Research Topics
Genomes and Genes
| Yu Tzu TaiSummaryAffiliation: Harvard University Country: USA Publications
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Detail Information
Publications
Bruton tyrosine kinase inhibition is a novel therapeutic strategy targeting tumor in the bone marrow microenvironment in multiple myelomaYu Tzu Tai
LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Multiple Myeloma Research, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA
Blood 120:1877-87. 2012..Together, these results delineate functional sequelae of Btk activation mediating osteolysis and growth of MM cells, supporting evaluation of PCI-32765 as a novel therapeutic in MM...
Role of B-cell-activating factor in adhesion and growth of human multiple myeloma cells in the bone marrow microenvironmentYu Tzu Tai
The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Cancer Res 66:6675-82. 2006....- 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... - Anti-CS1 humanized monoclonal antibody HuLuc63 inhibits myeloma cell adhesion and induces antibody-dependent cellular cytotoxicity in the bone marrow milieuYu Tzu Tai
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 112:1329-37. 2008..These results thus define the functional significance of CS1 in MM and provide the preclinical rationale for testing HuLuc63 in clinical trials, either alone or in combination... - 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... - 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... - Vascular endothelial growth factor-induced migration of multiple myeloma cells is associated with beta 1 integrin- and phosphatidylinositol 3-kinase-dependent PKC alpha activationKlaus Podar
Jerome Lipper Multiple Myeloma Research Center Dana Farber Cancer Institute and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 277:7875-81. 2002..Time-lapse phase contrast video microscopy (TLVM) studies confirm the importance of these signaling components in VEGF-triggered MM cell migration on fibronectin... - 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... - 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... - 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... - 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... - 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... - CD40 induces human multiple myeloma cell migration via phosphatidylinositol 3-kinase/AKT/NF-kappa B signalingYu Tzu Tai
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 101:2762-9. 2003.... - 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.... - 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 PKC in multiple myeloma: in vitro and in vivo effects of the novel, orally available small-molecule inhibitor enzastaurin (LY317615.HCl)Klaus Podar
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 109:1669-77. 2007.... - CD40 activation induces p53-dependent vascular endothelial growth factor secretion in human multiple myeloma cellsYu Tzu Tai
Department of Adult Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 99:1419-27. 2002..These studies demonstrate that CD40 induces VEGF secretion and MM cell migration, suggesting a role for CD40 in regulating MM homing and angiogenesis... - 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... - 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.... - Immunomodulatory effects of lenalidomide and pomalidomide on interaction of tumor and bone marrow accessory cells in multiple myelomaGullu Gorgun
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Blood 116:3227-37. 2010..These data therefore demonstrate that modulation of SOCS1 may enhance immune response and efficacy of IMiDs in MM... - Blockade of XBP1 splicing by inhibition of IRE1α is a promising therapeutic option in multiple myelomaNaoya Mimura
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA
Blood 119:5772-81. 2012..Taken together, our results demonstrate that blockade of XBP1 splicing by inhibition of IRE1α endoribonuclease domain is a potential therapeutic option in MM... - 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... - A high-affinity fully human anti-IL-6 mAb, 1339, for the treatment of multiple myelomaMariateresa Fulciniti
Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Clin Cancer Res 15:7144-52. 2009.... - Investigational agent MLN9708/2238 targets tumor-suppressor miR33b in MM cellsZe Tian
LeBow Institute for Myeloma Therapeutics and Jerome Lipper Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Blood 120:3958-67. 2012..Our results show that miR33b is a tumor suppressor that plays a role during MLN2238-induced apoptotic signaling in MM cells, and these data provide the basis for novel therapeutic strategies targeting miR33b in MM... 
The selective adhesion molecule inhibitor Natalizumab decreases multiple myeloma cell growth in the bone marrow microenvironment: therapeutic implicationsKlaus Podar
Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Boston, MA 02115, USA
Br J Haematol 155:438-48. 2011..Our data therefore provide the rationale for the clinical evaluation of Natalizumab, preferably in combination with novel agents (e.g. bortezomib) to enhance MM cytotoxicity and improve patient outcome...- Nuclear factor-kappaB p65 mediates tumor necrosis factor alpha-induced nuclear translocation of telomerase reverse transcriptase proteinMasaharu Akiyama
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 63:18-21. 2003..These studies suggest that NF-kappaB p65 plays a pivotal role in regulating telomerase by modulating its nuclear translocation... - Dual inhibition of canonical and noncanonical NF-κB pathways demonstrates significant antitumor activities in multiple myelomaClaire Fabre
Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA
Clin Cancer Res 18:4669-81. 2012.... - MHC class I chain-related protein A antibodies and shedding are associated with the progression of multiple myelomaMasahisa Jinushi
Department of Medical Oncology and Cancer Vaccine Center, Dana Farber Cancer Institute, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 105:1285-90. 2008..Together, these findings reveal that the alterations in the NKG2D pathway are associated with the progression from MGUS to MM and raise the possibility that anti-MICA monoclonal antibodies might prove therapeutic for these disorders... - Critical role for hematopoietic cell kinase (Hck)-mediated phosphorylation of Gab1 and Gab2 docking proteins in interleukin 6-induced proliferation and survival of multiple myeloma cellsKlaus Podar
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
J Biol Chem 279:21658-65. 2004.... - Hsp27 inhibits release of mitochondrial protein Smac in multiple myeloma cells and confers dexamethasone resistanceDharminder Chauhan
Jerome Lipper Multiple Myeloma Center, Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA
Blood 102:3379-86. 2003..Moreover, AS-Hsp27 overcomes interleukin-6 (IL-6)-mediated protection against Dex-induced apoptosis. These data demonstrate that Hsp27 inhibits the release of Smac, and thereby confers Dex resistance in MM cells... - Targeting NAD+ salvage pathway induces autophagy in multiple myeloma cells via mTORC1 and extracellular signal-regulated kinase (ERK1/2) inhibitionMichele Cea
LeBow Institute for Myeloma Therapeutics, Harvard Medical School, Boston, MA, USA
Blood 120:3519-29. 2012..Our data therefore define a key role of Nampt in MM biology, providing the basis for a novel targeted therapeutic approach... - Significant biological role of sp1 transactivation in multiple myelomaMariateresa Fulciniti
Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Boston, Massachusetts, USA
Clin Cancer Res 17:6500-9. 2011..We here provide experimental and clinical evidence that Sp1 plays an important regulatory role in multiple myeloma (MM) cell growth and survival... - Targeting the beta-catenin/TCF transcriptional complex in the treatment of multiple myelomaKumar Sukhdeo
Department of Medical Oncology, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 104:7516-21. 2007..Taken together, these data demonstrate the efficacy of disrupting the beta-catenin/TCF transcriptional complex to exploit tumor dependence on Wnt signaling as a therapeutic approach in the treatment of MM... - Halofuginone inhibits multiple myeloma growth in vitro and in vivo and enhances cytotoxicity of conventional and novel agentsMerav Leiba
Department of Medical Oncology, The LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
Br J Haematol 157:718-31. 2012..Taken together, these preclinical studies provide the preclinical framework for future clinical studies of HF in MM... - Perspectives for combination therapy to overcome drug-resistant multiple myelomaLaurence Catley
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Mayer 551, 44 Binney Street, Boston, MA 02115, USA
Drug Resist Updat 8:205-18. 2005..As an increasing number of other novel therapeutics is identified and mechanisms of resistance are elucidated, combinations of these drugs will be developed to optimize new therapeutic regimens... - 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... - Myeloma-specific multiple peptides able to generate cytotoxic T lymphocytes: a potential therapeutic application in multiple myeloma and other plasma cell disordersJooeun Bae
Dana Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02115, USA
Clin Cancer Res 18:4850-60. 2012.... - Potent in vitro and in vivo activity of an Fc-engineered humanized anti-HM1.24 antibody against multiple myeloma via augmented effector functionYu Tzu Tai
LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Multiple Myeloma Research, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Blood 119:2074-82. 2012..These results support clinical development of XmAb5592, both as a monotherapy and in combination with lenalidomide, to improve patient outcome of MM... - Alkyl phospholipid perifosine induces myeloid hyperplasia in a murine myeloma modelLaurence Catley
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Mass, USA
Exp Hematol 35:1038-46. 2007..We investigated the effects of perifosine on the peripheral blood, bone marrow, and spleen of mice inoculated with subcutaneous plasmacytomas... - Specific killing of multiple myeloma cells by (-)-epigallocatechin-3-gallate extracted from green tea: biologic activity and therapeutic implicationsMasood A Shammas
Veterans Administration Boston Health Care System, and Dana Farber Cancer Institute/Harvard Medical School, 44 Binney Street, D1B25, Boston, MA 02115, USA
Blood 108:2804-10. 2006..Expression of related genes at the protein level were also confirmed by Western blot analysis. These data demonstrate potent and specific antimyeloma activity of EGCG and provide the rationale for its clinical evaluation... - 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 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... - A novel immunogenic CS1-specific peptide inducing antigen-specific cytotoxic T lymphocytes targeting multiple myelomaJooeun Bae
Dana Farber Cancer Institute, Boston, MA 02115, USA
Br J Haematol 157:687-701. 2012..In conclusion, this study introduced a novel immunogenic HLA-A2-specific CS1(239-247) peptide capable of inducing antigen-specific CTL against MM cells that will provide a framework for its application as a novel MM immunotherapy... - 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... - Targeting PI3K and RAD51 in Barrett's adenocarcinoma: impact on DNA damage checkpoints, expression profile and tumor growthJagannath Pal
Department of Adult Oncology, Harvard Dana Farber Cancer Institute, Boston, MA, USA
Cancer Genomics Proteomics 9:55-66. 2012..Simultaneous suppression of PI3K and RAD51, especially in cells with lower AKT expression, can significantly reduce their proliferative potential... - 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... - 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... - Generation of antitumor invariant natural killer T cell lines in multiple myeloma and promotion of their functions via lenalidomide: a strategy for immunotherapyWeihua Song
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute Harvard Medical School, Boston, MA 02115, USA
Clin Cancer Res 14:6955-62. 2008..Therefore, the development of functional iNKT cells may provide a novel strategy for the immunotherapy in multiple myeloma... - Anti-DKK1 mAb (BHQ880) as a potential therapeutic agent for multiple myelomaMariateresa Fulciniti
Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 114:371-9. 2009..These results confirm DKK1 as an important therapeutic target in myeloma and provide the rationale for clinical evaluation of BHQ880 to improve bone disease and to inhibit MM growth... - 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... - Patupilone (epothilone B) inhibits growth and survival of multiple myeloma cells in vitro and in vivoBoris Lin
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA
Blood 105:350-7. 2005..Taken together, these preclinical findings suggest that patupilone may be a safe and effective drug in the treatment of MM, providing the framework for clinical studies to improve patient outcome in MM... - Pretreatment mitochondrial priming correlates with clinical response to cytotoxic chemotherapyTríona Ní Chonghaile
Department of Medical Oncology, Dana Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, USA
Science 334:1129-33. 2011..In contrast, chemoresistant cancers and normal tissues were poorly primed. Manipulation of mitochondrial priming might enhance the efficacy of cytotoxic agents... - Phenotypic and functional effects of heat shock protein 90 inhibition on dendritic cellJooeun Bae
Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
J Immunol 178:7730-7. 2007.... - Emerging therapies for multiple myelomaKlaus Podar
Dana Farber Cancer Institute, Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Boston, MA 02115, USA
Expert Opin Emerg Drugs 14:99-127. 2009..This article reviews the scientific rationale of new therapy regimens and newly identified therapeutic agents - small molecules as well as therapeutic antibodies - that hold promise to further improve outcome in MM... - 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.... - 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.... - 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... - 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.... - Clinical, radiographic, and biochemical characterization of multiple myeloma patients with osteonecrosis of the jawNoopur Raje
The Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02114, USA
Clin Cancer Res 14:2387-95. 2008..Osteonecrosis of the jaw (ONJ) has been reported in patients with a history of aminobisphosphonate use. This study was conducted in order to define ONJ clinically and radiographically and gain insights into its pathophysiology... - 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... - 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.... - Novel epitope evoking CD138 antigen-specific cytotoxic T lymphocytes targeting multiple myeloma and other plasma cell disordersJooeun Bae
Dana Farber Cancer Institute, Boston, MA, USA
Br J Haematol 155:349-61. 2011..In conclusion, a novel immunogenic CD138(260-268) (GLVGLIFAV) peptide can induce antigen-specific CTL, which might be useful for the treatment of MM patients with peptide-based vaccine or cellular immunotherapy strategies... - Establishment of BCWM.1 cell line for Waldenström's macroglobulinemia with productive in vivo engraftment in SCID-hu miceDaniel Ditzel Santos
Bing Center for Waldenstrom s Macroglobulinemia, Dana Farber Cancer Institute, Boston, Massachusetts, USA
Exp Hematol 35:1366-75. 2007.... - Identification of novel antigens with induced immune response in monoclonal gammopathy of undetermined significanceSimona Blotta
Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 114:3276-84. 2009..These findings demonstrate OFD1 as an important immune target and highlight its possible role in signal transduction and tumorigenesis in MGUS and 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... - Cytokines modulate telomerase activity in a human multiple myeloma cell lineMasaharu Akiyama
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 62:3876-82. 2002..These studies therefore demonstrate that telomerase activity is associated with cell growth, survival, and drug resistance in MM cells... - Aggresome induction by proteasome inhibitor bortezomib and alpha-tubulin hyperacetylation by tubulin deacetylase (TDAC) inhibitor LBH589 are synergistic in myeloma cellsLaurence Catley
Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
Blood 108:3441-9. 2006..These data confirm the potential clinical benefit of combining HDAC inhibitors with proteasome inhibitors, and provide insight into the mechanisms of synergistic anti-MM activity of bortezomib in combination with LBH589... - 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... - p38 MAPK inhibition enhances PS-341 (bortezomib)-induced cytotoxicity against multiple myeloma cellsTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Mayer 557, 44 Binney Street, Boston, MA 02115, USA
Oncogene 23:8766-76. 2004..These studies therefore provide the framework for clinical trials of SCIO-469 to enhance sensitivity and overcome resistance to PS-341, thereby improving patient outcome in MM... - Essential role of caveolae in interleukin-6- and insulin-like growth factor I-triggered Akt-1-mediated survival of multiple myeloma cellsKlaus Podar
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 278:5794-801. 2003..Taken together, this study identifies caveolin-1 and other structural membrane components as potential new therapeutic targets in multiple myeloma... - Effects of oligonucleotide N3'-->P5' thio-phosphoramidate (GRN163) targeting telomerase RNA in human multiple myeloma cellsMasaharu Akiyama
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Cancer Res 63:6187-94. 2003.... - MYD88 L265P in Waldenström macroglobulinemia, immunoglobulin M monoclonal gammopathy, and other B-cell lymphoproliferative disorders using conventional and quantitative allele-specific polymerase chain reactionLian Xu
Bing Center for Waldenstrom s Macroglobulinemia, Dana Farber Cancer Institute, Boston, MA 02215, USA
Blood 121:2051-8. 2013..The finding of this mutation in many IgM MGUS patients suggests that MYD88 L265P may be an early oncogenic event in WM pathogenesis... - Translocation of Ku86/Ku70 to the multiple myeloma cell membrane: functional implicationsYu-Tzu Tai
The Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA
Exp Hematol 30:212-20. 2002..Therefore, targeting Ku86 and Ku70, with blocking peptides for example, might serve as a novel treatment strategy in human MM... - Recombinant humanized anti-CD40 monoclonal antibody triggers autologous antibody-dependent cell-mediated cytotoxicity against multiple myeloma cellsToshiaki Hayashi
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
Br J Haematol 121:592-6. 2003..This study, therefore, both demonstrates that rhuCD40 mAb triggers autologous ADCC against patient MM cells and provides the framework for the clinical evaluation of rhuCD40 mAb immunotherapy to improve patient outcome in MM... - Bruton's tyrosine kinase: oncotarget in myelomaYu Tzu Tai
LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
Oncotarget 3:913-4. 2012.... - Antibody-based therapies in multiple myelomaYu Tzu Tai
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Bone Marrow Res 2011:924058. 2011.... - Tumour cell/dendritic cell fusions as a vaccination strategy for multiple myelomaNoopur Raje
Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA
Br J Haematol 125:343-52. 2004..These studies therefore demonstrated that MM/DC FC can trigger an autologous immune response to MM cells and formed the framework for a clinical trial currently underway... - Mitochondrial H2O2 regulates the angiogenic phenotype via PTEN oxidationKip M Connor
Centers for Immunology and Microbial Disease, Neuropharmacology and Neuroscience, and Cell Biology and Cancer Research, Albany Medical College, Albany, New York 12208, USA
J Biol Chem 280:16916-24. 2005.... - CD52 is expressed on human mast cells and is a potential therapeutic target in Waldenstrom's Macroglobulinemia and mast cell disordersDaniel Ditzel Santos
Bing Center for Waldenstrom s Macroglobulinemia, Dana Farber Cancer Institute
Clin Lymphoma Myeloma 6:478-83. 2006..One potential target of alemtuzumab is bone marrow mast cells (BMMCs), which provide growth and survival signaling for WM lymphoplasmacytic cells... - Neurospheres modified to produce glial cell line-derived neurotrophic factor increase the survival of transplanted dopamine neuronsThor Ostenfeld
Cambridge Centre for Brain Repair, University of Cambridge, Forvie Site, Cambridge, United Kingdom
J Neurosci Res 69:955-65. 2002....