Research Topics
| G D RoodmanSummaryAffiliation: University of Pittsburgh Country: USA Publications
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Detail Information
Publications
Biology of osteoclast activation in cancerG D Roodman
University of Texas Health Science Center at San Antonio and Audie Murphy Veterans Administration Hospital, San Antonio, TX 78284, USA
J Clin Oncol 19:3562-71. 2001..Understanding of the molecular mechanisms responsible for osteoclast activation in osteolytic metastases should lead to development of novel therapeutic approaches for this highly morbid and potentially fatal complication of cancer...- Role of stromal-derived cytokines and growth factors in bone metastasisG David Roodman
School of Medicine Hematology Oncology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA
Cancer 97:733-8. 2003..Bone is a storehouse of latent growth factors produced by stromal cells and osteoblasts that, when activated during osteoclastic bone resorption, can enhance the growth of tumor cells... - Mechanisms of bone metastasisG David Roodman
Department of Medicine, Division of Hematology-Oncology, University of Pittsburgh, School of Medicine/Hematology, The University of Pittsburgh Cancer Institute, Pittsburgh, PA 15213, USA
N Engl J Med 350:1655-64. 2004 - Macrophage inflammatory protein-1alpha is an osteoclastogenic factor in myeloma that is independent of receptor activator of nuclear factor kappaB ligandJ H Han
Department of Medicine/Hematology, University of Texas Health Science Center, San Antonio, TX 78284, USA
Blood 97:3349-53. 2001..Blood. 2001;97:3349-3353).. - Osteoclasts formed by measles virus-infected osteoclast precursors from hCD46 transgenic mice express characteristics of pagetic osteoclastsS V Reddy
Department of Medicine/Hematology, University of Texas Health Science Center, San Antonio, Texas 78229, USA
Endocrinology 142:2898-905. 2001.... - Ibandronate decreases bone disease development and osteoclast stimulatory activity in an in vivo model of human myelomaJ C Cruz
Department of Medicine, Texas Tech University, Lubbock, TX, USA
Exp Hematol 29:441-7. 2001..These data demonstrate that early treatment of ARH-77 mice with IB prior to development of myeloma bone disease decreases OSA and possibly retards the development of lytic lesions, but not eventual tumor burden... - Cell biology of the osteoclastG D Roodman
Department of Medicine, University of Texas Health Science Center, San Antonio, USA
Exp Hematol 27:1229-41. 1999..The recent development of osteoclast cell lines may make it possible for major advances to our understanding of the biology of the osteoclast to be realized in the near future... - ADAM8: a novel osteoclast stimulating factorS J Choi
Department of Medicine Hematology, University of Texas Health Science Center, San Antonio, USA
J Bone Miner Res 16:814-22. 2001..Western blot analysis confirmed that the soluble form of ADAM8 is present in normal marrow cultures. These data suggest that ADAM8 plays an important role in OCL formation and acts primarily at the later stages of OCL differentiation... - Osteoclast inhibitory peptide 2 inhibits osteoclast formation via its C-terminal fragmentS J Choi
Department of Medicine/Hematology, University of Texas Health Science Center, San Antonio, USA
J Bone Miner Res 16:1804-11. 2001..These data show that the CTF of OIP-2, rather than the mature enzyme, mediates the inhibitory effects of OIP-2 through a putative receptor on OCL precursors... 
Pathogenesis of myeloma bone diseaseG D Roodman
Veterans Affairs Pittsburgh Healthcare System, Department of Medicine Hematology Oncology, University of Pittsburgh, Pittsburgh, PA 15240, USA
Leukemia 23:435-41. 2009..The basis for this severe imbalance between increased osteoclastic bone resorption and decreased bone formation has been a topic of intensive investigation over the last several years and will be reviewed in this article...
Annexin II increases osteoclast formation by stimulating the proliferation of osteoclast precursors in human marrow culturesC Menaa
Department of Medicine Hematology, University of Texas Health Science Center, San Antonio, Texas 78284, USA Audie Murphy Veterans Administration Hospital, San Antonio, Texas 78284, USA
J Clin Invest 103:1605-13. 1999..Taken together, these data suggest that AXII stimulates OCL formation by activating T cells through a putative receptor to secrete GM-CSF. GM-CSF then expands the OCL precursor pool to enhance OCL formation...- Studies in Paget's disease and their relevance to oncologyG D Roodman
Department of Medicine/Hematology, University of Texas Health Science Center, San Antonio, TX, USA
Semin Oncol 28:15-21. 2001..Paget's disease provides an ideal model in which to investigate the efficacy of the new third-generation bisphosphonates in the treatment of bone metastases as well as nonmalignant bone disease... - Antisense inhibition of macrophage inflammatory protein 1-alpha blocks bone destruction in a model of myeloma bone diseaseS J Choi
Department of Medicine/Hematology, University of Texas Health Science Center, San Antonio, Texas, USA
J Clin Invest 108:1833-41. 2001..These data support an important role for MIP-1alpha in cell homing, survival, and bone destruction in MM... - A murine model of inflammatory bone diseaseT A Hentunen
Department of Medicine Hematology, University of Texas Health Science Center, San Antonio, USA
Bone 26:183-8. 2000.... - Interleukin-6 enhances hypercalcemia and bone resorption mediated by parathyroid hormone-related protein in vivoJ de la Mata
Department of Medicine, University of Texas Health Science Center, San Antonio 78284, USA
J Clin Invest 95:2846-52. 1995..We conclude that IL-6 stimulatory effects on osteoclast precursors may enhance the effects of other bone resorption factors that act at later stages in the osteoclast lineage... - Paget's disease of bone: a disease of the osteoclastS V Reddy
Department of Medicine, Division of Hematology, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX, USA
Rev Endocr Metab Disord 2:195-201. 2001..1). The basis for the abnormalities detected in Paget's disease and the role that the paramyxoviruses may play in this disease are still unclear... - Myeloma bone diseaseN S Callander
Department of Medicine/Hematology, University of Texas Health Science Center, San Antonio, TX, USA
Semin Hematol 38:276-85. 2001..Treatment of myeloma bone disease includes radiation therapy, vertebroplasty, surgery, and bisphosphonates. New developments on the pathogenesis and treatment of myeloma bone disease present great opportunities to combat bone disease... - Assignment of OSTF1 to human chromosome bands 12q24.1-->q24.2 by in situ hybridizationR Schaub
Department of Cellular and Structural Biology, The University of Texas Health Science Center, San Antonio, TX 78284, USA
Cytogenet Cell Genet 88:87-8. 2000 - Treatment strategies for bone diseaseG D Roodman
Department of Medicine Hematology Oncology, VA Pittsburgh Healthcare System, University of Pittsburgh, Pittsburgh, PA 15240, USA
Bone Marrow Transplant 40:1139-46. 2007..New therapies that can target both the tumor as well as the severe bone disease should be on the horizon to treat this devastating complication of myeloma... - Tumor necrosis factor enhances parathyroid hormone-related protein-induced hypercalcemia and bone resorption without inhibiting bone formation in vivoH L Uy
Department of Medicine, University of Texas Health Sciences Center, San Antonio 78284 7877, USA
Cancer Res 57:3194-9. 1997.... - Isolation and characterization of a cDNA clone encoding a novel peptide (OSF) that enhances osteoclast formation and bone resorptionS Reddy
Department of Medicine Hematology Endocrinology, the Veterans Administration Medical Center and The University of Texas Health Science Center, San Antonio, USA
J Cell Physiol 177:636-45. 1998.... - Genetic linkage of Paget disease of the bone to chromosome 18qJ D Cody
Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78284, USA
Am J Hum Genet 61:1117-22. 1997..40, with the genetic marker D18S42, a marker tightly linked to the FEO locus. This demonstrates that the gene(s) responsible for FEO and that for Paget disease are either closely linked or the same locus... - Cloning and characterization of the 5'-flanking region of the mouse tartrate-resistant acid phosphatase geneS V Reddy
Department of Medicine, University of Texas Health Science Center, San Antonio
J Bone Miner Res 8:1263-70. 1993..The availability of the TRAP promoter may also permit production of transgenic mice, which can be used to develop previously unavailable osteoclast cell lines... - Mutation of the sequestosome 1 (p62) gene increases osteoclastogenesis but does not induce Paget diseaseNoriyoshi Kurihara
VA Pittsburgh Healthcare System, Research and Development, Pittsburgh, Pennsylvania 15240, USA
J Clin Invest 117:133-42. 2007.... - Combination mammalian target of rapamycin inhibitor rapamycin and HSP90 inhibitor 17-allylamino-17-demethoxygeldanamycin has synergistic activity in multiple myelomaLanie K Francis
University of Pittsburgh Cancer Institute, Division of Hematology/Oncology, Department of Internal Medicine, Pittsburgh, Pennsylvania, USA
Clin Cancer Res 12:6826-35. 2006..CONCLUSIONS: These studies provide the basis for potential clinical evaluation of this combination for multiple myeloma patients... - SDX-308, a nonsteroidal anti-inflammatory agent, inhibits NF-kappaB activity, resulting in strong inhibition of osteoclast formation/activity and multiple myeloma cell growthRentian Feng
Division of Hematology Oncology, University of Pittsburgh Cancer Institute, PA 15232, USA
Blood 109:2130-8. 2007..We propose that SDX-308 is a promising therapeutic candidate to inhibit multiple myeloma growth and osteoclast activity and that it should receive attention for further study... - Eosinophil chemotactic factor-L (ECF-L) enhances osteoclast formation by increasing in osteoclast precursors expression of LFA-1 and ICAM-1Veronica Garcia-Palacios
Department of Medicine, Division of Hematology Oncology, University of Pittsburgh, Pittsburgh, PA, USA
Bone 40:316-22. 2007..Taken together, these results demonstrate that ECF-L enhances RANKL and 1,25-(OH)2D3-induced OCL formation by increasing adhesive interactions between OCL precursors through increased expression of ICAM-1 and LFA-1... - Alpha9beta1: a novel osteoclast integrin that regulates osteoclast formation and functionHongwei Rao
Medicine Hematology Oncology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
J Bone Miner Res 21:1657-65. 2006..Antibody to alpha(9) inhibited OCL formation in human marrow cultures, and OCLs from alpha(9) knockout mice had a defect in actin ring reorganization and an impaired bone resorption capacity... - Chemokines in multiple myelomaRohit Aggarwal
Department of Internal Medicine, University of Pittsburgh, Pittsburgh, PA 15240, USA
Exp Hematol 34:1289-95. 2006.... - Multiple myeloma bone disease: Pathophysiology of osteoblast inhibitionNicola Giuliani
Cattedra e Unità Operativa UO di Ematologia Centro Trapianti Midollo Osseo CTMO, Universita degli Studi di Parma, Italy
Blood 108:3992-6. 2006..Recently, the biologic mechanisms involved in the osteoblast inhibition induced by MM cells have begun to be elucidated. In this article, the pathophysiology underlying osteoblast inhibition in MM is reviewed... - Eosinophil chemotactic factor-L (ECF-L) enhances osteoclast formation by increasing ICAM-1 expressionVeronica Garcia-Palacios
Medicine/Hematology-Oncology (111-H, University Drive C, Pittsburgh, PA 15240, USA
Ann N Y Acad Sci 1068:240-3. 2006..Furthermore, ECF-L Fc did not enhance OCL formation by ICAM-1 knockout (KO) cells. Increased expression of ICAM-1 by ECF-L appears to be critical for its effects on OCL formation... - Bone-breaking cancer treatmentG David Roodman
Nat Med 13:25-6. 2007 - Ultrastructure of bone cells in Paget's disease of boneFrederick R Singer
John Wayne Cancer Institute, Santa Monica, California 90404, USA
J Bone Miner Res 21:P51-4. 2006 - Experimental models of Paget's diseaseNoriyoshi Kurihara
University of Pittsburgh, Department of Medicine/Hematology-Oncology, Pittsburgh, Pennsylvania, USA
J Bone Miner Res 21:P55-7. 2006..CONCLUSION: These results show that expression of MVNP in OCL in vivo results in a bone phenotype that is characteristic of PD... - New potential targets for treating myeloma bone diseaseG David Roodman
Department of Medicine Hematology Oncology, University of Pittsburgh and VA Pittsburgh Healthcare System, Medicine Hematology Oncology, Pittsburgh, Pennsylvania 15240, USA
Clin Cancer Res 12:6270s-6273s. 2006..The basis for both the increased bone destruction and decreased bone formation has been a topic of extensive investigation during the last several years... - 1alpha,25-Dihydroxyvitamin D(3)-26,23-lactam analogues function as vitamin D receptor antagonists in human and rodent cellsSeiichi Ishizuka
Teijin Institute for Bio Medical Research, Hino, Tokyo, Japan
J Steroid Biochem Mol Biol 110:269-77. 2008..In contrast, (23S)-25-deoxy-1alpha-hydroxyvitamin D(3)-26,23-lactone, which only blocks human VDR, these vitamin D antagonists can block VDR in human cells and rodent cells... - Bone building with bortezomibG David Roodman
Office of Research and Development, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania 15240, USA
J Clin Invest 118:462-4. 2008.... - Pathophysiology of myeloma bone diseaseFlavia R Esteve
University of Pittsburgh, Medicine Hematology Oncology, 5150 Centre Avenue, Pittsburgh, PA 15213, USA
Best Pract Res Clin Haematol 20:613-24. 2007..In addition, we also review the emerging data on novel targeted therapies aimed at ameliorating myeloma bone disease... - Perspective on the osteoclast: an angiogenic cell?Frank C Cackowski
University of Pittsburgh School of Medicine, Hematology Oncology, Pittsburgh, Pennsylvania, USA
Ann N Y Acad Sci 1117:12-25. 2007.... - Pathophysiology of multiple myeloma bone diseaseSuzanne Lentzsch
Division of Hematology Oncology, Department of Medicine, University of Pittsburgh, and Division of Hematology Oncology, Veterans Administration Pittsburgh Healthcare System, Research and Development, PA 15232, USA
Hematol Oncol Clin North Am 21:1035-49, viii. 2007..In this article, the pathophysiology underlying the imbalanced bone remodeling and potential new strategies for the treatment of bone disease in multiple myeloma are reviewed... - RANK ligand as a therapeutic target for bone metastases and multiple myelomaG David Roodman
University of Pittsburgh School of Medicine and VA Medical Center, VA Pittsburgh Healthcare System, Research and Development 151 U, Pittsburgh, PA 15240, USA
Cancer Treat Rev 34:92-101. 2008..This manuscript will review how RANKL contributes to skeletal complications of cancer and the development of targeted, mechanism-based drugs that inhibit RANKL... - SDX-308 and SDX-101, non-steroidal anti-inflammatory drugs, as therapeutic candidates for treating hematologic malignancies including myelomaSuzanne Lentzsch
University of Pittsburgh Cancer Institute, Division of Hematology Oncology, Pittsburgh, PA 15232, USA
Arch Pharm (Weinheim) 340:511-6. 2007..This review covers future application of SDX-308 as an anti-myeloma drug regulating increased osteoclast activity... - Monocyte chemotactic protein-1 mediates prostate cancer-induced bone resorptionYi Lu
Department of Medicine, University of Pittsburgh, University Drive, Pittsburgh, PA 15240, USA
Cancer Res 67:3646-53. 2007..This study may provide novel therapeutic targets for treatment of prostate cancer skeletal metastasis... - Role of the microenvironment in multiple myeloma bone diseaseAlissa Huston
University of Pittsburgh Cancer Institute, and VA Pittsburgh Healthcare System, Research and Development, PA 15240, USA
Future Oncol 2:371-8. 2006.... - Normalizing the bone marrow microenvironment with p38 inhibitor reduces multiple myeloma cell proliferation and adhesion and suppresses osteoclast formationAaron N Nguyen
Scios Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
Exp Cell Res 312:1909-23. 2006..Collectively, these results suggest that SCIO-469 treatment can suppress factors in the bone marrow microenvironment to inhibit MM cell proliferation and adhesion and also to alleviate osteolytic activation in MM... - Paget disease of boneG David Roodman
Department of Medicine, Division of Hematology Oncology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15240, USA
J Clin Invest 115:200-8. 2005..In this review, the pathophysiology of PD and evidence for both a genetic and a viral etiology for PD will be discussed... - (23S)-25-Dehydro-1{alpha}-hydroxyvitamin D3-26,23-lactone, a vitamin D receptor antagonist that inhibits osteoclast formation and bone resorption in bone marrow cultures from patients with Paget's diseaseSeiichi Ishizuka
Veterans Affairs Pittsburgh Healthcare System, Research and Development (151-U, University Drive, Pittsburgh, Pennsylvania 15240, USA
Endocrinology 146:2023-30. 2005..These results demonstrate that TEI-9647 can suppress the excessive bone resorption and OCL formation seen in marrow cultures from patients with PD... - Vitamin D antagonist, TEI-9647, inhibits osteoclast formation induced by 1alpha,25-dihydroxyvitamin D3 from pagetic bone marrow cellsSeiichi Ishizuka
Department of Bone and Calcium Metabolism, Teijin Institute for Bio Medical Research, Hino, Tokyo, Japan
J Steroid Biochem Mol Biol 89:331-4. 2004..These results suggest that TEI-9647 acts directly on osteoclast precursors and osteoclasts, and that TEI-9647 may be a novel agent to suppress the excessive bone resorption and osteoclast formation in patients with Paget's disease... - Role of TAFII-17, a VDR binding protein, in the increased osteoclast formation in Paget's DiseaseNoriyoshi Kurihara
Department of Medicine/Hematology and Oncology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
J Bone Miner Res 19:1154-64. 2004..TAFII-17 can bind VDR at low concentrations of 1,25(OH)2D3. These results suggest that MVNP expression in Paget's OCL precursors increases expression of a component(s) of the VDR transcription complex that can increase OCL formation... - MIP-1 alpha and myeloma bone diseaseG David Roodman
Bone Biology Center, University of Pittsburgh Medical Center, University of Pittsburgh, PA 15261, USA
Cancer Treat Res 118:83-100. 2004.... - Pathogenesis of myeloma bone diseaseG David Roodman
Department of Medicine Hematology Oncology, University of Pittsburgh, Pittsburgh, PA 15213, USA
Blood Cells Mol Dis 32:290-2. 2004..This overview will focus on the factors recently identified that appear to play an important role in the bone destructive process in myeloma... - Functional role for heat shock factors in the transcriptional regulation of human RANK ligand gene expression in stromal/osteoblast cellsJennifer L Roccisana
Department of Medicine Division of Hematology, The University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA
J Biol Chem 279:10500-7. 2004..These data further suggest that HSF-2 is a downstream target of b-FGF to induce RANKL expression in stromal/osteoblast cells, and that HSF may play an important role in modulating RANKL gene expression in the bone microenvironment... - IL-3 expression by myeloma cells increases both osteoclast formation and growth of myeloma cellsJun Won Lee
Department of Medicine, Hematology Oncology Division, University of Pittsburgh, and Department of Vetrerans Affairs Medical Center, PA 15213, USA
Blood 103:2308-15. 2004..These data suggest that increased IL-3 levels in the bone marrow microenvironment of MM patients with imbalanced AML-1A and AML-1B expression can increase bone destruction and tumor cell growth... - Role of the bone marrow microenvironment in multiple myelomaG David Roodman
Center for Bone Biology, Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, Pennsylvania 15261, USA
J Bone Miner Res 17:1921-5. 2002..In addition, potential therapeutic agents under investigation, which included RANKL antagonists, protein prenylation inhibitors, and osteoblast growth factors, were discussed... - SV40 T antigen and telomerase are required to obtain immortalized human adult bone cells without loss of the differentiated phenotypeChristian Darimont
Nestle Research Center, 1000 Lausanne 26, Switzerland
Cell Growth Differ 13:59-67. 2002..These results demonstrate that reconstitution of telomerase activity in transformed SV40 T-antigen human osteoblast precursors or marrow stromal cells leads to the generation of immortalized cells with a preserved phenotype... - MIP-1alpha utilizes both CCR1 and CCR5 to induce osteoclast formation and increase adhesion of myeloma cells to marrow stromal cellsYasuo Oba
Department of Medicine Hematology Oncology Division, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA
Exp Hematol 33:272-8. 2005..Several chemokine receptors (CCR1, CCR5, and CCR9) mediate the effects of MIP-1alpha. In this study, we determined which of these mediates the effects of MIP-1alpha on human OCL formation and myeloma cells... - The role of immune cells and inflammatory cytokines in Paget's disease and multiple myelomaLori A Ehrlich
Department of Medicine/Hematology-Oncology, University of Pittsburgh, Pittsburgh, PA 15240, USA
Immunol Rev 208:252-66. 2005..This article discusses the role of immune cells and inflammatory cytokines and chemokines in the increased OCL activity in PD and MM bone disease, as well as the potential role of interleukin-3 in the suppression of OBL activity in MM... - Regulation of osteoclast differentiationG David Roodman
University of Pittsburgh, School of Medicine Hematology Oncology, VA Pittsburgh Healthcare System, R and D 151 U, Room 2E 113, University Drive C, Pittsburgh, PA 15240, USA
Ann N Y Acad Sci 1068:100-9. 2006..OCL differentiation is controlled by exogenous hormones and cytokines as well as autocrine-paracrine factors that positively or negatively regulate OCL proliferation and differentiation... - IL-3 is a potential inhibitor of osteoblast differentiation in multiple myelomaLori A Ehrlich
Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA
Blood 106:1407-14. 2005..These data suggest that IL-3 plays a dual role in the bone destructive process in myeloma by both stimulating osteoclasts and indirectly inhibiting osteoblast formation... - Expression of measles virus nucleocapsid protein in osteoclasts induces Paget's disease-like bone lesions in miceNoriyoshi Kurihara
Medicine/Hem-Onc, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
J Bone Miner Res 21:446-55. 2006..CONCLUSIONS: These results show that persistent expression of the MVNP gene in cells of the OCL lineage can induce pagetic-like bone lesions in vivo... - Annexin II stimulates RANKL expression through MAPKFanghong Li
Department of Medicine Hematology Oncology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
J Bone Miner Res 20:1161-7. 2005..Thus, both GM-CSF and RANKL are required for AX-II stimulation of OCL formation... - Cloning and characterization of the annexin II receptor on human marrow stromal cellsGanwei Lu
Medicine Hematology Oncology, University of Pittsburgh, Pittsburgh, Pennsylvania 15240, USA
J Biol Chem 281:30542-50. 2006..Importantly, the annexin II receptor antibody dose-dependently blocked the stimulatory effects of annexin II on human osteoclast formation, demonstrating that the receptor mediates the effects of annexin II on osteoclast formation... - Eosinophil chemotactic factor-L (ECF-L): a novel osteoclast stimulating factorYasuo Oba
Department of Medicine Hematology Oncology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
J Bone Miner Res 18:1332-41. 2003..ECF-L enhanced OCL formation without increasing RANKL levels. Anti-ECF-L inhibited RANKL-induced OCL formation. These results support a potent role of ECF-L in osteoclastogenesis... - AML-1A and AML-1B regulation of MIP-1alpha expression in multiple myelomaSun J Choi
Department of Medicine Hematology Oncology, University of Pittsburgh, PA, USA
Blood 101:3778-83. 2003..The data suggest that strategies that enhance AML-1B expression or decrease AML-1A in MM cells may be beneficial therapeutically... - Legumain expression in relation to clinicopathologic and biological variables in colorectal cancerRaghavendra Vasudeva Murthy
Department of Oncology, Institute of Biomedicine and Surgery, University of Linkoping, S 581 85 Linkoping, Sweden
Clin Cancer Res 11:2293-9. 2005..However, there is no study examining the relationship of legumain expression to clinocopathologic and biological variables in colorectal cancers... - Mechanisms of regulation of CXCR4/SDF-1 (CXCL12)-dependent migration and homing in multiple myelomaYazan Alsayed
University of Pittsburgh Cancer Institute, Division of Hematology Oncology, Department of Internal Medicine, University of Pittsburgh, PA, USA
Blood 109:2708-17. 2007..This study, therefore, demonstrates that SDF-1/CXCR4 is a critical regulator of MM homing and that it provides the framework for inhibitors of this pathway to be used in future clinical trials to abrogate MM trafficking... - Myeloma bone disease: pathogenesis and treatmentG David Roodman
Center of Bone Biology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA
Oncology (Williston Park) 19:983-4, 986. 2005..multiplemyeloma.org and are published on a regular basis in ONCOLOGY. For more information about the interactive series, see the MMRF ad on page 1089... - High bone turnover markers predict poor outcome in patients with bone metastasisG David Roodman
J Clin Oncol 23:4821-2. 2005 - Paget's disease-a VDR coactivator disease?Noriyoshi Kurihara
Department of Medicine Hematology, University of Pittsburgh, Kaufmann Medical Building, Suite 601, 3471 Fifth Avenue, Pittsburgh, PA 15213, USA
J Steroid Biochem Mol Biol 89:321-5. 2004.... - Advances in treating metastatic bone cancer: summary statement for the First Cambridge ConferenceAllan Lipton
Milton S Hershey Medical Center, Penn State University College of Medicine, Hershey, Pennsylvania 17033 0850, USA, and Department of Oncology, Norwegian Radium Hospital, Oslo, Norway
Clin Cancer Res 12:6209s-6212s. 2006..The conclusions reached during the 2-day meeting are summarized in this article and presented in more detail in the individual articles and accompanying discussion sessions that comprise the conference proceedings... - Tumor lysis syndrome following thalidomide and dexamethasone therapy for newly diagnosed multiple myelomaAlissa Huston
Exp Hematol 34:1616. 2006 - Sequence analysis of measles virus nucleocapsid transcripts in patients with Paget's diseaseWilliam E Friedrichs
Department of Medicine/Hematology, University of Texas Health Science Center, San Antonio, USA
J Bone Miner Res 17:145-51. 2002..These findings are consistent with the presence of a chronic MV infection in affected sites from these patients with Paget's disease...