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CD4 T cell stimulation with or without chronic lymphocytic leukemia (CLL) cells present

ABSTRACT: CD4 T cell stimulation with or without chronic lymphocytic leukemia (CLL) cells present

PROVIDER: PRJNA797099 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17616000_1.fastq.gz	Fastqsanger.gz
	SRR17616000_2.fastq.gz	Fastqsanger.gz
	SRR17616001_1.fastq.gz	Fastqsanger.gz
	SRR17616001_2.fastq.gz	Fastqsanger.gz
	SRR17616002_1.fastq.gz	Fastqsanger.gz

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CD4 T cell stimulation with or without chronic lymphocytic leukemia (CLL) cells present

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CD40 stimulation of chronic lymphocytic leukemia (CLL) cells

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RNAseq of Chronic Lymphocytic Leukaemia with and without anti-IgM treatment at 6 hrs and 24 hrs post-stimulation

Project description:Series of Chronic Lymphocytic Leukaemia (mix of U-CLL and M-CLL) with and without anti-IgM stimulation of the B cell receptor. RNA acquired at 6hrs and 24hrs post stimulation.

2022-02-21 | E-MTAB-11195 | biostudies-arrayexpress

Temporal transcriptional response from primary human chronic lymphocytic leukemia (CLL)-cells after B-cell receptor stimulation.

Project description:The B-cell receptor (BCR) signaling is crucial for the pathophysiology of most leukemias and lymphomas originated from mature B lymphocytes and has emerged as a new therapeutic target, especially for chronic lymphocytic leukemia (CLL). However, the precise mechanisms by which BCR signaling controls neoplastic B-cell proliferation are ill characterized. This work was performed using primary leukemic cells of untreated patients at initial stage of CLL (Binet stage A / Rai 0) presenting biological characteristics of aggressive form of the disease (unmutated IGHV genes and ZAP70 protein expression). In order to mimic the primary leukemogenic step occurring in vivo, this study focused on the BCR-dependent proliferation of CLL cells induced ex vivo using anti-IgM, together with mandatory co-stimulating factors (CD40L, IL-4 and IL-21) (Schleiss, Sci Rep, 2019). Cell proliferation was objectivized by the emergence of proliferative clusters and the presence of more than 25% of CLL cells that did undergo division within the cell culture at day 6. To capture the specific actors of the proliferative response in these samples, we also included non-proliferating control CLL samples. Gene expression was analyzed by RNA-seq before stimulation (T0) and at the time points 1h, 1h30, 3h30, 6h30, 12h, 24h, 48h and 96h after cell stimulation (n=54 data points), the latest time points corresponding to the emergence of the proliferation clusters.

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RNA-Seq of primary chronic lymphocytic leukaemia (CLL) tumours treated with anti-IgM antibodies against isotype control treated tumours

Project description:Chronic lymphocytic leukemia (CLL) is a highly heterogenous disease, with vastly diverse phenotypes that cause differing clinical courses ranging from benign disease (requiring no treatment), to a rapidly progressive disease and may require aggressive treatment therapy. Key to the B cell is the B-cell receptor (BCR); CLL utilises the BCR to evade apoptosis and promote proliferation and drug resistance through cross-talk between the TME and through BCR activation. Our experiments engage the BCR to determine downstream impact of BCR stimulation on gene expression in CLL (6 hours after stimulation).

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Project description:The B-cell receptor (BCR) signaling is crucial for the pathophysiology of chronic lymphocytic leukemia (CLL). Although the BCR has recently emerged as a new therapeutic target the precise mechanisms by which BCR signaling controls neoplastic B-cell proliferation are still ill characterized. Here, by comparing proliferating vs. non-proliferating cells from aggressive CLL patients, we longitudinally characterized the transcriptional and proteomic response of CLL cells after BCR engagement ex vivo. Of the 5,733 genes and/or proteins which expression was modulated after BCR activation, we identified a CLL proliferative signature including 430 genes and 374 proteins. Mathematical modelling of this signature revealed a nested sub-regulatory network comprising transcription factors activated within hours after cell activation linked to proteins involved in cell proliferation days after stimulation. The mining of this core cellular program sustaining primary human cancer cells proliferation provides an evidence based-resource for innovative therapeutic perspectives.

2021-03-29 | PXD013573 | Pride

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2021-09-08 | PXD013696 | Pride