Research Topics
Genomes and Genes
| Klaus PodarSummaryAffiliation: Harvard University Country: USA Publications
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Detail Information
Publications
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....
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... - 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... - 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... - 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... - 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.... - 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.... - 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.... - 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... - 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.... - 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... - 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... - 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... - 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... - 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... - 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.... - 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.... - 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... - 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... - 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... - 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... - 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.... - 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... - 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... - 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.... - 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... - 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.... - 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... - 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.... - 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... - 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... - 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... - 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... - 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... - 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.... - 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: 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... - 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.... - 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... - 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... - Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive oxygen speciesJeong H Kim
Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
Blood 105:1717-23. 2005..Finally, these results hint at novel targets for drug development that may aid traditional therapy... - 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... - 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.... - 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... - Combination of the mTOR inhibitor rapamycin and CC-5013 has synergistic activity in multiple myelomaNoopur Raje
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, VA Boston Healthcare System and Harvard Medical School, Boston, MA 02115, USA
Blood 104:4188-93. 2004..These studies, therefore, provide the framework for clinical evaluation of mTOR inhibitors combined with IMiDs to improve patient outcome in MM... 
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...- Combination therapy with interleukin-6 receptor superantagonist Sant7 and dexamethasone induces antitumor effects in a novel SCID-hu In vivo model of human multiple myelomaPierfrancesco Tassone
Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute and VA Boston Healthcare System, Harvard Medical School, Boston, Massachusetts 02115, USA
Clin Cancer Res 11:4251-8. 2005.... - Superoxide-dependent and -independent mitochondrial signaling during apoptosis in multiple myeloma cellsDharminder Chauhan
Department of Medical Oncology, The Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Oncogene 22:6296-300. 2003.... - 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... - 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... - Biologic sequelae of I{kappa}B kinase (IKK) inhibition in multiple myeloma: therapeutic implicationsTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Blood 113:5228-36. 2009..Combination therapy targeting these kinases therefore represents a promising treatment strategy in MM... - Perifosine, an oral bioactive novel alkylphospholipid, inhibits Akt and induces in vitro and in vivo cytotoxicity in human multiple myeloma cellsTeru Hideshima
Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Mayer 557, 44 Binney Street, Boston, MA 02115, USA
Blood 107:4053-62. 2006..Taken together, our data provide the rationale for clinical trials of perifosine 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... - 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... - 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... - 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.... - 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... - 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... - VEGF induces Mcl-1 up-regulation and protects multiple myeloma cells against apoptosisSteven Le Gouill
Jerome Lipper Multiple Myeloma Center Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA
Blood 104:2886-92. 2004..Our studies therefore demonstrate that VEGF-induced MM cell proliferation and survival are mediated via Mcl-1, providing the preclinical framework for novel therapeutics targeting Mcl-1 and/or VEGF to improve patient outcome in MM... - 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... - Multiple myelomaMarc S Raab
LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Multiple Myeloma Research, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
Lancet 374:324-39. 2009..This treatment framework promises to improve outcome not only for patients with multiple myeloma, but also with other haematological malignancies and solid tumours... - The Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenesGerlinde Wernig
Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
Blood 111:3751-9. 2008..Overall, our results suggest that constitutive activation of Jak2 requires an intact FERM domain for a transforming phenotype, and is necessary for activation of the major target of Jak2, STAT5... - 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... - Critical role for Gab2 in transformation by BCR/ABLMartin Sattler
Dana Farber Cancer Institute, Department of Adult Oncology, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
Cancer Cell 1:479-92. 2002..Our results identify Gab2 and its associated proteins as key determinants of the lineage and severity of BCR/ABL transformation... - 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... - 2-Methoxyestradiol overcomes drug resistance in multiple myeloma cellsDharminder Chauhan
Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02215, USA
Blood 100:2187-94. 2002..They provide a framework for the use of 2ME2, either alone or in combination with Dex, to overcome drug resistance and to improve outcome in MM... - A novel small molecule met inhibitor induces apoptosis in cells transformed by the oncogenic TPR-MET tyrosine kinaseMartin Sattler
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 63:5462-9. 2003..The characterization of SU11274 as an effective inhibitor of Met tyrosine kinase activity illustrates the potential of targeting for Met therapeutic use in cancers associated with activated forms of this kinase... - Effects of PKC412, nilotinib, and imatinib against GIST-associated PDGFRA mutants with differential imatinib sensitivityEllen Weisberg
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
Gastroenterology 131:1734-42. 2006..In this study, we compare the effects of 3 tyrosine kinase inhibitors, PKC412 and nilotinib, and imatinib, on 2 GIST-related PDGFRA mutants, V561D and D842V, which possess differential sensitivity to imatinib... - The malignant clone and the bone-marrow environmentKlaus Podar
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Best Pract Res Clin Haematol 20:597-612. 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... - 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 signalling pathways for the treatment of multiple myelomaKlaus Podar
Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Expert Opin Ther Targets 9:359-81. 2005..Close collaboration between basic researchers and clinicians will be required to further improve our knowledge of MM pathophysiologically in order to translate advances from the bench to the bedside and improve patient outcome... - Inhibition of VEGF signaling pathways in multiple myeloma and other malignanciesKlaus Podar
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Cell Cycle 6:538-42. 2007..Our own and others' work suggest that VEGF-inhibitors e.g., the small molecule VEGF receptor inhibitor pazopanib, may also improve patient outcome in MM... - Blockade of ubiquitin-conjugating enzyme CDC34 enhances anti-myeloma activity of Bortezomib/Proteasome inhibitor PS-341Dharminder Chauhan
Department of Medical Oncology, Harvard Medical School, The Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
Oncogene 23:3597-602. 2004.... - The therapeutic role of targeting protein kinase C in solid and hematologic malignanciesKlaus Podar
Dana Farber Cancer Institute, Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, 44 Binney Street, Boston, MA 02115, USA
Expert Opin Investig Drugs 16:1693-707. 2007..Therefore, it is necessary to further dissect the relative contribution of PKC isozymes in the development and progression of specific tumors in order to identify therapeutic opportunities, using either PKC inhibitors or PKC activators... - Targeting the vascular endothelial growth factor pathway in the treatment of multiple myelomaKlaus Podar
Dana Farber Cancer Institute, Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Boston, MA 02115, USA
Expert Rev Anticancer Ther 7:551-66. 2007..Important contributing effectors are tumor cell-stroma cell and cell-extracellular matrix contacts, the bone marrow vasculature, and a variety of cytokines and growth factors in the bone marrow milieu...