GEO DataSets

(Submitter supplied) Inactivating mutations in the NF-kB inhibitor NFKBIE are frequent in chronic lymphocytic leukemia (CLL) and have been associated with accelerated disease progression and inferior responses to chemotherapy. To further understand the role of NFKBIE mutations in CLL, we disrupted by CRISPR/Cas9 editing the NFKBIE gene in CLL cells derived from the Eμ-TCL1 transgenic mouse model and investigated how this will affect CLL growth and response to B cell receptor inhibitor treatment. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

22 Samples

Download data: TXT

(Submitter supplied) The clinical efficacy displayed by ibrutinib in chronic lymphocytic leukemia (CLL) has been challenged by the frequent emergence of resistant clones. The ibrutinib target, Bruton's tyrosine kinase (BTK), is essential for B-cell receptor signaling, and most resistant cases carry mutations in BTK or PLCG2, a downstream effector target of BTK. Recent findings show that MI-2, a small molecule inhibitor of the para-caspase MALT1, is effective in preclinical models of another type of BCR pathway-dependent lymphoma. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

6 Samples

Download data: TXT

(Submitter supplied) Chronic lymphocytic leukemia (CLL) cell survival and growth is fueled by aberrant activation of various pro-survival signaling pathways within tumor niches. Specifically, B-cell receptor (BCR) signaling, toll-like receptor signaling, and supportive cellular interactions drive constitutive activation of NF-κB signaling and transcription of proliferative/pro-survival genes. Directly targeting the NF-κB pathway has been a challenge, however, herein, we investigated SpiD3, a spirocyclic dimer and novel NF-κB pathway inhibitor in preclinical models of CLL. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21697

9 Samples

Download data: XLSX

(Submitter supplied) The RNA splicing factor SF3B1 is recurrently mutated in chronic lymphocytic leukemia (CLL), but its functional role in the pathogenesis of this disease has not been firmly established. Here, we show that conditional expression of heterozygous Sf3b1-K700E mutation in mouse B lineage cells disrupts pre-mRNA splicing, alters B-cell development and function, and induces a state of cellular senescence. B-cell restricted expression of this mutation combined with Atm deletion led to the overcoming of cellular senescence, together with enhanced genome instability and the development of clonal B220+CD5+ CLL cells in elderly mice at low penetrance. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL9185

17 Samples

Download data: XLSX

(Submitter supplied) Deletion of the short arm of chromosome 17 (17p-) is one of the most critical genetic variants used in B-CLL risk stratification. The tumor suppressor TP53 maps to this region, and its loss or mutation significantly accelerates B-CLL progression, hampers response to chemotherapy, and shortens survival. While florescent in situ hybridization (FISH) analyses for 17p deletions are routinely performed during clinical diagnoses, mutational analyses of the TP53 gene is not widely available and thus its mutational status is often unknown in patients with CLL. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

15 Samples

Download data: TXT

(Submitter supplied) CLL cells obtained from patients with CLL were treated with MLN4924 to determine whether NFkB transcription targets were affected by the drug.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

22 Samples

Download data: TXT

(Submitter supplied) Our project is based on the hypothesis that ibrutinib could interfere with chronic lymphocytic leukemia (CLL) microenvironment, modulating the immune response. The aim of the project is to understand if and how ibrutinib modifies the tumor microenvironment accessory cells in CLL, specifically nurse like cells (NLC).

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

20 Samples

Download data: TXT