The anti-human leukocyte antigen-DR monoclonal antibody 1D09C3 activates the mitochondrial cell death pathway and exerts a potent antitumor activity in lymphoma-bearing nonobese diabetic/severe combined immunodeficient mice.

@article{CarloStella2006TheAL,
  title={The anti-human leukocyte antigen-DR monoclonal antibody 1D09C3 activates the mitochondrial cell death pathway and exerts a potent antitumor activity in lymphoma-bearing nonobese diabetic/severe combined immunodeficient mice.},
  author={C. Carlo-Stella and M. Di Nicola and M. Turco and L. Cleris and C. Lavazza and P. Longoni and M. Milanesi and M. Magni and M. Ammirante and A. Leone and Z. Nagy and W. Gioffr{\`e} and F. Formelli and A. Gianni},
  journal={Cancer research},
  year={2006},
  volume={66 3},
  pages={
          1799-808
        }
}
The fully human anti-HLA-DR antibody 1D09C3 has been shown to delay lymphoma cell growth in severe combined immunodeficient (SCID) mice. The present study was aimed at (a) investigating the mechanism(s) of 1D09C3-induced cell death and (b) further exploring the therapeutic efficacy of 1D09C3 in nonobese diabetic (NOD)/SCID mice. The chronic lymphocytic leukemia cell line JVM-2 and the mantle cell lymphoma cell line GRANTA-519 were used. Generation of reactive oxygen species (ROS) and… Expand
Therapy of B-cell malignancies by anti-HLA-DR humanized monoclonal antibody, IMMU-114, is mediated through hyperactivation of ERK and JNK MAP kinase signaling pathways.
TLDR
IMMU-114 induced disease-free survival in tumor-bearing SCID mice with early-stage disease and in models that are relatively resistant to anti-CD20 monoclonal antibodies; antibody-induced hyperactivation of ERK and JNK mitogen activated protein kinase signaling pathways are also required. Expand
IFN-gamma enhances the antimyeloma activity of the fully human anti-human leukocyte antigen-DR monoclonal antibody 1D09C3.
TLDR
IFN-gamma-induced up-regulation of HLA-DR results in a potent enhancement of the in vivo antimyeloma activity of 1D09C3, and no mice experienced any apparent treatment-related toxicity. Expand
Perifosine and sorafenib combination induces mitochondrial cell death and antitumor effects in NOD/SCID mice with Hodgkin lymphoma cell line xenografts
TLDR
In vivo xenograft studies demonstrated a significant reduction in tumor burden, an increased survival time, and an increased apoptosis and necrosis in perifosine/sorafenib-treated animals compared with mice receiving single agents, and these data provide a rationale for clinical trials using perifOSine/ sorAFenib combination. Expand
Effective induction of cell death on adult T-cell leukaemia cells by HLA-DRbeta-specific small antibody fragment isolated from human antibody phage library.
TLDR
S1T-A3 diabody is a small antibody fragment with agonistic activity to induce cell death through HLA-DR, the first report elucidating that diabODY specific to HLA -DR is effective to induce the cell death in T- cell malignancy especially adult T-cell leukaemic cell line. Expand
Antitumor activity of human CD34+ cells expressing membrane-bound tumor necrosis factor-related apoptosis-inducing ligand.
TLDR
Results show that CD34-TRAil+ cells might be an efficient vehicle for mTRAIL delivery to tumors, where they exert a potent antitumor effect possibly mediated by both direct tumor cell killing and indirect vascular-disrupting mechanisms. Expand
The in vitro biological activity of the HLA-DR-binding clinical IgG4 antibody 1D09C3 is a consequence of the disruption of cell aggregates and can be abrogated by Fab arm exchange.
TLDR
The results indicate that the activity of 1D09C3 in vitro may have been a consequence of assay design rather than an ability to induce HLA-DR-dependent cell death, and this antibody undergoes Fab arm exchange in the presence of IgG4. Expand
Inactivation of PI3k/Akt signaling pathway and activation of caspase-3 are involved in tanshinone I-induced apoptosis in myeloid leukemia cells in vitro
TLDR
It is concluded that the induction of apoptosis by Tan I in these leukemia cells is mainly related to the disruption of Δψm, the upregulation of Bax expression, and the activation of caspase-3. Expand
In vitro and in vivo sensitization of SW620 metastatic colon cancer cells to CDDP-induced apoptosis by the nitric oxide donor DETANONOate: Involvement of AIF.
TLDR
Findings underscore the potential therapeutic application of NO donors and subtoxic chemotherapeutic drugs in the treatment of advanced colon cancer resistant to conventional chemotherAPEutic agents. Expand
The mechanism of killing of B-lymphoma cells by 111In-conjugated antibodies
  • M. J. Mattes
  • Medicine, Biology
  • International journal of radiation biology
  • 2008
TLDR
Apoptosis was activated in at least four of the five cell lines tested, and participated in the killing of the cells, which may lead to a better understanding of the role of apoptosis in tumor cell cytotoxicity. Expand
BIM upregulation and ROS-dependent necroptosis mediate the antitumor effects of the HDACi Givinostat and Sorafenib in Hodgkin lymphoma cell line xenografts
TLDR
Gene expression profiling indicated that the synergistic effects of Givinostat/Sorafenib treatment are associated with the modulation of cell cycle and cell death pathways, and Knockdown experiments identified BIM as a key signaling molecule that mediates Giv inostat /SorAFenib-induced oxidative death of HL cells. Expand
...
1
2
3
4
...

References

SHOWING 1-10 OF 64 REFERENCES
Hu1D10 induces apoptosis concurrent with activation of the AKT survival pathway in human chronic lymphocytic leukemia cells.
TLDR
It is demonstrated that Hu1D10 induces caspase-independent apoptosis following secondary cross-linking in primary chronic lymphocytic leukemia (CLL) cells, and data suggest that Hu 1D10 ligation in CLL cells induces death and survival signals for which combination therapies may be designed to greatly enhance efficiency of both Hu2D10 and other class II antibodies in development. Expand
Lymphoma models for B-cell activation and tolerance: anti-immunoglobulin M treatment induces growth arrest by preventing the formation of an active kinase complex which phosphorylates retinoblastoma gene product in G1.
  • L. Joseph, S. Ezhevsky, D. Scott
  • Biology, Medicine
  • Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
  • 1995
TLDR
It is suggested that anti-mu-mediated growth arrest is due to the direct or indirect inactivation of an active kinase complex capable of pRB phosphorylation, and its effect on a cyclin:kinase complex that can act on pRB in murine B-lymphoma cells. Expand
Complement-mediated cell death induced by rituximab in B-cell lymphoproliferative disorders is mediated in vitro by a caspase-independent mechanism involving the generation of reactive oxygen species.
TLDR
It is suggested that CD20, CD59, and complement have a role in the in vitro cytotoxic effect of rituximab, which is mediated by a caspase-independent process that involves ROS generation. Expand
Lymphoma regression induced by monoclonal anti-idiotypic antibodies correlates with their ability to induce Ig signal transduction and is not prevented by tumor expression of high levels of bcl-2 protein.
TLDR
A strong correlation is found between the ability of an anti-Id MoAb to induce an increase in tyrosine phosphorylation in vitro and its ability to induce a tumor regression in the patient and the level of bcl-2 expressed by the tumor cells was not correlated with clinical response to anti- Id MoAb treatment. Expand
Apoptosis of malignant human B cells by ligation of CD20 with monoclonal antibodies.
TLDR
It is suggested that ligation of CD20 in vivo by anti-CD20 antibodies in the presence of FcR-expressing cells may initiate signal transduction events that induce elevation of [Ca2+]i and lead to apoptosis of malignant B cells, thereby contributing to the impressive tumor regressions observed in mouse models and clinical trials using anti- CD20 MoAbs. Expand
Ligation of IFN-gamma-induced HLA-DR molecules on fibroblasts induces RANTES expression via c-Jun N-terminal kinase (JNK) pathway.
TLDR
JNK-2 was one of the HLA-DR-mediated signal transduction pathways leading to RANTES production from fibroblasts when the DR molecules were ligated with L243, and JNK inhibitor nearly completely blocked tumor necrosis factor-alpha (TNF-alpha)-induced RantES production in GF. Expand
Fully human, HLA-DR-specific monoclonal antibodies efficiently induce programmed death of malignant lymphoid cells
TLDR
Although the expression of HLA-DR on normal hematopoietic cells is a potential safety concern, the antibodies caused no long-lasting hematological toxicity in primates, in vivo, and offer the potential for a novel therapeutic approach to lymphoid malignancies. Expand
Mitochondria control of cell death induced by anti-HLA-DR antibodies
TLDR
It is demonstrated that anti-HLA-DR-induced cell death is instead associated with a rapid disruption of the inner mitochondrial transmembrane potential, ΔΨm, a process that is significantly inhibited by Bcl-2 overexpression, and found that ΔΩm disruption results in the selective release of apoptosis-inducing factor (AIF) from the mitochondria. Expand
Mechanisms involved in the inhibition of growth of a human B lymphoma cell line, B104, by anti‐MHC class II antibodies
TLDR
It is demonstrated that cross‐linking of MHC class II molecules transduced the negative signals through intracellular mechanisms different from those present in the cross‐ linking of surface IgM. Expand
Growth inhibition of Epstein-Barr virus-transformed B cells by anti-HLA-DR antibody L243: possible relationship to L243-induced down-regulation of CD23 antigen expression.
TLDR
The possibility that the suppressive effect of L243 mab on LCL proliferation is due to down-regulation of CD23 antigen expression is discussed. Expand
...
1
2
3
4
5
...