-4956 | biostudies-arrayexpress

Proteomes of chromatin fractions derived from SU-DHL-5 cells

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human HG-3 B-lymphome cell line subclones

Project description:Genetic heterogeneity though common in tumors has been rarely documented in cell lines. To examine how often B-lymphoma cell lines are comprised of subclones, we performed immunoglobulin (Ig) heavy chain hypermutation analysis. Revealing that subclones are not rare in B-cell lymphoma cell lines, 6/49 Ig hypermutated cell lines (12%) consisted of subclones with individual Ig mutations. Subclones were also identified in 2/284 leukemia/lymphoma cell lines exhibiting bimodal CD marker expression. We successfully isolated 10 subclones from four cell lines HG3, SU-DHL-5, TMD-8, U-2932). Whole exome sequencing was performed to molecularly characterize these subclones. We in detail describe the clonal structure of cell line HG3, derived from chronic lymphocytic leukemia. HG3 consists of three lineages each bearing clone-specific aberrations, gene expression and DNA methylation patterns. While donor patient leukemic cells were CD5+ , two of three HG3 subclones had independently lost this marker. CD5 on HG3 cells was regulated by epigenetic/transcriptional mechanisms rather than by alternative splicing as reported hitherto. In conclusion, we show that the presence of subclones in cell lines carrying individual mutations and characterized by sets of differentially expressed genes is not uncommon. We show also that these subclones can be useful isogenic models for regulatory and functional studies.

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Genes expression of SU-DHL-2 cells treated with IL-17A

Project description:To further figure out the molecular mechanisms of IL-17A-mediated DLBCL cells growth, we used the Whole Human Genome Oligo Microarray (4×44K, Agilent Technologies) to identify genes expression. Six samples of SU-DHL-2 cells (2×10^6 cells/ml) co-cultured with or without IL-17A (200pg/ml) for 72hr in vivo. Three samples of SU-DHL-2 cells were all co-cultured with IL-17A , other three samples of SU-DHL-2 cells without IL-17A treatment were used as controls. Then, all these six samples of SU-DHL-2 cells were measured by microarray.

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Genes expression of SU-DHL-2 cells treated with IL-17A

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mRNA-seq of gemcitabine resistant pancreatic cancer cell line subclones derived from BxPC3

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