K C Anderson

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc A novel proteasome inhibitor NPI-0052 as an anticancer therapy
    D Chauhan
    Department of Medical Oncology, Harvard Medical School, Dana Farber Cancer Institute, The Jerome Lipper Multiple Myeloma Center, Boston, MA 02115, USA
    Br J Cancer 95:961-5. 2006
  2. pmc A novel rapid-onset high-penetrance plasmacytoma mouse model driven by deregulation of cMYC cooperating with KRAS12V in BALB/c mice
    Y Hu
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Multiple Myeloma Research, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Blood Cancer J 3:e156. 2013
  3. pmc Fatty acid synthase is a novel therapeutic target in multiple myeloma
    Yutaka Okawa
    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
    Br J Haematol 141:659-71. 2008
  4. ncbi request reprint Therapeutic advances in relapsed or refractory multiple myeloma
    Kenneth C Anderson
    Kraft Family Professor of Medicine, Harvard Medical School, Boston, Massachusetts, USA
    J Natl Compr Canc Netw 11:676-9. 2013
  5. doi request reprint The 39th David A. Karnofsky Lecture: bench-to-bedside translation of targeted therapies in multiple myeloma
    Kenneth C Anderson
    Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, 450 Brookline Ave, Boston, MA 02115 5450, USA
    J Clin Oncol 30:445-52. 2012
  6. pmc Proteasome inhibition, the pursuit of new cancer therapeutics, and the adaptor molecule p130Cas
    Dharminder Chauhan
    The 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
    BMC Biol 9:72. 2011
  7. pmc Targeting the UPS as therapy in multiple myeloma
    Dharminder Chauhan
    The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    BMC Biochem 9:S1. 2008
  8. doi request reprint Oncogenomics to target myeloma in the bone marrow microenvironment
    Kenneth C Anderson
    Dana Farber Cancer Institute, Medical Oncology, Boston, Massachusetts 02115, USA
    Clin Cancer Res 17:1225-33. 2011
  9. ncbi request reprint Development of effective new treatments for multiple myeloma
    Kenneth C Anderson
    Division of Hematologic Neoplasia, Dana Farber Cancer Institute, Boston, MA 02115, USA
    J Clin Oncol 23:7207-11. 2005
  10. ncbi request reprint Clinically relevant end points and new drug approvals for myeloma
    K C Anderson
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Leukemia 22:231-9. 2008

Research Grants

  1. CHARACTERIZATION OF GROWTH FACTOR RESPONSIVE B CELLS
    Kenneth Anderson; Fiscal Year: 1993
  2. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2005
  3. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2006
  4. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2007
  5. Host-Tumor Cell Interactions in Myeloma: Therapeutic Applications
    Kenneth Anderson; Fiscal Year: 2007
  6. Specialized Program of Research Excellence in Myeloma
    Kenneth Anderson; Fiscal Year: 2007
  7. Molecular Sequelae of Myeloma-Bone Marrow Interactions: Therapeutic Applications
    Kenneth Anderson; Fiscal Year: 2009
  8. Molecular Sequelae of Myeloma-Bone Marrow Interactions: Therapeutic Applications
    Constantine S Mitsiades; Fiscal Year: 2010
  9. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2004
  10. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2003

Detail Information

Publications203 found, 100 shown here

  1. pmc A novel proteasome inhibitor NPI-0052 as an anticancer therapy
    D Chauhan
    Department of Medical Oncology, Harvard Medical School, Dana Farber Cancer Institute, The Jerome Lipper Multiple Myeloma Center, Boston, MA 02115, USA
    Br J Cancer 95:961-5. 2006
    ..These preclinical studies provided the basis for Phase-I clinical trial of NPI-0052 in relapsed/refractory MM patients...
  2. pmc A novel rapid-onset high-penetrance plasmacytoma mouse model driven by deregulation of cMYC cooperating with KRAS12V in BALB/c mice
    Y Hu
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Multiple Myeloma Research, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Blood Cancer J 3:e156. 2013
    ....
  3. pmc Fatty acid synthase is a novel therapeutic target in multiple myeloma
    Yutaka Okawa
    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
    Br J Haematol 141:659-71. 2008
    ..This report demonstrated that inhibition of FAS has anti-tumour activity against MM cells, suggesting that it represents a novel therapeutic target in MM...
  4. ncbi request reprint Therapeutic advances in relapsed or refractory multiple myeloma
    Kenneth C Anderson
    Kraft Family Professor of Medicine, Harvard Medical School, Boston, Massachusetts, USA
    J Natl Compr Canc Netw 11:676-9. 2013
    ....
  5. doi request reprint The 39th David A. Karnofsky Lecture: bench-to-bedside translation of targeted therapies in multiple myeloma
    Kenneth C Anderson
    Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, 450 Brookline Ave, Boston, MA 02115 5450, USA
    J Clin Oncol 30:445-52. 2012
    ..Myeloma therefore represents a paradigm for targeting the tumor in its microenvironment, which has already markedly improved patient outcome in MM and has great potential in other hematologic malignancies and solid tumors as well...
  6. pmc Proteasome inhibition, the pursuit of new cancer therapeutics, and the adaptor molecule p130Cas
    Dharminder Chauhan
    The 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
    BMC Biol 9:72. 2011
    ..Zhao and Vuori describe this month in BMC Biology experiments indicating a novel role of the adaptor protein p130Cas in sensitivity to apoptosis induced not only by proteasome inhibitors but also by the unrelated drug doxorubicin...
  7. pmc Targeting the UPS as therapy in multiple myeloma
    Dharminder Chauhan
    The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    BMC Biochem 9:S1. 2008
    ..PUBLICATION HISTORY : Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com)...
  8. doi request reprint Oncogenomics to target myeloma in the bone marrow microenvironment
    Kenneth C Anderson
    Dana Farber Cancer Institute, Medical Oncology, Boston, Massachusetts 02115, USA
    Clin Cancer Res 17:1225-33. 2011
    ..This paradigm of targeting the tumor in its microenvironment has already extended median survival in MM from 3 to 7 to 8 years and has great potential to improve patient outcome in other hematologic malignancies and solid tumors as well...
  9. ncbi request reprint Development of effective new treatments for multiple myeloma
    Kenneth C Anderson
    Division of Hematologic Neoplasia, Dana Farber Cancer Institute, Boston, MA 02115, USA
    J Clin Oncol 23:7207-11. 2005
  10. ncbi request reprint Clinically relevant end points and new drug approvals for myeloma
    K C Anderson
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Leukemia 22:231-9. 2008
    ..This manuscript will therefore be a most valuable resource to provide the framework for the design of appropriate clinical trial strategies for more rapid new drug approval in myeloma...
  11. ncbi request reprint 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 cells
    Tanyel 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...
  12. doi request reprint New insights into therapeutic targets in myeloma
    Kenneth C Anderson
    Dana Farber Cancer Institute, Boston, MA 02215, USA
    Hematology Am Soc Hematol Educ Program 2011:184-90. 2011
    ..With continued rapid evolution of progress in these areas, MM will be a chronic illness with sustained complete response in a significant number of patients...
  13. ncbi request reprint Lenalidomide and thalidomide: mechanisms of action--similarities and differences
    Kenneth C Anderson
    Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Semin Hematol 42:S3-8. 2005
    ..Our understanding of the mechanism of action of these agents has provided a platform for exciting clinical trials evaluating combinations of thalidomide and lenalidomide with both conventional chemotherapy and newer targeted agents...
  14. ncbi request reprint Moving disease biology from the lab to the clinic
    Kenneth C Anderson
    Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer 97:796-801. 2003
    ..Future studies should define the utility of these agents as primary therapy, treatment for first relapse, and maintenance therapy...
  15. ncbi request reprint Targeted therapy of multiple myeloma based upon tumor-microenvironmental interactions
    Kenneth C Anderson
    The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, and Harvard Medical School, Boston, MA 02115, USA
    Exp Hematol 35:155-62. 2007
    ..Importantly, gene-array, proteomic, and cell-signaling studies have not only helped to identify in vivo mechanisms of action and drug resistance to novel agents, but also aided in the design of promising combination-therapy protocols...
  16. ncbi request reprint A strategic framework for novel drug development in multiple myeloma
    Kenneth C Anderson
    Department of Medicine, Harvard Medical School, Division of Hematologic Neoplasia, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Br J Haematol 138:153-9. 2007
  17. doi request reprint Preclinical activity of P276-00, a novel small-molecule cyclin-dependent kinase inhibitor in the therapy of multiple myeloma
    N Raje
    Division of Hematologic Malignancies, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02114, USA
    Leukemia 23:961-70. 2009
    ..Finally, in vivo efficacy of P276-00 was confirmed in an MM xenograft model. These studies form the basis of an ongoing phase I study in the treatment of relapsed/refractory MM...
  18. ncbi request reprint The role of tumor necrosis factor alpha in the pathophysiology of human multiple myeloma: therapeutic applications
    T Hideshima
    Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, MA 02115, USA
    Oncogene 20:4519-27. 2001
    ..Agents which act to inhibit TNFalpha may therefore abrogate the paracrine growth and survival advantage conferred by MM cell adhesion in the BM microenvironment...
  19. ncbi request reprint Adherence of multiple myeloma cells to bone marrow stromal cells upregulates vascular endothelial growth factor secretion: therapeutic applications
    D Gupta
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Leukemia 15:1950-61. 2001
    ..These data demonstrate the importance of stromal-MM cell interactions in regulating VEGF and IL-6 secretion, and suggest additional mechanisms whereby thalidomide and IMiD1-CC4047 act against MM cells in the BM millieu...
  20. pmc microRNA expression in the biology, prognosis, and therapy of Waldenstr├Âm macroglobulinemia
    Aldo M Roccaro
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Blood 113:4391-402. 2009
    ..These data indicate that microRNAs play a pivotal role in the biology of WM; represent important prognostic marker; and provide the basis for the development of new microRNA-based targeted therapies in WM...
  21. ncbi request reprint TRAIL/Apo2L ligand selectively induces apoptosis and overcomes drug resistance in multiple myeloma: therapeutic applications
    C S Mitsiades
    Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Blood 98:795-804. 2001
    ..These preclinical studies suggest that TRAIL/Apo2L can overcome conventional drug resistance and provide the basis for clinical trials of TRAIL-based treatment regimens to improve outcome in patients with MM. (Blood. 2001;98:795-804)..
  22. ncbi request reprint The proteasome inhibitor PS-341 inhibits growth, induces apoptosis, and overcomes drug resistance in human multiple myeloma cells
    T Hideshima
    Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 61:3071-6. 2001
    ..Given the acceptable animal and human toxicity profile of PS-341, these studies provide the framework for clinical evaluation of PS-341 to improve outcome for patients with this universally fatal hematological malignancy...
  23. pmc CXCR4 inhibitor AMD3100 disrupts the interaction of multiple myeloma cells with the bone marrow microenvironment and enhances their sensitivity to therapy
    Abdel 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...
  24. ncbi request reprint 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 growth
    Hiroshi 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
    ....
  25. ncbi request reprint Identification of genes regulated by dexamethasone in multiple myeloma cells using oligonucleotide arrays
    Dharminder 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...
  26. ncbi request reprint Identification of genes regulated by 2-methoxyestradiol (2ME2) in multiple myeloma cells using oligonucleotide arrays
    Dharminder 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...
  27. ncbi request reprint NF-kappa B as a therapeutic target in multiple myeloma
    Teru 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...
  28. ncbi request reprint Novel therapies targeting the myeloma cell and its bone marrow microenvironment
    T Hideshima
    Department of Adult Oncology, Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Semin Oncol 28:607-12. 2001
    ..These data indicate that VEGF plays a pivotal role not only in neoangiogenesis in MM BM but also in proliferation and migration of tumor cells...
  29. ncbi request reprint Vascular endothelial growth factor triggers signaling cascades mediating multiple myeloma cell growth and migration
    K Podar
    Jerome Lipper Multiple Myeloma Center, Dana-Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Blood 98:428-35. 2001
    ..These observations provide the framework for novel therapeutic strategies targeting VEGF signaling cascades in MM...
  30. ncbi request reprint beta-lapachone, a novel plant product, overcomes drug resistance in human multiple myeloma cells
    Deepak Gupta
    Jerome Lipper Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Exp Hematol 30:711-20. 2002
    ..1S); MM cell lines resistant to dexamethasone (MM.1R), melphalan (RPMI8226/LR5), doxorubicin (RPMI8226/DOX40), and mitoxantrone (RPMI8226/ MR20); and MM cells from patients (MM1-MM4)...
  31. ncbi request reprint A pivotal role for Mcl-1 in Bortezomib-induced apoptosis
    K Podar
    Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 022115, USA
    Oncogene 27:721-31. 2008
    ..To prevent relapse of MM in patients treated with Bortezomib, we therefore recommend the combination of Bortezomib with agents that induce MM cell death independent of Mcl-1...
  32. ncbi request reprint High-dose chemoradiotherapy and anti-B-cell monoclonal antibody-purged autologous bone marrow transplantation in mantle-cell lymphoma: no evidence for long-term remission
    A S Freedman
    Division of Hematologic Malignancies and Biostatistics, Dana Farber Cancer Institute, Boston, MA 02115, USA
    J Clin Oncol 16:13-8. 1998
    ....
  33. ncbi request reprint A novel Bcl-2/Bcl-X(L)/Bcl-w inhibitor ABT-737 as therapy in multiple myeloma
    D Chauhan
    The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Oncogene 26:2374-80. 2007
    ....
  34. doi request reprint Lenalidomide inhibits osteoclastogenesis, survival factors and bone-remodeling markers in multiple myeloma
    I Breitkreutz
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics, Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Leukemia 22:1925-32. 2008
    ..We conclude that both agents specifically target key factors in osteoclastogenesis, and could directly affect the MM-OCL-BMSCs activation loop in osteolytic bone disease...
  35. ncbi request reprint Molecular mechanisms mediating antimyeloma activity of proteasome inhibitor PS-341
    Teru 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...
  36. pmc Molecular sequelae of proteasome inhibition in human multiple myeloma cells
    Nicholas 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...
  37. ncbi request reprint MLN120B, a novel IkappaB kinase beta inhibitor, blocks multiple myeloma cell growth in vitro and in vivo
    Teru 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
    ..The purpose of this study is to delineate the biological significance of IkappaB kinase (IKK) beta inhibition in multiple myeloma cells in the context of bone marrow stromal cells (BMSC) using a novel IKKbeta inhibitor MLN120B...
  38. ncbi request reprint Insulin-like growth factor-1 induces adhesion and migration in human multiple myeloma cells via activation of beta1-integrin and phosphatidylinositol 3'-kinase/AKT signaling
    Yu 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...
  39. ncbi request reprint Ku86 variant expression and function in multiple myeloma cells is associated with increased sensitivity to DNA damage
    Y T Tai
    Department of Adult Oncology, Dana Farber Cancer Institute, and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA
    J Immunol 165:6347-55. 2000
    ..Coupled with a recent report that Ku86 activity correlates with resistance to radiation and chemotherapy, these results have implications for the potential role of Ku86 as a novel therapeutic target...
  40. pmc AT7519, A novel small molecule multi-cyclin-dependent kinase inhibitor, induces apoptosis in multiple myeloma via GSK-3beta activation and RNA polymerase II inhibition
    L Santo
    Jerome Lipper Multiple Myeloma Disease Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Oncogene 29:2325-36. 2010
    ..These results offer new insights into the crucial, yet controversial role of GSK-3beta in MM and show significant anti-MM activity of AT7519, providing the rationale for its clinical evaluation in MM...
  41. ncbi request reprint Thalidomide and immunomodulatory derivatives augment natural killer cell cytotoxicity in multiple myeloma
    F E Davies
    Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Blood 98:210-6. 2001
    ..Thus in vitro and in vivo data support the hypothesis that Thal may mediate its anti-MM effect, at least in part, by modulating NK cell number and function...
  42. ncbi request reprint Tumor cell expression of CD59 is associated with resistance to CD20 serotherapy in patients with B-cell malignancies
    S P Treon
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston Massachusetts 02115, USA
    J Immunother 24:263-71. 2001
    ..A prospective, clinical study is assessing the role of these antigens in mediating rituximab resistance...
  43. ncbi request reprint Toxicity and efficacy of defined doses of CD4(+) donor lymphocytes for treatment of relapse after allogeneic bone marrow transplant
    E P Alyea
    Divisions of Hematologic Malignancies and Biostatistics, Dana Farber Cancer Institute, Boston, MA, USA
    Blood 91:3671-80. 1998
    ....
  44. ncbi request reprint Molecular characterization of PS-341 (bortezomib) resistance: implications for overcoming resistance using lysophosphatidic acid acyltransferase (LPAAT)-beta inhibitors
    Teru 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...
  45. ncbi request reprint A novel orally active proteasome inhibitor induces apoptosis in multiple myeloma cells with mechanisms distinct from Bortezomib
    Dharminder 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...
  46. ncbi request reprint Antitumor activity of lysophosphatidic acid acyltransferase-beta inhibitors, a novel class of agents, in multiple myeloma
    Teru 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...
  47. doi request reprint p38 mitogen-activated protein kinase inhibitor LY2228820 enhances bortezomib-induced cytotoxicity and inhibits osteoclastogenesis in multiple myeloma; therapeutic implications
    Kenji 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...
  48. ncbi request reprint Arsenic trioxide inhibits growth of human multiple myeloma cells in the bone marrow microenvironment
    Toshiaki 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...
  49. pmc The use of novel agents in the treatment of relapsed and refractory multiple myeloma
    J P Laubach
    Department of Medical Oncology, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA, USA
    Leukemia 23:2222-32. 2009
    ..This review focuses on the role of thalidomide, lenalidomide and bortezomib in relapsed and refractory MM, with additional discussion dedicated to emerging drugs in relapsed MM that may prove beneficial to patients with this disease...
  50. doi request reprint A novel role for CCL3 (MIP-1╬▒) in myeloma-induced bone disease via osteocalcin downregulation and inhibition of osteoblast function
    S Vallet
    Division of Hematology and Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA
    Leukemia 25:1174-81. 2011
    ..Our results show that CCL3, in addition to its known catabolic activity, reduces bone formation by inhibiting OB function, and therefore contributes to OB/OC uncoupling in MM...
  51. ncbi request reprint Novel etodolac analog SDX-308 (CEP-18082) induces cytotoxicity in multiple myeloma cells associated with inhibition of beta-catenin/TCF pathway
    H Yasui
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
    Leukemia 21:535-40. 2007
    ..Importantly, growth of MM cells adherent to bone marrow (BM) stromal cells is also significantly inhibited by SDX-308. Our data therefore indicate that the novel etodolac analog SDX-308 can target MM cells in the BM milieu...
  52. ncbi request reprint Didox, a ribonucleotide reductase inhibitor, induces apoptosis and inhibits DNA repair in multiple myeloma cells
    N Raje
    Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Boston, MA 02114, USA
    Br J Haematol 135:52-61. 2006
    ..7 as determined by the Chou-Talalay method. These studies therefore provide the preclinical rationale for evaluation of Didox, alone and in combination with DNA-damaging agents, to improve patient outcome in MM...
  53. doi request reprint Aurora kinase A is a target of Wnt/beta-catenin involved in multiple myeloma disease progression
    Jui 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...
  54. ncbi request reprint Targeting mitochondria to overcome conventional and bortezomib/proteasome inhibitor PS-341 resistance in multiple myeloma (MM) cells
    Dharminder 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...
  55. ncbi request reprint The biological sequelae of stromal cell-derived factor-1alpha in multiple myeloma
    Teru 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
    ....
  56. ncbi request reprint Combination therapy with interleukin-6 receptor superantagonist Sant7 and dexamethasone induces antitumor effects in a novel SCID-hu In vivo model of human multiple myeloma
    Pierfrancesco 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
    ....
  57. ncbi request reprint The vascular endothelial growth factor receptor tyrosine kinase inhibitor PTK787/ZK222584 inhibits growth and migration of multiple myeloma cells in the bone marrow microenvironment
    Boris 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...
  58. ncbi request reprint The bortezomib/proteasome inhibitor PS-341 and triterpenoid CDDO-Im induce synergistic anti-multiple myeloma (MM) activity and overcome bortezomib resistance
    Dharminder 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...
  59. ncbi request reprint NVP-LAQ824 is a potent novel histone deacetylase inhibitor with significant activity against multiple myeloma
    Laurence 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...
  60. pmc PI3K/p110{delta} is a novel therapeutic target in multiple myeloma
    Hiroshi 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...
  61. ncbi request reprint Transforming growth factor beta receptor I kinase inhibitor down-regulates cytokine secretion and multiple myeloma cell growth in the bone marrow microenvironment
    Toshiaki 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
    ....
  62. ncbi request reprint Moving disease biology from the laboratory to the clinic
    Kenneth C Anderson
    Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Semin Oncol 29:17-20. 2002
    ....
  63. ncbi request reprint The proteasome inhibitor PS-341 potentiates sensitivity of multiple myeloma cells to conventional chemotherapeutic agents: therapeutic applications
    Nicholas 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...
  64. ncbi request reprint The proteasome inhibitor bortezomib induces apoptosis in human retinoblastoma cell lines in vitro
    Vassiliki Poulaki
    Angiogenesis Laser Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts 02114, USA
    Invest Ophthalmol Vis Sci 48:4706-19. 2007
    ..NF-kappaB, which is constitutively active in human retinoblastoma cells and promotes their survival, represents a therapeutic target for patients with this malignancy...
  65. ncbi request reprint Biological pathways and in vivo antitumor activity induced by Atiprimod in myeloma
    P Neri
    Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Leukemia 21:2519-26. 2007
    ..Taken together, these data demonstrate the in vitro and in vivo antitumor activity of Atip, delineate potential molecular targets triggered by this agent, and provide a preclinical rational for its clinical evaluation in MM...
  66. ncbi request reprint Isolation and characterization of human multiple myeloma cell enriched populations
    Y T Tai
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    J Immunol Methods 235:11-9. 2000
    ..This immunomagnetic bead depletion method therefore permits the ready isolation of homogeneous populations of patient MM cells for use in both cellular and molecular studies...
  67. ncbi request reprint Concepts in the use of TRAIL/Apo2L: an emerging biotherapy for myeloma and other neoplasias
    N Mitsiades
    Department of Adult Oncology, Dana Farber Cancer Institute, Boston MA 02115, USA
    Expert Opin Investig Drugs 10:1521-30. 2001
    ..These studies provide a framework for the use of TRAIL/Apo2L as a single agent or as part of combination therapy for the treatment of MM...
  68. ncbi request reprint Biologic sequelae of interleukin-6 induced PI3-K/Akt signaling in multiple myeloma
    T Hideshima
    Jerome Lipper Multiple Myeloma Center, Department of Adult Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Oncogene 20:5991-6000. 2001
    ..Our data therefore suggest that PI3-K/Akt signaling mediates growth, survival, and cell cycle regulatory effects of IL-6 in MM...
  69. ncbi request reprint Novel biologically based therapies for myeloma
    K C Anderson
    Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer J 7:S19-23. 2001
    ..Adenoviral purging prior to autotransplantation and in vivo and ex vivo stimulation of autoimmune cells are discussed as potential approaches to address these problems...
  70. ncbi request reprint Targeting MEK1/2 blocks osteoclast differentiation, function and cytokine secretion in multiple myeloma
    Iris 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...
  71. doi request reprint Antimyeloma activity of the orally bioavailable dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235
    Douglas W McMillin
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 69:5835-42. 2009
    ..g., dexamethasone and doxorubicin) or novel (e.g., bortezomib) anti-MM agents showed lack of antagonism. These results indicate that BEZ235 merits clinical testing, alone and in combination with other agents, in MM...
  72. ncbi request reprint Cytotoxic activity of the maytansinoid immunoconjugate B-B4-DM1 against CD138+ multiple myeloma cells
    Pierfrancesco Tassone
    Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
    Blood 104:3688-96. 2004
    ....
  73. pmc Bortezomib induces canonical nuclear factor-kappaB activation in multiple myeloma cells
    Teru 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...
  74. ncbi request reprint A novel carbohydrate-based therapeutic GCS-100 overcomes bortezomib resistance and enhances dexamethasone-induced apoptosis in multiple myeloma cells
    Dharminder 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
    ....
  75. ncbi request reprint Immunomodulatory drug CC-5013 overcomes drug resistance and is well tolerated in patients with relapsed multiple myeloma
    Paul 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...
  76. ncbi request reprint Novel therapies for multiple myeloma
    Toshiaki 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
  77. ncbi request reprint Regulation of vascular endothelial growth factor expression by insulin-like growth factor I in thyroid carcinomas
    Vassiliki Poulaki
    Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts 02114, USA
    J Clin Endocrinol Metab 88:5392-8. 2003
    ....
  78. doi request reprint Ascorbic acid inhibits antitumor activity of bortezomib in vivo
    G Perrone
    Department of Medical Oncology, LeBow Institute for Myeloma Therapeutics and Jerome Lipper Myeloma Center, Harvard Medical School, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Leukemia 23:1679-86. 2009
    ....
  79. pmc The Akt pathway regulates survival and homing in Waldenstrom macroglobulinemia
    Xavier 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...
  80. pmc MicroRNAs 15a and 16 regulate tumor proliferation in multiple myeloma
    Aldo M Roccaro
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    Blood 113:6669-80. 2009
    ..These data indicate that microRNAs play a pivotal role in the biology of MM and represent important targets for novel therapies in MM...
  81. pmc Honokiol overcomes conventional drug resistance in human multiple myeloma by induction of caspase-dependent and -independent apoptosis
    Kenji 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...
  82. ncbi request reprint Novel inosine monophosphate dehydrogenase inhibitor VX-944 induces apoptosis in multiple myeloma cells primarily via caspase-independent AIF/Endo G pathway
    Kenji 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
    ....
  83. pmc Janus kinase inhibitor INCB20 has antiproliferative and apoptotic effects on human myeloma cells in vitro and in vivo
    Renate 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
    ....
  84. ncbi request reprint Functional significance of novel neurotrophin-1/B cell-stimulating factor-3 (cardiotrophin-like cytokine) for human myeloma cell growth and survival
    Renate 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...
  85. pmc Selective inhibition of chymotrypsin-like activity of the immunoproteasome and constitutive proteasome in Waldenstrom macroglobulinemia
    Aldo M Roccaro
    Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Blood 115:4051-60. 2010
    ..These findings suggest that targeting i20S and c20S CT-L activity by ONX0912 represents a valid antitumor therapy in WM...
  86. ncbi request reprint Targeting p38 MAPK inhibits multiple myeloma cell growth in the bone marrow milieu
    Teru 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...
  87. ncbi request reprint Activation of NF-kappaB and upregulation of intracellular anti-apoptotic proteins via the IGF-1/Akt signaling in human multiple myeloma cells: therapeutic implications
    Constantine 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...
  88. pmc A proto-oncogene BCL6 is up-regulated in the bone marrow microenvironment in multiple myeloma cells
    Teru Hideshima
    Jerome Lipper Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 115:3772-5. 2010
    ....
  89. ncbi request reprint Vascular endothelial growth factor-induced migration of multiple myeloma cells is associated with beta 1 integrin- and phosphatidylinositol 3-kinase-dependent PKC alpha activation
    Klaus 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...
  90. ncbi request reprint Patupilone (epothilone B) inhibits growth and survival of multiple myeloma cells in vitro and in vivo
    Boris 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...
  91. pmc Proteasome inhibitors disrupt the unfolded protein response in myeloma cells
    Ann Hwee Lee
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115 6017, USA
    Proc Natl Acad Sci U S A 100:9946-51. 2003
    ..Identification of compounds that target the activity of IRE1 alpha/XBP-1 may yield novel therapies for the treatment of multiple myeloma and other malignancies that rely on an intact UPR...
  92. pmc Telomerase inhibitor GRN163L inhibits myeloma cell growth in vitro and in vivo
    M A Shammas
    Department of Medicine, VA Boston Healthcare System, MA, USA
    Leukemia 22:1410-8. 2008
    ..Furthermore, GRN163L-induced myeloma cell death could be significantly enhanced by Hsp90 inhibitor 17AAG. These data provide the preclinical rationale for clinical evaluation of GRN163L in myeloma and in combination with 17AAG...
  93. pmc Blockade of the MEK/ERK signalling cascade by AS703026, a novel selective MEK1/2 inhibitor, induces pleiotropic anti-myeloma activity in vitro and in vivo
    Kihyun 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...
  94. ncbi request reprint Blockade of Hsp27 overcomes Bortezomib/proteasome inhibitor PS-341 resistance in lymphoma cells
    Dharminder 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...
  95. pmc JS-K has potent anti-angiogenic activity in vitro and inhibits tumour angiogenesis in a multiple myeloma model in vivo
    Tanyel Kiziltepe
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA, USA
    J Pharm Pharmacol 62:145-51. 2010
    ..We have designed a prodrug class that releases nitric oxide on metabolism by GST. O(2)-(2,4-Dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate (JS-K, a member of this class) has potent antineoplastic activity...
  96. ncbi request reprint FTY720 induces apoptosis in multiple myeloma cells and overcomes drug resistance
    Hiroshi 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...
  97. pmc Dual targeting of the proteasome regulates survival and homing in Waldenstrom macroglobulinemia
    Aldo 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...
  98. ncbi request reprint Novel therapies for multiple myeloma
    Joan J Ryoo
    Harvard Medical School, MA, USA
    Blood Rev 16:167-74. 2002
    ..In targeting tumor biology, these therapies serve as a model of treatment with great potential for improving outcomes in patients with MM...
  99. ncbi request reprint In vivo and in vitro cytotoxicity of R-etodolac with dexamethasone in glucocorticoid-resistant multiple myeloma cells
    Paola 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...
  100. ncbi request reprint Inhibition of Akt induces significant downregulation of survivin and cytotoxicity in human multiple myeloma cells
    Teru 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...
  101. ncbi request reprint GW654652, the pan-inhibitor of VEGF receptors, blocks the growth and migration of multiple myeloma cells in the bone marrow microenvironment
    Klaus Podar
    Department of Medical Oncology, Jerome Lipper Multiple Myeloma Center, Harvard Medical School, Boston, MA 02115, USA
    Blood 103:3474-9. 2004
    ....

Research Grants22

  1. CHARACTERIZATION OF GROWTH FACTOR RESPONSIVE B CELLS
    Kenneth Anderson; Fiscal Year: 1993
    ..Although these studies are encouraging, relapses suggest that improvements in ablative therapies in vivo and/or marrow purging methods in vitro are needed...
  2. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2005
    ..abstract_text> ..
  3. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2006
    ..abstract_text> ..
  4. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2007
    ..abstract_text> ..
  5. Host-Tumor Cell Interactions in Myeloma: Therapeutic Applications
    Kenneth Anderson; Fiscal Year: 2007
    ..Ultimately our goal is to validate MM-host cell interactions as a target for novel therapeutics to improve patient outcome in MM. ..
  6. Specialized Program of Research Excellence in Myeloma
    Kenneth Anderson; Fiscal Year: 2007
    ..abstract_text> ..
  7. Molecular Sequelae of Myeloma-Bone Marrow Interactions: Therapeutic Applications
    Kenneth Anderson; Fiscal Year: 2009
    ....
  8. Molecular Sequelae of Myeloma-Bone Marrow Interactions: Therapeutic Applications
    Constantine S Mitsiades; Fiscal Year: 2010
    ....
  9. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2004
    ..abstract_text> ..
  10. Role of Cytokines in Myeloma Pathogenesis
    Kenneth Anderson; Fiscal Year: 2003
    ..abstract_text> ..
  11. KSHV AND VIL6 IN THE PATHOGENESIS OF MULTIPLE MYELOMA
    Kenneth Anderson; Fiscal Year: 1999
    ..The PI's proposed experiments will define the significance of KSHV infection and MM and may provide the basis for novel treatment approaches which target KSHV or vIL-6 in MM. ..
  12. CHARACTERIZATION OF GROWTH FACTOR RESPONSIVE B CELLS
    Kenneth Anderson; Fiscal Year: 1992
    ..Although these studies are encouraging, relapses suggest that improvements in ablative therapies in vivo and/or marrow purging methods in vitro are needed...
  13. KSHV AND VIL6 IN THE PATHOGENESIS OF MULTIPLE MYELOMA
    Kenneth Anderson; Fiscal Year: 2000
    ..The PI's proposed experiments will define the significance of KSHV infection and MM and may provide the basis for novel treatment approaches which target KSHV or vIL-6 in MM. ..
  14. KSHV AND VIL6 IN THE PATHOGENESIS OF MULTIPLE MYELOMA
    Kenneth Anderson; Fiscal Year: 2001
    ..The PI's proposed experiments will define the significance of KSHV infection and MM and may provide the basis for novel treatment approaches which target KSHV or vIL-6 in MM. ..
  15. KSHV AND VIL6 IN THE PATHOGENESIS OF MULTIPLE MYELOMA
    Kenneth Anderson; Fiscal Year: 2002
    ..The PI's proposed experiments will define the significance of KSHV infection and MM and may provide the basis for novel treatment approaches which target KSHV or vIL-6 in MM. ..
  16. Molecular Sequelae of Myeloma-Bone Marrow Interactions: Therapeutic Applications
    KENNETH C contact ANDERSON; Fiscal Year: 2011
    ....