Cell cycle progression of chronic lymphocytic leukemia cells is controlled by cyclin D2, cyclin D3, cyclin-dependent kinase (cdk) 4 and the cdk inhibitor p27

Decker, Thomas; Schneller, Folker; Hipp, Susanne; Miething, Cornelius; Jähn, Thomas; Duyster, Justus; Peschel, Christian

doi:10.1038/sj.leu.2402389

Cited by 95 publications

(95 citation statements)

References 48 publications

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“…33 Importantly, no activating mutations in VEGFRs have been described in CLL, indicating that survival effects depend on VEGF binding to the receptor rather than being ligand To induce CLL proliferation, cells were stimulated with DSP30 (100 U/ml) and interleukin (IL)-2 as described elsewhere. 29 Proliferating CLL cells form cluster of cells and can be identified by phase-microscopy (upper panel). After 48 h, cells sorafenib was added for additional 24 h to the culture at 10 mM.…”

Section: Discussionmentioning

confidence: 99%

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Sorafenib induces cell death in chronic lymphocytic leukemia by translational downregulation of Mcl-1

et al. 2011

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Section: Discussionmentioning

confidence: 99%

“…CLL cells were stimulated with CpG oligonucleotides and interleukin-2. 28,29 After 72 h, cells form clusters of proliferative cells (Figure 5b, white circles in the light microscopy image). BrdU staining of cells confirmed that CLL cells were proliferating.…”

Section: Sorafenib Induces Cell Death In Proliferating and Stromal-cementioning

confidence: 99%

Sorafenib induces cell death in chronic lymphocytic leukemia by translational downregulation of Mcl-1

et al. 2011

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“…Therefore, a different approach was taken by our group using a combination of an immunostimulatory CpG-oligonucleotide DSP30 and IL-2 that has already been reported to effectively induce cell cycle progression of CLL cells in vitro. 10 With this approach in our first preliminary study, 125 of 132 (94.7%) cases could be successfully stimulated for metaphase generation and 101 of 125 (80.8%) cases showed chromosomal aberrations. 11 Therefore, the objective of this study was to evaluate a large cohort of CLL to further analyse the additional information provided by CBA in comparison to interphase FISH.…”

Section: Introductionmentioning

confidence: 88%

Comprehensive genetic characterization of CLL: a study on 506 cases analysed with chromosome banding analysis, interphase FISH, IgVH status and immunophenotyping

et al. 2007

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In CLL data from chromosome banding analysis (CBA) have been scarce due to the low proliferative activity of CLL cells in vitro. We improved the cultivation technique using an immunostimulatory CpG-oligonucleotide DSP30 and IL-2. A total of 506 CLL samples were analysed with CBA and interphase FISH using probes for the detection of trisomy 12, IgH rearrangements and deletions of 6q21, 11q22.3 (ATM), 13q14 (D13S25 and D13S319) and 17p13 (TP53). A total of 500 of 506 (98.8%) cases were successfully stimulated for metaphase generation and are subject to this study. Aberrations were detected in 415 of 500 (83.0%) cases by CBA and in 392 of 500 (78.4%) cases by FISH. CBA detected 832 abnormalities and FISH only 502. Therefore, CBA offers important information in addition to FISH. (1) CLL is characterized mainly by genomic imbalances and reciprocal translocations are rare. (2) A subgroup with complex aberrant karyotype (16.4%) is identified which is associated with an unmutated IgV H status and CD38 expression (P ¼ 0.034 and 0.02, respectively). (3) Additional abnormalities are detectable providing new biological insights into different CLL subclasses revealing a much more heterogeneous pattern of cytogenetic abnormalities as assumed so far based on FISH data only. Therefore, prospective clinical trials should evaluate the prognostic impact of newly available CBA data.

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“…One key characteristic of CLL, as assessed by flow cytometry‐based analysis is the accumulation of clonal B cells arrested in the early G0/1 phase of the cell cycle 47, 48. A possible explanation why the cytokinesis defect described here has not previously been reported is that conventional flow cytometry does not easily distinguish between cells in the G1 or cytokinesis part of the cell cycle and that a majority of cells in cytokinesis are counted as G1 cells because of the break of the cytoplasmic bridge 49…”

Section: Discussionmentioning

confidence: 99%

Cytokinesis arrest and multiple centrosomes in B cell chronic lymphocytic leukaemia

Rogne

Svaerd

Madsen‐Østerbye

et al. 2018

J Cellular Molecular Medi

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Cytokinesis failure leads to the emergence of tetraploid cells and multiple centrosomes. Chronic lymphocytic leukaemia (CLL) is the most common haematological malignancy in adults and is characterized by clonal B cell expansion. Here, we show that a significant number of peripheral blood CLL cells are arrested in cytokinesis and that this event occurred after nuclear envelope reformation and before cytoplasmic abscission. mRNA expression data showed that several genes known to be crucial for cell cycle regulation, checkpoint and centromere function, such as ING4, ING5, CDKN1A and CDK4, were significantly dysregulated in CLL samples. Our results demonstrate that CLL cells exhibit difficulties in completing mitosis, which is different from but may, at least in part, explain the previously reported accumulation of CLL cells in G0/1.

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Cell cycle progression of chronic lymphocytic leukemia cells is controlled by cyclin D2, cyclin D3, cyclin-dependent kinase (cdk) 4 and the cdk inhibitor p27

Cited by 95 publications

References 48 publications

Sorafenib induces cell death in chronic lymphocytic leukemia by translational downregulation of Mcl-1

Sorafenib induces cell death in chronic lymphocytic leukemia by translational downregulation of Mcl-1

Comprehensive genetic characterization of CLL: a study on 506 cases analysed with chromosome banding analysis, interphase FISH, IgVH status and immunophenotyping

Cytokinesis arrest and multiple centrosomes in B cell chronic lymphocytic leukaemia

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