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The proteasome inhibitor PS-341 inhibits growth, induces apoptosis, and overcomes drug resistance in human multiple myeloma cells.
TLDR
It is demonstrated that the proteasome inhibitor PS-341 both acts directly on MM cells and alters cellular interactions and cytokine secretion in the BM millieu to inhibit tumor cell growth, induce apoptosis, and overcome drug resistance. Expand
NF-kappa B as a therapeutic target in multiple myeloma.
TLDR
It is demonstrated that specific targeting of NF-kappaB can overcome the growth and survival advantage conferred both by tumor cell binding to BMSCs and cytokine secretion in the BM milieu. Expand
A novel orally active proteasome inhibitor induces apoptosis in multiple myeloma cells with mechanisms distinct from Bortezomib.
TLDR
It is shown that the novel proteasome inhibitor NPI-0052 induces apoptosis in MM cells resistant to conventional and Bortezomib therapies, which provides the rationale for clinical protocols evaluating NPI -0052, alone and together with Bortzomib, to improve patient outcome in MM. Expand
Inhibition of the insulin-like growth factor receptor-1 tyrosine kinase activity as a therapeutic strategy for multiple myeloma, other hematologic malignancies, and solid tumors.
TLDR
NVP-ADW742 monotherapy or its combination with cytotoxic chemotherapy had significant antitumor activity in an orthotopic xenograft MM model, providing in vivo proof of principle for therapeutic use of selective IGF-1R inhibitors in cancer. Expand
Multiple myeloma cell adhesion-induced interleukin-6 expression in bone marrow stromal cells involves activation of NF-kappa B.
TLDR
The data suggest that the NF-kappa B site is one of the essential regulatory elements for MM cell adhesion-induced IL-6 transcription in BMSCs, and may provide new therapeutic strategies based on interruption of IL- 6 mediated tumor cell growth. Expand
Molecular sequelae of proteasome inhibition in human multiple myeloma cells
TLDR
The molecular sequelae of PS-341 treatment in MM cells are characterized and the rationale for future clinical trials of this promising agent, in combination with conventional and novel therapies, to improve patient outcome in MM is explained. Expand
The role of tumor necrosis factor α in the pathophysiology of human multiple myeloma: therapeutic applications
TLDR
Agents which act to inhibit TNFα may abrogate the paracrine growth and survival advantage conferred by MM cell adhesion in the BM microenvironment. Expand
Thalidomide and its analogs overcome drug resistance of human multiple myeloma cells to conventional therapy.
TLDR
Clinical activity of Thal against MM that is refractory to conventional therapy is demonstrated and mechanisms of anti-tumor activity of thalidomide and its potent analogs (immunomodulatory drugs [IMiDs]) are delineated. Expand
Biologic sequelae of interleukin-6 induced PI3-K/Akt signaling in multiple myeloma
TLDR
It is shown that PI3-K/Akt signaling mediates growth, survival, and cell cycle regulatory effects of IL-6 in MM, and LY294002 completely abrogates this signaling cascade. Expand
Small-molecule inhibition of proteasome and aggresome function induces synergistic antitumor activity in multiple myeloma.
TLDR
It is demonstrated that tubacin combined with bortezomib mediates significant anti-MM activity, providing the framework for clinical evaluation of combined therapy to improve patient outcome in MM. Expand
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