Project description:To examine the existence of lymphoma initiating cells, we used an anaplastic large cell lymphoma mouse model. Established NPM-ALK+ lymphomas contained a heterogeneous cell composition ranging from mature T-cells to undifferentiated hematopoietic stem cells. To investigate the underlying mechanisms and activated pathways of lymphoma initiating cells we used gene expression analyses. These analyses unmasked stem-cell-like transcriptional regulation exclusively of the DN3/DN4 lymphoma T-cell subpopulation.
Project description:Global proteomics profiling of anaplastic large cell lymphoma cell lines DEL, SU-DHL-1 (ALK+), Mac-1, Mac-2A (ALK-) as well as Hodgkin lymphoma cell lines L-428, L-540, L-1236 and HDLM-2.
Project description:Anaplastic Large Cell Lymphoma (ALCL) is a mature T-cell lymphoma that can present as a systemic or primary cutaneous disease. Systemic ALCL represents 2-5% of adult lymphoma but up to 30% of all pediatric cases. Two subtypes of systemic ALCL are currently recognized on the basis of the presence of a translocation involving the Anaplastic Lymphoma Kinase ALK gene. Despite considerable progress, several questions remain open regarding the pathogenesis of both ALCL subtypes. To investigate the molecular pathogenesis and to assess the relationship between the ALK(+) and ALK(-)ALCL subtypes, we performed a genome-wide DNA profiling using high density, single nucleotide polymorphism (SNP) arrays (SNP-array) on a series of 63 cases and seven cell lines. The commonest lesions were losses at 17p13 and at 6q21, encompassing the TP53 and PRDM1 genes respectively. The latter gene, coding for BLIMP1, was inactivated by multiple mechanisms, more frequently, but not exclusively, in ALK(-)ALCL. In vitro and in vivo experiments showed that that PRDM1 is a tumor suppressor gene in ALCL models, likely acting as an anti-apoptotic agent. Losses of TP53 and/or PRDM1 were present in 52% of ALK(-)ALCL, and in 29% of all ALCL cases with a clinical implication. Genomic profiling of Anaplastic Large Cell Lymphoma
Project description:Analysis of differential gene expression in human non-Hodgkin`s lymphoma cell lines and a primary leukaemic tumor sample of large cell anaplastic type in comparison with Hodgkin`s lymphoma cell lines and other non-Hodgkin`s lymphoma samples and non-neoplastic lymphocytes Experiment Overall Design: Samples were analyzed to be compared to publically available data sets
Project description:Analysis of differential gene expression in human non-Hodgkin`s lymphoma cell lines and a primary leukaemic tumor sample of large cell anaplastic type in comparison with Hodgkin`s lymphoma cell lines and other non-Hodgkin`s lymphoma samples and non-neoplastic lymphocytes Keywords: cell type comparison
Project description:Anaplastic Large Cell Lymphoma (ALCL) is propagated by cancer stem cells which are identified by their ability to efflux dye and hence reside in the side population (SP) on FACS analysis. In order to understand the origins of these ALCL SP cells we purified SP and main population (MP; SP-depleted) cell from the ALCL cell line SUDHL-1. On comparison of the gene expression signatures derived from these 2 cellular populations distinct branches dividing the SP and MP populations present indicating that they are distinct subsets within the bulk tumour. We sought to obtain pure populations of SP and MP cells from human SUDHL-1 Anaplastic Large Cell Lymphoma (ALCL) cell line. SUDHL-1 cells were stained with Hoechst 33342 dye, analysed using MoFlo Cell Sorter with UV lasers. The cells were then sorted in triplicates and subjected to RNA extraction. The extracted RNA was subjected to gene expression microarray using the Affymetrix Human Gene 1.0 ST Array.
Project description:To identify genes and pathways involved in the pathogenesis of Hodgkin Lymphoma (HL) and Anaplastic Large Cell Lymphoma (ALCL) , we used the Ontario Cancer Institute (OCI) Human 27k arrays (UNH Homo sapiens 19K8 array), to study the expression profiling in pairs of HL-derived cell lines (KMH2 and L428) and ALCL-derived cell lines (DEL and SR-786).
Project description:Anaplastic Large Cell Lymphoma (ALCL) is a mature T-cell lymphoma that can present as a systemic or primary cutaneous disease. Systemic ALCL represents 2-5% of adult lymphoma but up to 30% of all pediatric cases. Two subtypes of systemic ALCL are currently recognized on the basis of the presence of a translocation involving the Anaplastic Lymphoma Kinase ALK gene. Despite considerable progress, several questions remain open regarding the pathogenesis of both ALCL subtypes. To investigate the molecular pathogenesis and to assess the relationship between the ALK(+) and ALK(-)ALCL subtypes, we performed a genome-wide DNA profiling using high density, single nucleotide polymorphism (SNP) arrays (SNP-array) on a series of 63 cases and seven cell lines. The commonest lesions were losses at 17p13 and at 6q21, encompassing the TP53 and PRDM1 genes respectively. The latter gene, coding for BLIMP1, was inactivated by multiple mechanisms, more frequently, but not exclusively, in ALK(-)ALCL. In vitro and in vivo experiments showed that that PRDM1 is a tumor suppressor gene in ALCL models, likely acting as an anti-apoptotic agent. Losses of TP53 and/or PRDM1 were present in 52% of ALK(-)ALCL, and in 29% of all ALCL cases with a clinical implication.