Research Topics
Genomes and Genes
| Teru HideshimaSummaryAffiliation: Harvard University Country: USA Publications
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Detail Information
Publications
CXCR4 inhibitor AMD3100 disrupts the interaction of multiple myeloma cells with the bone marrow microenvironment and enhances their sensitivity to therapyAbdel Kareem Azab
Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Blood 113:4341-51. 2009..These experiments provide a proof of concept for the use of agents that disrupt interaction with the microenvironment for enhancement of efficacy of cytotoxic agents in cancer therapy...
Histone deacetylase inhibitors in the treatment for multiple myelomaTeru Hideshima
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute and Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA
Int J Hematol 97:324-32. 2013..Many HDAC inhibitors have already shown significant anti-MM activities in preclinical studies and are under evaluation in clinical trials...- Biologic impact of proteasome inhibition in multiple myeloma cells--from the aspects of preclinical studiesTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA
Semin Hematol 49:223-7. 2012..Importantly, multiple myeloma (MM) cells are considered to have lower threshold against these stresses than other cell types, which makes these cells sensitive to proteasome inhibitors... - Preclinical studies of novel targeted therapiesTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Hematol Oncol Clin North Am 21:1071-91, viii-ix. 2007.... - Mechanism of action of proteasome inhibitors and deacetylase inhibitors and the biological basis of synergy in multiple myelomaTeru Hideshima
Dana Farber Cancer Institute, Boston, MA 02115, USA
Mol Cancer Ther 10:2034-42. 2011..Data from the studies summarized here have been used as the rationale for the implementation of phase II and III clinical trials of DACi, alone and combined with bortezomib, in relapsed and refractory multiple myeloma... 
Current therapeutic uses of lenalidomide in multiple myelomaTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Expert Opin Investig Drugs 15:171-9. 2006..Therefore, lenalidomide represents a new class of antitumour agents that is useful in the treatment of MM. Lenalidomide has received fast track designation from the FDA for the treatment of MM and myelodysplastic syndromes...- Novel therapies in MM: from the aspect of preclinical studiesTeru Hideshima
Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, 450 Brookline Avenue, Boston, MA 02215, USA
Int J Hematol 94:344-54. 2011..Currently they are under evaluation in preclinical studies, as single agents and/or in combination, to improve outcome of MM patients... - A novel Aurora-A kinase inhibitor MLN8237 induces cytotoxicity and cell-cycle arrest in multiple myelomaGullu Gorgun
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 115:5202-13. 2010..MLN8237 is currently in phase 1 and phase 2 clinical trials in patients with advanced malignancies, and our preclinical results suggest that MLN8237 may be a promising novel targeted therapy in MM... - Targeting mitochondria to overcome conventional and bortezomib/proteasome inhibitor PS-341 resistance in multiple myeloma (MM) cellsDharminder Chauhan
Dana-Farber Cancer Institute, 44 Binney St, Boston, MA 02215, USA
Blood 104:2458-66. 2004..Together, these preclinical studies suggest that combining bortezomib with PK may enhance its clinical efficacy, reduce attendant toxicity, and overcome conventional and bortezomib resistance in patients with relapsed refractory MM... - CS1 promotes multiple myeloma cell adhesion, clonogenic growth, and tumorigenicity via c-maf-mediated interactions with bone marrow stromal cellsYu Tzu Tai
LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 113:4309-18. 2009..These studies provide direct evidence of the role of CS1 in myeloma pathogenesis, define molecular mechanisms regulating its effects, and further support novel therapies targeting CS1 in MM... - Molecular characterization of PS-341 (bortezomib) resistance: implications for overcoming resistance using lysophosphatidic acid acyltransferase (LPAAT)-beta inhibitorsTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Oncogene 24:3121-9. 2005..Our studies therefore demonstrate that LPAAT-beta inhibitor CT-32615 triggers necrosis, even in PS-341-resistant DHL-4 cells, providing the framework for its evaluation to overcome clinical PS-341 resistance and improve patient outcome... - Arsenic trioxide inhibits growth of human multiple myeloma cells in the bone marrow microenvironmentToshiaki Hayashi
The Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Mol Cancer Ther 1:851-60. 2002..These studies provide the rationale for clinical trials of As2O3, either alone or together with dexamethasone, to overcome classical drug resistance and improve outcome in patients with MM... - Identification of genes regulated by 2-methoxyestradiol (2ME2) in multiple myeloma cells using oligonucleotide arraysDharminder Chauhan
The Jerome Lipper Multiple Myeloma Center, The Department of Medical Oncology, Cancer Biology, Boston Veteran Affairs Healthcare System, Boston, MA, USA
Blood 101:3606-14. 2003..These studies may therefore allow improved therapeutic use of 2ME2, based upon targeting genes that regulate MM cell growth and survival... - BIRB 796 enhances cytotoxicity triggered by bortezomib, heat shock protein (Hsp) 90 inhibitor, and dexamethasone via inhibition of p38 mitogen-activated protein kinase/Hsp27 pathway in multiple myeloma cell lines and inhibits paracrine tumour growthHiroshi Yasui
Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Br J Haematol 136:414-23. 2007.... - Functional interaction of plasmacytoid dendritic cells with multiple myeloma cells: a therapeutic targetDharminder Chauhan
The LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Myeloma Research, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Cell 16:309-23. 2009..Our study therefore validates targeting pDC-MM interactions as a therapeutic strategy to overcome drug resistance in MM... - Targeting MEK induces myeloma-cell cytotoxicity and inhibits osteoclastogenesisYu Tzu Tai
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 110:1656-63. 2007..Taken together, these results show that AZD6244 targets both MM cells and OCs in the BM microenvironment, providing the preclinical framework for clinical trials to improve patient outcome in MM... - The bortezomib/proteasome inhibitor PS-341 and triterpenoid CDDO-Im induce synergistic anti-multiple myeloma (MM) activity and overcome bortezomib resistanceDharminder Chauhan
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA
Blood 103:3158-66. 2004..Together, these findings provide the framework for clinical evaluation of CDDO-Im, either alone or in combination with bortezomib, to overcome drug resistance and improve patient outcome in MM... - PI3K/p110{delta} is a novel therapeutic target in multiple myelomaHiroshi Ikeda
LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Harvard Medical School, Boston, MA, USA
Blood 116:1460-8. 2010..Our studies therefore show that PI3K/p110delta is a novel therapeutic target in MM and provide the basis for clinical evaluation of CAL-101 to improve patient outcome in MM... - Proteasomal degradation of topoisomerase I is preceded by c-Jun NH2-terminal kinase activation, Fas up-regulation, and poly(ADP-ribose) polymerase cleavage in SN38-mediated cytotoxicity against multiple myelomaLaurence Catley
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02215, USA
Cancer Res 64:8746-53. 2004..These findings have clinical significance, because identification of downstream apoptotic signaling after topoisomerase I inhibition will both elucidate mechanisms of resistance and optimize future combination chemotherapy against MM... - The biological sequelae of stromal cell-derived factor-1alpha in multiple myelomaTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, and Harvard Medical School, Boston, Massachusetts 02115, USA
Mol Cancer Ther 1:539-44. 2002.... - Transforming growth factor beta receptor I kinase inhibitor down-regulates cytokine secretion and multiple myeloma cell growth in the bone marrow microenvironmentToshiaki Hayashi
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Clin Cancer Res 10:7540-6. 2004.... - p38 mitogen-activated protein kinase inhibitor LY2228820 enhances bortezomib-induced cytotoxicity and inhibits osteoclastogenesis in multiple myeloma; therapeutic implicationsKenji Ishitsuka
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Br J Haematol 141:598-606. 2008..These results suggest that LY represents a promising novel targeted approach to improve MM patient outcome both by enhancing the effect of bortezomib and by reducing osteoskeletal events... - Targeting MEK1/2 blocks osteoclast differentiation, function and cytokine secretion in multiple myelomaIris Breitkreutz
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Br J Haematol 139:55-63. 2007..The present study therefore provides a preclinical rationale for the evaluation of AZD6244 as a potential new therapy for patients with MM... - A novel carbohydrate-based therapeutic GCS-100 overcomes bortezomib resistance and enhances dexamethasone-induced apoptosis in multiple myeloma cellsDharminder Chauhan
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 65:8350-8. 2005.... - MLN120B, a novel IkappaB kinase beta inhibitor, blocks multiple myeloma cell growth in vitro and in vivoTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Clin Cancer Res 12:5887-94. 2006..These studies provide the framework for clinical evaluation of MLN120B, alone and in combined therapies, trials of these novel agents to improve patient outcome in multiple myeloma... - Inhibition of Akt induces significant downregulation of survivin and cytotoxicity in human multiple myeloma cellsTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Br J Haematol 138:783-91. 2007..These preclinical studies provide the framework for clinical trials of bortezomib with Perifosine to improve patient outcome in MM... - SDX-101, the R-enantiomer of etodolac, induces cytotoxicity, overcomes drug resistance, and enhances the activity of dexamethasone in multiple myelomaHiroshi Yasui
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Mayer 557, 44 Binney St, Boston, MA 02115, USA
Blood 106:706-12. 2005..Our data, therefore, indicate that R-etodolac circumvents drug resistance in MM cells at clinically relevant concentrations, targets Mcl-1, and can be synergistically combined with Dex... - Mechanisms by which SGN-40, a humanized anti-CD40 antibody, induces cytotoxicity in human multiple myeloma cells: clinical implicationsYu-Tzu Tai
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA
Cancer Res 64:2846-52. 2004..1S cells and patient MM cells. Taken together, these results provide the preclinical rationale for the evaluation of SGN-40 as a potential new therapy to improve patient outcome in MM... - NVP-LAQ824 is a potent novel histone deacetylase inhibitor with significant activity against multiple myelomaLaurence Catley
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Blood 102:2615-22. 2003..Finally, a study using NVP-LAQ824 in a preclinical murine myeloma model provides in vivo relevance to our in vitro studies. Taken together, these findings provide the framework for NVP-LAQ824 as a novel therapeutic in MM... - GW654652, the pan-inhibitor of VEGF receptors, blocks the growth and migration of multiple myeloma cells in the bone marrow microenvironmentKlaus Podar
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Harvard Medical School, Boston, MA 02115, USA
Blood 103:3474-9. 2004.... - Antitumor activity of lysophosphatidic acid acyltransferase-beta inhibitors, a novel class of agents, in multiple myelomaTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 63:8428-36. 2003..Our data therefore demonstrate for the first time that inhibiting LPAAT-beta induces cytotoxicity in MM cells in the bone marrow milieu, providing the framework for clinical trials of these novel agents in MM... - Bortezomib induces canonical nuclear factor-kappaB activation in multiple myeloma cellsTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 114:1046-52. 2009..Moreover, IKKbeta inhibitors enhanced bortezomib-induced cytotoxicity. Our studies therefore suggest that bortezomib-induced cytotoxicity cannot be fully attributed to inhibition of canonical NF-kappaB activity in MM cells... - Molecular mechanisms whereby immunomodulatory drugs activate natural killer cells: clinical applicationToshiaki Hayashi
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
Br J Haematol 128:192-203. 2005..These studies defined the mechanisms whereby IMiDs trigger NK cell-mediated tumour-cell lysis, further supporting their therapeutic use in MM... - Molecular mechanisms mediating antimyeloma activity of proteasome inhibitor PS-341Teru Hideshima
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Blood 101:1530-4. 2003..Inhibition of JNK activity abrogates PS-341-induced MM cell death. These studies identify molecular targets of PS-341 and provide the rationale for the development of second-generation, more targeted therapies... - FTY720 induces apoptosis in multiple myeloma cells and overcomes drug resistanceHiroshi Yasui
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 65:7478-84. 2005..These results suggest that FTY720 overcomes drug resistance in multiple myeloma cells and provide the rationale for its clinical evaluation to improve patient outcome in multiple myeloma... - The proteasome inhibitor PS-341 potentiates sensitivity of multiple myeloma cells to conventional chemotherapeutic agents: therapeutic applicationsNicholas Mitsiades
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 101:2377-80. 2003..These studies, therefore, provide the framework for clinical use of this agent in combination with conventional chemotherapy... - Molecular sequelae of proteasome inhibition in human multiple myeloma cellsNicholas Mitsiades
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 99:14374-9. 2002..These data provide both insight into the molecular mechanisms of antitumor activity of PS-341 and the rationale for future clinical trials of PS-341, in combination with conventional and novel therapies, to improve patient outcome in MM... - Seliciclib (CYC202 or R-roscovitine), a small-molecule cyclin-dependent kinase inhibitor, mediates activity via down-regulation of Mcl-1 in multiple myelomaNoopur Raje
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Mayer 557, 44 Binney St, Boston, MA 02115, USA
Blood 106:1042-7. 2005..Finally, combination studies of seliciclib with doxorubicin and bortezomib show in vitro synergism, providing the rationale for testing these drug combinations to improve patient outcome in MM... - Immunomodulatory drug lenalidomide (CC-5013, IMiD3) augments anti-CD40 SGN-40-induced cytotoxicity in human multiple myeloma: clinical implicationsYu-Tzu Tai
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Res 65:11712-20. 2005.... - A novel orally active proteasome inhibitor induces apoptosis in multiple myeloma cells with mechanisms distinct from BortezomibDharminder Chauhan
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Cell 8:407-19. 2005..Combining NPI-0052 and Bortezomib induces synergistic anti-MM activity. Our study therefore provides the rationale for clinical protocols evaluating NPI-0052, alone and together with Bortezomib, to improve patient outcome in MM... - Janus kinase inhibitor INCB20 has antiproliferative and apoptotic effects on human myeloma cells in vitro and in vivoRenate Burger
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Mol Cancer Ther 8:26-35. 2009.... - Combination of proteasome inhibitors bortezomib and NPI-0052 trigger in vivo synergistic cytotoxicity in multiple myelomaDharminder Chauhan
The LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Myeloma Research, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 111:1654-64. 2008..Taken together, our study provides the preclinical rationale for clinical protocols evaluating bortezomib together with NPI-0052 to improve patient outcome in MM... - beta-lapachone, a novel plant product, overcomes drug resistance in human multiple myeloma cellsDeepak Gupta
Jerome Lipper Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Exp Hematol 30:711-20. 2002..CONCLUSION: These studies provide a framework for clinical evaluation of beta-lapachone to improve the outcome for patients with MM... - Targeting mitochondrial factor Smac/DIABLO as therapy for multiple myeloma (MM)Dharminder Chauhan
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 109:1220-7. 2007..Our study therefore provides the rationale for clinical protocols evaluating LBW242, alone and together with other anti-MM agents, to improve patient outcome in MM... - 5-Azacytidine, a DNA methyltransferase inhibitor, induces ATR-mediated DNA double-strand break responses, apoptosis, and synergistic cytotoxicity with doxorubicin and bortezomib against multiple myeloma cellsTanyel Kiziltepe
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Mol Cancer Ther 6:1718-27. 2007..Taken together, these data provide the preclinical rationale for the clinical evaluation of 5-azacytidine, alone and in combination with doxorubicin and bortezomib, to improve patient outcome in MM... - Azaspirane (N-N-diethyl-8,8-dipropyl-2-azaspiro [4.5] decane-2-propanamine) inhibits human multiple myeloma cell growth in the bone marrow milieu in vitro and in vivoMakoto Hamasaki
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Mayer 557, 44 Binney St, Boston, MA 02115, USA
Blood 105:4470-6. 2005..These results, therefore, show that azaspirane both induces MM cell apoptosis and inhibits cytokine secretion in the BM milieu, providing the framework for clinical trials to improve patient outcome in MM... - Human anti-CD40 antagonist antibody triggers significant antitumor activity against human multiple myelomaYu-Tzu Tai
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 65:5898-906. 2005..These results provide the preclinical rationale for clinical trials of CHIR-12.12 to improve patient outcome in multiple myeloma... - Honokiol overcomes conventional drug resistance in human multiple myeloma by induction of caspase-dependent and -independent apoptosisKenji Ishitsuka
Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
Blood 106:1794-800. 2005..Taken together, our results provide the preclinical rationale for clinical protocols of HNK to improve patient outcome in MM... - Caveolin-1 is required for vascular endothelial growth factor-triggered multiple myeloma cell migration and is targeted by bortezomibKlaus Podar
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA
Cancer Res 64:7500-6. 2004.... - Inhibition of the insulin-like growth factor receptor-1 tyrosine kinase activity as a therapeutic strategy for multiple myeloma, other hematologic malignancies, and solid tumorsConstantine S Mitsiades
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
Cancer Cell 5:221-30. 2004.... - MLN3897, a novel CCR1 inhibitor, impairs osteoclastogenesis and inhibits the interaction of multiple myeloma cells and osteoclastsSonia Vallet
Jerome Lipper Multiple Myeloma Disease Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Blood 110:3744-52. 2007..Our results therefore show novel biologic sequelae of CCL3 and its inhibition in both osteoclastogenesis and MM cell growth, providing the preclinical rationale for clinical trials of MLN3897 to treat OBD in MM... - A proto-oncogene BCL6 is up-regulated in the bone marrow microenvironment in multiple myeloma cellsTeru Hideshima
Jerome Lipper Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 115:3772-5. 2010.... - The monoclonal antibody nBT062 conjugated to cytotoxic Maytansinoids has selective cytotoxicity against CD138-positive multiple myeloma cells in vitro and in vivoHiroshi Ikeda
Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute Harvard Medical School, Boston, Massachusetts 02115, USA
Clin Cancer Res 15:4028-37. 2009..We investigated the antitumor effect of murine/human chimeric CD138-specific monoclonal antibody nBT062 conjugated with highly cytotoxic maytansinoid derivatives against multiple myeloma (MM) cells in vitro and in vivo... - The small-molecule VEGF receptor inhibitor pazopanib (GW786034B) targets both tumor and endothelial cells in multiple myelomaKlaus Podar
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 103:19478-83. 2006.... - Insulin-like growth factor-1 induces adhesion and migration in human multiple myeloma cells via activation of beta1-integrin and phosphatidylinositol 3'-kinase/AKT signalingYu Tzu Tai
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Res 63:5850-8. 2003..Moreover, they define the functional association of IGF-IR and beta1 integrin in mediating MM cell homing, providing the preclinical rationale for novel treatment strategies targeting IGF-I/IGF-IR in MM... - In vivo and in vitro cytotoxicity of R-etodolac with dexamethasone in glucocorticoid-resistant multiple myeloma cellsPaola Neri
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Br J Haematol 134:37-44. 2006..These data indicate that R-etodolac overcomes resistance to Dex in glucocorticoid-resistant MM cells, providing the framework for clinical trials of R-etodolac combined with Dex, to improve patient outcome in MM... - JNK-dependent release of mitochondrial protein, Smac, during apoptosis in multiple myeloma (MM) cellsDharminder Chauhan
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 278:17593-6. 2003..These findings demonstrate that activation of JNK is an obligatory event for the release of Smac during stress-induced apoptosis in MM cells... - Novel inosine monophosphate dehydrogenase inhibitor VX-944 induces apoptosis in multiple myeloma cells primarily via caspase-independent AIF/Endo G pathwayKenji Ishitsuka
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Oncogene 24:5888-96. 2005.... - Bortezomib mediates antiangiogenesis in multiple myeloma via direct and indirect effects on endothelial cellsAldo Maria Roccaro
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 66:184-91. 2006..These data, therefore, delineate the mechanisms of the antiangiogenic effects of bortezomib on multiple myeloma cells in the bone marrow milieu... - Functional significance of novel neurotrophin-1/B cell-stimulating factor-3 (cardiotrophin-like cytokine) for human myeloma cell growth and survivalRenate Burger
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Br J Haematol 123:869-78. 2003..In conclusion, BSF-3 is a novel myeloma growth and survival factor with a potential role in the pathophysiology of the disease... - Targeting PKC: a novel role for beta-catenin in ER stress and apoptotic signalingMarc S Raab
LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 113:1513-21. 2009..Moreover, we identify p73 as a potential novel therapeutic target in MM. Based on these and previous data, enzastaurin is currently under clinical investigation in a variety of hematologic malignancies, including MM... - Aplidin, a marine organism-derived compound with potent antimyeloma activity in vitro and in vivoConstantine S Mitsiades
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Res 68:5216-25. 2008..The profile of the anti-MM activity of Aplidin in our preclinical models provided the framework for its clinical testing in MM, which has already provided favorable preliminary results... - Proteasome inhibitor PS-341 abrogates IL-6 triggered signaling cascades via caspase-dependent downregulation of gp130 in multiple myelomaTeru Hideshima
Department of Adult Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Jerome Lipper Multiple Myeloma Center, 44 Binney Street, Boston, MA 02155, USA
Oncogene 22:8386-93. 2003..Importantly, this effect on cytokine-induced gp130 signaling cascades may account, at least in part, for the remarkable preclinical sensitivity and clinical responses achieved in MM with PS-341 treatment... - Up-regulation of c-Jun inhibits proliferation and induces apoptosis via caspase-triggered c-Abl cleavage in human multiple myelomaKlaus Podar
Jerome Lipper Multiple Myeloma Center, Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Cancer Res 67:1680-8. 2007..Finally, our data suggest that this mechanism may not only be restricted to MM but may also be important in a broad range of malignancies including erythroleukemia and solid tumors... - Identification of genes regulated by dexamethasone in multiple myeloma cells using oligonucleotide arraysDharminder Chauhan
The Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, MA 02115, USA
Oncogene 21:1346-58. 2002..These studies may therefore allow improved therapeutic uses of Dex, based upon targeting genes that regulate MM cell growth and survival... - NF-kappa B as a therapeutic target in multiple myelomaTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 277:16639-47. 2002..Furthermore, they provide the framework for clinical evaluation of novel MM therapies based upon targeting NF-kappaB... - Dual inhibition of akt/mammalian target of rapamycin pathway by nanoparticle albumin-bound-rapamycin and perifosine induces antitumor activity in multiple myelomaDiana Cirstea
Leebow Institute of Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Disease Center, Dana Farber Cancer Institute
Mol Cancer Ther 9:963-75. 2010..Mol Cancer Ther; 9(4); 963-75. (c)2010 AACR... - Aurora kinase A is a target of Wnt/beta-catenin involved in multiple myeloma disease progressionJui Dutta-Simmons
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 114:2699-708. 2009..Our data provide evidence for a novel functional link between beta-catenin and Aurora kinase A, underscoring a critical role of these pathways in MM disease progression... - Cytotoxic activity of the maytansinoid immunoconjugate B-B4-DM1 against CD138+ multiple myeloma cellsPierfrancesco Tassone
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
Blood 104:3688-96. 2004.... - Immunomodulatory drug CC-5013 overcomes drug resistance and is well tolerated in patients with relapsed multiple myelomaPaul G Richardson
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Blood 100:3063-7. 2002..Our study therefore provides the basis for the evaluation of CC-5013, either alone or in combination, to treat patients with MM at earlier stages of disease... - [Proteasome inhibitor bortezomib as an anticancer drug]Hiroshi Yasui
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, USA
Tanpakushitsu Kakusan Koso 51:1251-6. 2006 - Blockade of the MEK/ERK signalling cascade by AS703026, a novel selective MEK1/2 inhibitor, induces pleiotropic anti-myeloma activity in vitro and in vivoKihyun Kim
Department of Medical Oncology, The LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Br J Haematol 149:537-49. 2010..Our results therefore support clinical evaluation of AS703026, alone or in combination with other anti-MM agents, to improve patient outcome... - Targeting angiogenesis via a c-Myc/hypoxia-inducible factor-1alpha-dependent pathway in multiple myelomaJing Zhang
Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Boston, MA 02115, USA
Cancer Res 69:5082-90. 2009..Our data, therefore, identify Hif-1alpha as a novel molecular target in MM and add another facet to anti-MM drug activity... - Blockade of Hsp27 overcomes Bortezomib/proteasome inhibitor PS-341 resistance in lymphoma cellsDharminder Chauhan
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Cancer Res 63:6174-7. 2003..These findings provide the first evidence that Hsp27 confers PS-341 resistance... - The vascular endothelial growth factor receptor tyrosine kinase inhibitor PTK787/ZK222584 inhibits growth and migration of multiple myeloma cells in the bone marrow microenvironmentBoris Lin
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 62:5019-26. 2002..The demonstrated anti-MM activity of PTK787, coupled with its antiangiogenic effects, provides the framework for clinical trials of this agent to overcome drug resistance and improve outcome in MM... - The Akt pathway regulates survival and homing in Waldenstrom macroglobulinemiaXavier Leleu
Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Blood 110:4417-26. 2007..These results provide understanding of biological effects of Akt pathway in WM and provide the framework for clinical evaluation of perifosine in WM patients... - Targeting p38 MAPK inhibits multiple myeloma cell growth in the bone marrow milieuTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 101:703-5. 2003..These studies therefore identify p38 MAPK as a novel therapeutic target to overcome drug resistance and improve patient outcome in MM... - Dual targeting of the proteasome regulates survival and homing in Waldenstrom macroglobulinemiaAldo M Roccaro
Medical Oncology, Dana Farber Cancer Institute, and Harvard Medical School, Boston, MA 02115, USA
Blood 111:4752-63. 2008..Theses studies enhance our understanding of the biologic role of the proteasome pathway in WM, and provide the preclinical basis for clinical trials of combinations of proteasome inhibitors in WM... - Activation of NF-kappaB and upregulation of intracellular anti-apoptotic proteins via the IGF-1/Akt signaling in human multiple myeloma cells: therapeutic implicationsConstantine S Mitsiades
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, MA 02115, USA
Oncogene 21:5673-83. 2002..Importantly, they provide the basis for future clinical trials in MM combining conventional or novel agents with strategies designed to neutralize IGF-1... - Gene expression analysis of B-lymphoma cells resistant and sensitive to bortezomibReshma Shringarpure
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA
Br J Haematol 134:145-56. 2006.... - In vitro anti-myeloma activity of the Aurora kinase inhibitor VE-465Joseph M Negri
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Br J Haematol 147:672-6. 2009..Combinations with dexamethasone (Dex), doxorubicin (Doxo) and bortezomib showed no antagonism. Our study highlights the potential role of the tumour microenvironment in modulating the activity of this drug class... - Novel therapies for multiple myelomaToshiaki Hayashi
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA
Br J Haematol 120:10-7. 2003 - Immunomodulatory drug costimulates T cells via the B7-CD28 pathwayRichard LeBlanc
Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA
Blood 103:1787-90. 2004.... - Proteasome inhibitor therapy in multiple myelomaDharminder Chauhan
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
Mol Cancer Ther 4:686-92. 2005.... - Targeting Akt and heat shock protein 90 produces synergistic multiple myeloma cell cytotoxicity in the bone marrow microenvironmentAlissa Huston
James P Wilmot Cancer Center, University of Rochester, Rochester, New York, USA
Clin Cancer Res 14:865-74. 2008.... - Apoptotic signaling induced by immunomodulatory thalidomide analogs in human multiple myeloma cells: therapeutic implicationsNicholas Mitsiades
Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 99:4525-30. 2002..These studies both delineate the mechanism of action of IMiDs against MM cells in vitro and form the basis for clinical trials of these agents, alone and coupled with conventional and other novel therapies, to improve outcome in MM... - Proteasome inhibition as a novel therapeutic target in human cancerS Vincent Rajkumar
Division of Hematology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
J Clin Oncol 23:630-9. 2005..This article discusses proteasome inhibition as a novel therapeutic target in cancer and focuses on the development, mechanism of action, and current clinical experience with bortezomib... - Proteasome inhibitor PS-341 inhibits human myeloma cell growth in vivo and prolongs survival in a murine modelRichard LeBlanc
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 62:4996-5000. 2002.... - Effects of PS-341 on the activity and composition of proteasomes in multiple myeloma cellsMikael Altun
Department of Pathology, Harvard Medical School, Boston, Massachusetts, USA
Cancer Res 65:7896-901. 2005..These data suggest that PS-341 targets both normal and immunoproteasome species to a similar extent in myeloma cells... - Combination mammalian target of rapamycin inhibitor rapamycin and HSP90 inhibitor 17-allylamino-17-demethoxygeldanamycin has synergistic activity in multiple myelomaLanie K Francis
University of Pittsburgh Cancer Institute, Division of Hematology/Oncology, Department of Internal Medicine, Pittsburgh, Pennsylvania, USA
Clin Cancer Res 12:6826-35. 2006..CONCLUSIONS: These studies provide the basis for potential clinical evaluation of this combination for multiple myeloma patients... - FQPD, a novel immunomodulatory drug, has significant in vitro activity in multiple myelomaShaji Kumar
Division of Hematology, Mayo Clinic, Rochester, MN, USA
Br J Haematol 132:698-704. 2006..Our studies therefore demonstrated in vitro anti-MM activity of FQPD and provide the rationale for its in vivo evaluation in animal models and derived clinical trials... - Targeting NF-kappaB in Waldenstrom macroglobulinemiaXavier Leleu
Medical Oncology, Dana Farber Cancer Institute, and Harvard Medical School, Boston, MA, USA
Blood 111:5068-77. 2008..Moreover, a combination of these drugs with the CD20 monoclonal antibody rituximab further increased their cytotoxic activity. Thus, effective WM therapy may require combination regimens targeting the NF-kappaB pathway...