ArticleLeukemia2015
Basal Ca(2+) signaling is particularly increased in mutated chronic lymphocytic leukemia.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- ACOX1-mediated peroxisomal fatty acid oxidation contributes to metabolic reprogramming and survival in chronic lymphocytic leukemia.Leukemia · 2024Article
- Stealth-Engineered Albumin-Coated Nanoparticles for Targeted Therapy: Effective Drug Delivery and Tumor Suppression in Xenograft-Zebrafish Model.International journal of nanomedicine · 2024Article
- B cell receptor signaling and associated pathways in the pathogenesis of chronic lymphocytic leukemia.Frontiers in oncology · 2024Review
- Proteogenomics refines the molecular classification of chronic lymphocytic leukemia.Nature communications · 2022Article
- Nanocarriers as a Delivery Platform for Anticancer Treatment: Biological Limits and Perspectives in B-Cell Malignancies.Pharmaceutics · 2022Review
- Targeting metabolic reprogramming in chronic lymphocytic leukemia.Experimental hematology & oncology · 2022Review
- SIRPα on Mouse B1 Cells Restricts Lymphoid Tissue Migration and Natural Antibody Production.Frontiers in immunology · 2020Article
- Responsiveness of chronic lymphocytic leukemia cells to B-cell receptor stimulation is associated with low expression of regulatory molecules of the nuclear factor-κB pathway.Haematologica · 2020Article
- Identifying lncRNA-mediated regulatory modules via ChIA-PET network analysis.BMC bioinformatics · 2019Article
- STIM1 at the plasma membrane as a new target in progressive chronic lymphocytic leukemia.Journal for immunotherapy of cancer · 2019Observational
- Calcium-RasGRP2-Rap1 signaling mediates CD38-induced migration of chronic lymphocytic leukemia cells.Blood advances · 2018Article
- CD5 expression promotes IL-10 production through activation of the MAPK/Erk pathway and upregulation of TRPC1 channels in B lymphocytes.Cellular & molecular immunology · 2018Article
- Cell lines generated from a chronic lymphocytic leukemia mouse model exhibit constitutive Btk and Akt signaling.Oncotarget · 2017Article
- Genome-wide DNA methylation profiling integrated with gene expression profiling identifiesClinical epigenetics · 2017Article
- New human single chain anti-idiotypic antibody against benzo[a]pyrene.Central-European journal of immunology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
On the basis of somatic hypermutation status of their B-cell antigen receptor (BCR) genes, chronic lymphocytic leukemia (CLL) patients can be divided into unmutated CLL (U-CLL) or mutated CLL (M-CLL). Approximately 30% of CLL patients express a stereotypic BCR, which may indicate that specific antigenic stimulation is driving CLL pathogenesis. Recently, it was reported that BCRs from CLL cells are capable of antigen-independent, cell-autonomous signaling, through recognition of an internal framework 2 (FR2) BCR epitope. We hypothesized that the level of cell-autonomous signaling may differ between CLL subgroups. Therefore, we analyzed Ca(2+) signaling in a series of primary stereotypic or heterogeneous U-CLL and M-CLL (n=68) and healthy controls (n=14). We confirmed that basal Ca(2+) signaling in CLL cells is higher than in normal B cells. Interestingly, we found that basal signaling was particularly increased in M-CLL. The degree of basal signaling did not correlate with membrane immunoglobulin levels, HCDR3 characteristics or FR2/FR3 sequence. We conclude that the level of basal Ca(2+) signaling is not uniformly enhanced in CLL B cells, but is associated with CLL immunoglobulin heavy chain V mutational status, reflecting a distinct cellular origin and possibly a different anergic state induced by repetitive or continuous antigen binding in vivo.
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