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A phase 2 study of bortezomib in relapsed, refractory myeloma.
- P. Richardson, B. Barlogie, +18 authors K. Anderson
- The New England journal of medicine
- 26 June 2003
Bortezomib, a member of a new class of anticancer drugs, is active in patients with relapsed multiple myeloma that is refractory to conventional chemotherapy. Expand
The proteasome inhibitor PS-341 inhibits growth, induces apoptosis, and overcomes drug resistance in human multiple myeloma cells.
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
Anti-CS1 humanized monoclonal antibody HuLuc63 inhibits myeloma cell adhesion and induces antibody-dependent cellular cytotoxicity in the bone marrow milieu.
The functional significance of CS1 in MM is defined and the preclinical rationale for testing HuLuc63 in clinical trials is provided, either alone or in combination. Expand
Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets
- T. Hideshima, C. Mitsiades, G. Tonon, P. Richardson, K. Anderson
- Nature Reviews Cancer
- 1 August 2007
Recent oncogenomic studies have further advanced the understanding of the molecular pathogenesis of multiple myeloma, providing the framework for new prognostic classification and identifying new therapeutic targets. Expand
A novel orally active proteasome inhibitor induces apoptosis in multiple myeloma cells with mechanisms distinct from Bortezomib.
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
NF-kappa B as a therapeutic target in multiple myeloma.
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
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.
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
Molecular sequelae of proteasome inhibition in human multiple myeloma cells
- N. Mitsiades, C. Mitsiades, +11 authors K. Anderson
- Biology, Medicine
- Proceedings of the National Academy of Sciences…
- 21 October 2002
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
- T. Hideshima, D. Chauhan, R. Schlossman, P. Richardson, K. Anderson
- Biology, Medicine
- 27 July 2001
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.
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