Unknown,Transcriptomics,Genomics,Proteomics

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Bortezomib resistance in Mantle Cell Lymphoma (MCL) is associated with plasmacytic differentiation

ABSTRACT: Bortezomib-induced resistant MCL cell lines (HBL2 BR and JEKO BR) were generated by continuous cultured of corresponding parental cell lines (HBL2 PT and JEKO PT) with increasing bortezomib concentrations The IC50 of bortezomib of BR cell lines was 80 fold higher than the IC50 of the parental clone for HBL2-BR and 40 fold higher for JEKO-BR.RNA was isolated from cells collected at different time points within the period of one month in triplicate for HBL2 and in duplicate for JEKO subclones. This material was used for gene expression analysis using Affymetrix platform. Keywords: RNA Comparision of gene expression profiling in matched pairs of PT and BR cell lines

ORGANISM(S): Homo sapiens

SUBMITTER: Patricia Perez-Galan

PROVIDER: E-GEOD-20915 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Primary effusion lymphomas (PELs) are specifically associated with KSHV/HHV-8 infection, and most frequently occur in HIV-positive individuals as lymphomatous effusions in the serous cavities without a detectable solid tumor mass. Most PELs have concomitant EBV infection, suggesting that EBV is an important pathogenetic co-factor, although other as yet unidentified cofactors, such as cellular genetic alterations, are also likely to play a role. Lymphomatous effusions that lack KSHV also occur; these are frequently EBV-associated in the setting of HIV infection. Here we used gene expression profile analysis to determine the viral impact on cellular gene expression and the pathogenesis of these lymphomatous effusions. We used the Affymetrix HG-U133A microarray to analyze the gene expression profile of these effusion lymphomas (three virologic groups: KSHV-positive EBV-positive PELs, KSHV-positive EBV-negative PELs and KSHV-negative EBV-positive lymphomatous effusions). Nine cell lines derived from patients with lymphomatous effusions (three from each virologic group and each cell line was done in duplicates.) and three PEL patient samples were used in the study. Our results suggest that KSHV-positive PELs are very different from KSHV-negative lymphomatous effusions, and the genes that are differentially expressed include apoptosis regulators, cell cycle regulators, transcriptional factors and signal transduction regulators. KSHV clearly plays a dominant role in the phenotype of PEL. Within the KSHV-positive PELs, two subgroups can be identified, which were correlated with their EBV viral status. Among these genes (45 gene probes), four were regulators of the MAP kinase pathway that were up-regulated in the KSHV-positive, EBV-negative PELs, suggesting that in the absence of EBV, events that lead to the activation of the MAP kinase pathway may act as a cofactor for the development of PEL. Next we determined whether we could predict the viral status of the three primary patient cases of PEL based on the 45 gene probes that were differentially expressed in KSHV-positive cell lines according to EBV status (pt. 1: KSHV-positive, EBV-positive; Pt. 2: KSHV-positive, low proportion of EBV-positive; pt. 3: KSHV-positive EBV-negative), and we could. Samples: KSHV-positive EBV-positive cell lines: BC-1, BC-2, BC-5 KSHV-positive EBV-negative cell lines: BC-3, BCBL-1, PEL-5 KSHV-negative EBV-positive cell lines: IBL4, SM1, BCKN-1 Patient 1: KSHV-positive, EBV-positive Patient 2: KSHV-positive, EBV-positive (low number of positive cells) Patient 3: KSHV-positive, EBV-negative.

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Bortezomib resistance in Mantle Cell Lymphoma (MCL) is associated with plasmacytic differentiation

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