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Mixed-species RNAseq analysis of human lymphoma cell adhesion to mouse stromal cells identifies a core gene set that is also differentially expressed in the lymph node microenvironment of MCL and CLL patients.

ABSTRACT: Mixed-species RNAseq analysis of human lymphoma cell adhesion to mouse stromal cells identifies a core gene set that is also differentially expressed in the lymph node microenvironment of MCL and CLL patients.

OTHER RELATED OMICS DATASETS IN: GSE99501

PROVIDER: PRJNA388663 | ENA |

REPOSITORIES: ENA

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Mixed-species RNAseq analysis of human lymphoma cell adhesion to mouse stromal cells identifies a core gene set that is also differentially expressed in the lymph node microenvironment of MCL and CLL patients.

Project description:Background:A subset of hematological cancer patients is refractory to treatment or suffer relapse, due in part to minimal residual disease, whereby some cancer cells survive treatment via microenvironment interaction. Cell-adhesion mediated drug resistance is an important mechanism, whereby cancer cells receive survival signals via interaction with e.g. stromal cells. No genome-wide studies of in vitro systems have yet been performed to compare gene expression in different cell subsets within a co-culture and cells grown separately. Results: Using RNAseq and species-specific read mapping, we compared transcript levels in human Jeko-1 mantle cell lymphoma (MCL) cells stably adhered to stromal cells or in suspension within a co-culture and in separate culture as well as mouse MS-5 stromal cells in co-culture or in separate culture. 1050 differentially expressed transcripts in adherent MCL cells identified 24 functional categories that together represent four main functional themes, anti-apoptosis, B-cell signaling, cell adhesion/migration and early mitosis. Comparison with previous MCL and chronic lymphocytic leukemia (CLL) patient data identified 116 genes that are differentially regulated in all three studies. From these genes we suggest a gene signature (CCL3, CCL4, DUSP4, ETV5, ICAM1, IL15RA, IL21R, IL4I1, MFSD2A, NFKB1, NFKBIE, SEMA7A, TMEM2) characteristic of cells undergoing cell-adhesion mediated microenvironment signaling in MCL/ CLL cells. Conclusions: The model system developed and characterized here together with suggested signature genes can be used in future studies of pathways that mediate increased cancer cell survival and drug resistance mechanisms.

2018-06-12 | GSE99501 | GEO

Comparison of CLL and MCL primary cells obtained from a patient with MCL variant Richter syndrome

Project description:Comparison of CLL and MCL primary cells obtained from a patient with MCL variant Richter syndrome

2016-07-13 | GSE84286 | GEO

Gene expression analysis of 3 MCL and 3 CLL cell lines

Project description:Microarray-based gene expression analysis identified genes differentially expressed in 3 MCL and 3 CLL cell lines compared to the lymphoblastoid non-tumor cell line LCL_WEI.

2010-06-03 | GSE16412 | GEO

Gene expression analysis of 6 MCL and 18 CLL patient samples

Project description:Microarray-based gene expression analysis identified genes differentially expressed in 6 MCL and 18 CLL patient samples compared in independent analyses to CD19 selected healthy donor B-cell samples.

2010-06-03 | GSE16411 | GEO

Expression profiles of SOX11-positive and SOX11-negative Mantle Cell Lymphoma (MCL) primary samples from lymph node and reactive lymph nodes (RLN).

Project description:Gene expression profiles were obtained via Nanostring nCounter Expression Assay (PanCancer Immune Profiling Panel, Nanostring Technologies, Hamburg, Germany). We aimed to obtain the differential immune gene expression comparing the lymph node microenvironment of SOX11-positive and SOX11-negative MCL primary samples and non-neoplastic nodal samples (RLN).

2021-12-01 | GSE141539 | GEO

The lymph node microenvironment promotes B-cell receptor signaling, NF-κB activation, and tumor proliferation in chronic lymphocytic leukemia (CLL)

2010-10-01 | GSE21029 | GEO

The lymph node microenvironment promotes B-cell receptor signaling, NF-κB activation, and tumor proliferation in chronic lymphocytic leukemia (CLL)

Project description:To elucidate effects of tumor host interactions in vivo in CLL, purified tumor cells were obtained concurrently from blood, bone marrow and/or lymph node and analyzed by gene expression profiling. Keywords: RNA Comparision of gene expression profiling in matched pairs of peripheral blood (PB) vs. bone marrow (BM) or lymph nodes (LN) derived CLL cells

2010-10-01 | E-GEOD-21029 | biostudies-arrayexpress

Macrophages confer survival signals via CCR1-dependent translational MCL-1 induction in chronic lymphocytic leukemia.

Project description:Protective interactions with bystander cells in micro-environmental niches such as lymph nodes (LNs) contribute to survival and therapy resistance of chronic lymphocytic leukemia (CLL) cells. This is caused by a shift in expression of BCL-2 family members. Pro-survival proteins BCL-XL, BFL-1, and MCL-1 are upregulated by LN-residing T cells through CD40L interaction, presumably via NF-κB signaling. Macrophages also reside in the LN, and are assumed to provide important supportive functions for CLL cells. However, if and how macrophages are able to induce survival is incompletely known. We first established that macrophages induced survival due to an exclusive upregulation of MCL-1. Next, we investigated the mechanism underlying MCL-1 induction by macrophages in comparison with CD40L. Genome-wide expression profiling of in vitro macrophage- and CD40L-stimulated CLL cells indicated activation of the PI3K-AKT-mTOR pathway, which was confirmed in ex vivo CLL LN material. Inhibition of PI3K-AKT-mTOR signaling abrogated MCL-1 upregulation and survival by macrophages as well asCD40 stimulation. MCL-1 can be regulated at multiple levels, and we established that AKT leads to increased MCL-1 translation, but does not affect MCL-1 transcription or protein stabilization. Furthermore, among macrophage-secreted factors that could activate AKT, we found that induction of MCL-1 and survival critically depended on C-C Motif Chemokine Receptor-1 (CCR1). In conclusion, this study indicates that two distinct micro-environmental factors, CD40L and macrophages, signal via CCR1 to induce AKT activation resulting in translational stabilization of MCL-1, and hence can contribute to CLL cell survival.

2017-02-11 | GSE94801 | GEO

Direct in vivo evidence for B-cell receptor and NF-KB activation in mantle cell lymphoma: role of the lymph node microenvironment and activating mutations. [Affymetrix]

Project description:We provide direct in vivo evidence for activation of the BCR and canonical NF-KB pathways in MCL that, in the absence of activating mutations, is dependent on the lymph node microenvironment. This finding provides a mechanistic explanation for the surprising efficacy of ibrutinib for the treatment of this type of lymphoma. Mutations in components of the BCR and NF-KB pathways are associated with cell-autonomous signaling and resistance to ibrutinib. Lymph node biopsies and peripheral blood samples were obtained from 55 patients with previously untreated MCL. The samples are distributed into 3 groups: peripheral blood (purified CD19, N=17), unpurified lymph node biopsy (mixed tissue biopsy, N=34), and purified lymph node (purified CD19 Tumor, N=4).

2016-07-15 | E-GEOD-70910 | biostudies-arrayexpress

Lymph node myeloid cells

Project description:Lymph node myeloid cells

| PRJNA895429 | ENA