Basic fibroblast growth factor (bFGF) upregulates the expression of bcl-2 in B cell chronic lymphocytic leukemia cell lines resulting in delaying apoptosis

König, Andrea; Menzel, Thomas P.; Lynen, S; Wrazel, Laura; Rosén, Anders; Al‐Katib, Ayad; Raveché, Elizabeth; Gabrilove, Janice

doi:10.1038/sj.leu.2400556

Cited by 162 publications

(89 citation statements)

References 8 publications

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“…Investigation of other regulators of the G1 to S transition in SLVL is clearly indicated. Additionally, a wider study of CDK dysregulation in other low grade B cell malignancies may be productive, particularly since drugs which inhibit cyclin dependent kinases are currently under development (Konig et al, 1997). This study demonstrates a novel mechanism for increased CDK6 expression, which may function in an oncogenic manner, and provides direct evidence that dysregulation of key elements of the G1 stage of the cell cycle is implicated in the pathogenesis of SLVL/ SMZL.…”

Section: Discussionmentioning

confidence: 80%

Dysregulation of cyclin dependent kinase 6 expression in splenic marginal zone lymphoma through chromosome 7q translocations

et al. 1999

Oncogene

130

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The increased or inappropriate expression of genes with oncogenic properties through speci®c chromosome translocations is an important event in the pathogenesis of Bcell lymphoproliferative diseases. Recent studies have found deletions or translocations of chromosome 7q to be the most common cytogenetic abnormality observed in SLVL, a leukemic variant of SMZL, with the q21 ± q22 region being most frequently a ected. In three patients with translocations between chromosomes 2 and 7, the cloning of the breakpoints at 7q21 revealed that each was located within a small region of DNA 3.6 kb upstream of the transcription start site of cyclin dependent kinase 6 (CDK6). In each case the translocation event was consistent with aberrant VJ recombination between the immunoglobulin light chain region (Ig kappa) on chromosome 2p12 and DNA sequences at 7q21, resembling the heptamer recombination site. The t(7;21) breakpoint in an additional patient with splenic marginal zone lymphoma (SMZL), resided 66 kb telomeric to the t(2;7) breakpoints juxtaposing CDK6 to an uncharacterized transcript. In two of the SLVL patient samples, the CDK6 protein was found to be markedly over expressed. These results suggest that dysregulation of CDK6 gene expression contributes to the pathogenesis of SLVL and SMZL.

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Section: Discussionmentioning

confidence: 80%

Dysregulation of cyclin dependent kinase 6 expression in splenic marginal zone lymphoma through chromosome 7q translocations

et al. 1999

Oncogene

130

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“…Of note, in prostate cancer cell lines, the levels of FGF-2 and FGFR1 have been shown to increase proportionally to the degree of cancer aggressiveness and castration resistance (Nakamoto et al, 1992;Cronauer et al, 1997). The analysis of tumor specimens has shown that enhanced FGF signaling results in increased proliferation, invasiveness and resistance to therapy in several solid and hematological malignancies (Menzel et al, 1996;Konig et al, 1997;Song et al, 2000;Sezer et al, 2001;Acevedo et al, 2009;Turner et al, 2010). Moreover, hemi-or homozygous inactivation of Fgf-2 alleles in TRAMP mice with transgenic prostate adenocarcinoma resulted in increased survival by inhibiting progression toward a poorly differentiated and highly metastatic phenotype (Polnaszek et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Control of tumor and microenvironment cross-talk by miR-15a and miR-16 in prostate cancer

et al. 2011

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The interaction between cancer cells and microenvironment has a critical role in tumor development and progression. Although microRNAs regulate all the major biological mechanisms, their influence on tumor microenvironment is largely unexplored. Here, we investigate the role of microRNAs in the tumor-supportive capacity of stromal cells. We demonstrated that miR-15 and miR-16 are downregulated in fibroblasts surrounding the prostate tumors of the majority of 23 patients analyzed. Such downregulation of miR-15 and miR-16 in cancer-associated fibroblasts (CAFs) promoted tumor growth and progression through the reduced post-transcriptional repression of Fgf-2 and its receptor Fgfr1, which act on both stromal and tumor cells to enhance cancer cell survival, proliferation and migration. Moreover, reconstitution of miR-15 and miR-16 impaired considerably the tumor-supportive capability of stromal cells in vitro and in vivo. Our data suggest a molecular circuitry in which miR-15 and miR-16 and their correlated targets cooperate to promote tumor expansion and invasiveness through the concurrent activity on stromal and cancer cells, thus providing further support to the development of therapies aimed at reconstituting miR-15 and miR-16 in advanced prostate cancer.

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“…The same upregulation of bcl-2 expression has been reported in chronic lymphocytic leukemia cell lines and related to bFGF stimulation. 7 Without speculating about the underlying mechanisms, we showed that apoptosis was reduced in the presence of fibroblasts for all patients having high levels of bFGF. Interestingly, four out of six patients having normal levels of bFGF showed no influence of fibroblasts on apoptosis.…”

Section: Figurementioning

confidence: 99%

The growth of highly proliferative acute lymphoblastic leukemia may be independent of stroma and/or angiogenesis

Schneider

Vasse

et al. 2001

Leukemia

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Basic fibroblast growth factor (bFGF) upregulates the expression of bcl-2 in B cell chronic lymphocytic leukemia cell lines resulting in delaying apoptosis

Abstract: Basic fibroblast growth factor (bFGF) is a pleiotropic cytokine blebbing, cell shrinkage, chromatin condensation and fragwhich has recently been shown to delay fludarabine-induced mentation. 9 The proto-oncogene bcl-2, an inner mitochon- shown to occur infrequently in CLL.

Cited by 162 publications

References 8 publications

Dysregulation of cyclin dependent kinase 6 expression in splenic marginal zone lymphoma through chromosome 7q translocations

Dysregulation of cyclin dependent kinase 6 expression in splenic marginal zone lymphoma through chromosome 7q translocations

Control of tumor and microenvironment cross-talk by miR-15a and miR-16 in prostate cancer

The growth of highly proliferative acute lymphoblastic leukemia may be independent of stroma and/or angiogenesis

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