Survivin is expressed on CD40 stimulation and interfaces proliferation and apoptosis in B-cell chronic lymphocytic leukemia

Granziero, Luisa; Ghia, Paolo; Circosta, Paola; Gottardi, Daniela; Strola, Giuliana; Geuna, Massimo; Montagna, Licia; Piccoli, P; Chilosi, Marco; Caligaris-Cappio, Federico

doi:10.1182/blood.v97.9.2777

Cited by 295 publications

(301 citation statements)

References 43 publications

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“…This cell cycle progression was previously described for malignant B cells stimulated by CD40L. 7,32,33 While we could observe a shift of the relative number of cells in S phase after BCR ligation in our study (data not shown), there are some conflicting results with regard to the effects of BCR engagement on survival and cell cycle progression of CLL cells. Engagement of surface IgM was described to elicit a strong survival program in B-CLL cells, which is associated with the inhibition of caspase activity and activation of NF-kB.…”

Section: Aav Gene Transfer Into B-cll By Bcr-stimulation Dm Kofler Et Alsupporting

confidence: 69%

Engagement of the B-cell antigen receptor (BCR) allows efficient transduction of ZAP-70-positive primary B-CLL cells by recombinant adeno-associated virus (rAAV) vectors

Büning

Mayr

et al. 2004

Gene Ther

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Section: Aav Gene Transfer Into B-cll By Bcr-stimulation Dm Kofler Et Alsupporting

confidence: 69%

Engagement of the B-cell antigen receptor (BCR) allows efficient transduction of ZAP-70-positive primary B-CLL cells by recombinant adeno-associated virus (rAAV) vectors

Büning

Mayr

et al. 2004

Gene Ther

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“…The in vitro data on mononuclear cells from peripheral blood or bone marrow indicated that B-CLL cells expressed survivin in concert with CD40 and that survivin was the only IAP whose expression was induced by the CD40 ligand (CD40L) [36]. CD40 belongs to the TNF receptor superfamily [37], and its stimulation rescues B-CLL cells from apoptosis and induces proliferation [38].…”

Section: Discussionmentioning

confidence: 99%

Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL)

et al. 2005

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Inhibitor of apoptosis protein (IAP)-family proteins suppress apoptotic signaling in normal/neoplastic cells in various settings. To determine the apoptosis-resistant mechanism in adult acute mixed lineage leukemia (AMLL) with biphenotypic blasts responsible for resistance against chemotherapy, the expression levels of IAP-family proteins in AMLL bone marrow cells were analyzed by quantitative RT-PCR. The overall expression levels of IAPs were higher than those in control, AML, and ALL cells. A significant difference for the expression of survivin was observed between AMLL and AML (P < 0.05), and differences between AMLL and ALL were significant for the expression of survivin (P < 0.05), NAIP (P < 0.05), and XIAP (P < 0.05). These findings suggest that higher expression of various IAPs is associated with the chemotherapy-resistant nature of this specific type of leukemia. Am.

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“…49 Furthermore, Bcl-X L expression in B-CLL cells is maintained through NF-kB and the expression of X-chromosome-linked inhibitor of apoptosis protein (XIAP) and FLIP in B-CLL has been linked to the constitutive PI3K-dependent NF-kB activation. 46 ALL B-precursor ALL is associated in 25-30% of adult cases, and 5% of childhood cases with the t(9;22) chromosomal translocation also found in 95% of chronic myeloid leukemia (CML, see below).…”

Section: B-cllmentioning

confidence: 99%

Targeting NF-κB in hematologic malignancies

et al. 2006

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The transcription factor nuclear factor kappa B (NF-jB) can intervene in oncogenesis by virtue of its capacity to regulate the expression of a plethora of genes that modulate apoptosis, and cell survival as well as proliferation, inflammation, tumor metastasis and angiogenesis. Different reports demonstrate the intrinsic activation of NF-jB in lymphoid and myeloid malignancies, including preneoplastic conditions such as myelodysplastic syndromes, underscoring its implication in malignant transformation. Targeting intrinsic NF-jB activation, as well as its upstream and downstream regulators, may hence constitute an additional approach to the oncologist's armamentarium. Several small inhibitors of the NF-jB-activatory kinase IjB kinase, of the proteaseome, or of the DNA binding of NF-jB subunits are under intensive investigation. Currently used cytotoxic agents can induce NF-jB activation as an unwarranted side effect, which confers apoptosis suppression and hence resistance to these drugs. Thus, NF-jB inhibitory molecules may be clinically useful, either as single therapeutic agents or in combination with classical chemotherapeutic agents, for the treatment of hematological malignancies.

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Survivin is expressed on CD40 stimulation and interfaces proliferation and apoptosis in B-cell chronic lymphocytic leukemia

Cited by 295 publications

References 43 publications

Engagement of the B-cell antigen receptor (BCR) allows efficient transduction of ZAP-70-positive primary B-CLL cells by recombinant adeno-associated virus (rAAV) vectors

Engagement of the B-cell antigen receptor (BCR) allows efficient transduction of ZAP-70-positive primary B-CLL cells by recombinant adeno-associated virus (rAAV) vectors

Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL)

Targeting NF-κB in hematologic malignancies

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