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Article ; Online: Pathogenesis of myeloma bone disease.

Roodman, G D

2009 Volume 23, Issue 3, Page(s) 435–441

Abstract: Bone disease in multiple myeloma (MM) is characterized by lytic bone lesions, which can cause severe bone pain, pathologic fractures and hypercalcemia. However, the lytic bone disease in MM differs from that in other cancer patients who have lytic bone ... ...

Abstract	Bone disease in multiple myeloma (MM) is characterized by lytic bone lesions, which can cause severe bone pain, pathologic fractures and hypercalcemia. However, the lytic bone disease in MM differs from that in other cancer patients who have lytic bone metastases. Although increased osteoclastic bone destruction is involved in MM and other tumors involving bone, in contrast to other tumors, once the MM tumor burden exceeds 50% in a local area, osteoblast activity is either suppressed or absent. 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.
MeSH term(s)	Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents/therapeutic use ; Boronic Acids/therapeutic use ; Bortezomib ; Cell Adhesion ; Cytokines/secretion ; Denosumab ; Fractures, Spontaneous/etiology ; Fractures, Spontaneous/physiopathology ; Glucocorticoids/adverse effects ; Glucocorticoids/therapeutic use ; Humans ; Hypercalcemia/etiology ; Hypercalcemia/physiopathology ; Immunologic Factors/therapeutic use ; Interleukins/physiology ; Multiple Myeloma/complications ; Multiple Myeloma/secretion ; Neoplasm Proteins/physiology ; Osteoblasts/pathology ; Osteoclasts/physiology ; Osteolysis/chemically induced ; Osteolysis/etiology ; Osteolysis/physiopathology ; Pyrazines/therapeutic use ; RANK Ligand/therapeutic use ; Stromal Cells/physiology ; Wnt Proteins/physiology
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; Boronic Acids ; Cytokines ; Glucocorticoids ; Immunologic Factors ; Interleukins ; Neoplasm Proteins ; Pyrazines ; RANK Ligand ; Wnt Proteins ; Denosumab (4EQZ6YO2HI) ; Bortezomib (69G8BD63PP)
Language	English
Publishing date	2009-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/leu.2008.336
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Zs.A 2295: Show issues

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Article: Treatment strategies for bone disease.

Roodman, G D

Bone marrow transplantation

2007 Volume 40, Issue 12, Page(s) 1139–1146

Abstract: Multiple myeloma is characterized by extensive bone destruction with little or no new bone formation. A multiplicity of factors including receptor activator NF-kappaB (RANKL), macrophage inflammatory protein-1alpha, interleukin-3 and interleukin-6 can ... ...

Abstract	Multiple myeloma is characterized by extensive bone destruction with little or no new bone formation. A multiplicity of factors including receptor activator NF-kappaB (RANKL), macrophage inflammatory protein-1alpha, interleukin-3 and interleukin-6 can induce osteoclast formation in myeloma and drive the bone destructive process. Furthermore, factors are also produced either in the microenvironment or by myeloma cells themselves, which inhibit osteoblast differentiation and new bone formation. The combination of increased osteoclast formation with little or no bone repair in response to the previous bone destruction explains the severity of the bone disease in myeloma. Studies of the pathophysiology of myeloma bone disease have identified several novel therapeutic targets. These include antibodies to RANKL, chemokine receptor antagonists, which block the effects of chemokines on osteoclast differentiation and proteasome antagonists, which can affect both RANKL production and osteoprotegerin levels as well as inhibit osteoclast and enhance osteoblast differentiation. In addition, many of the new biologic agents being used for the treatment of patients with myeloma also further inhibit the bone destructive process. 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.
MeSH term(s)	Bone Diseases/etiology ; Bone Diseases/therapy ; Drug Delivery Systems/methods ; Humans ; Multiple Myeloma/complications ; Multiple Myeloma/drug therapy ; Osteolysis/etiology ; Osteolysis/pathology
Language	English
Publishing date	2007-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	632854-4
ISSN	1476-5365 ; 0268-3369 ; 0951-3078
ISSN (online)	1476-5365
ISSN	0268-3369 ; 0951-3078
DOI	10.1038/sj.bmt.1705802
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Zs.A 2168: Show issues

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Article: Mechanisms of bone resorption in myeloma.

Roodman, G D

Journal of musculoskeletal & neuronal interactions

2003 Volume 3, Issue 4, Page(s) 271–2; discussion 292–4

Language	English
Publishing date	2003-12
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2041366-X
ISSN	1108-7161
ISSN	1108-7161
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Zs.A 5401: Show issues

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Article ; Online: Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction.

Sabol, Hayley M / Amorim, Tânia / Ashby, Cody / Halladay, David / Anderson, Judith / Cregor, Meloney / Sweet, Megan / Nookaew, Intawat / Kurihara, Noriyoshi / Roodman, G David / Bellido, Teresita / Delgado-Calle, Jesus

Neoplasia (New York, N.Y.)

2022 Volume 28, Page(s) 100785

Abstract: In multiple myeloma (MM), communication via Notch signaling in the tumor niche stimulates tumor progression and bone destruction. We previously showed that osteocytes activate Notch, increase Notch3 expression, and stimulate proliferation in MM cells. We ...

Abstract	In multiple myeloma (MM), communication via Notch signaling in the tumor niche stimulates tumor progression and bone destruction. We previously showed that osteocytes activate Notch, increase Notch3 expression, and stimulate proliferation in MM cells. We show here that Notch3 inhibition in MM cells reduced MM proliferation, decreased Rankl expression, and abrogated the ability of MM cells to promote osteoclastogenesis. Further, Notch3 inhibition in MM cells partially prevented the Notch activation and increased proliferation induced by osteocytes, demonstrating that Notch3 mediates MM-osteocyte communication. Consistently, pro-proliferative and pro-osteoclastogenic pathways were upregulated in CD138
MeSH term(s)	Animals ; Cell Communication ; Humans ; Mice ; Multiple Myeloma/metabolism ; Multiple Myeloma/pathology ; Osteocytes/metabolism ; Osteocytes/pathology ; Osteogenesis ; Osteolysis ; Receptor, Notch3/genetics ; Receptor, Notch3/metabolism ; Signal Transduction
Chemical Substances	NOTCH3 protein, human ; Receptor, Notch3
Language	English
Publishing date	2022-04-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2022.100785
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Zs.A 5203: Show issues

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Article: Biology of osteoclast activation in cancer.

Roodman, G D

Journal of clinical oncology : official journal of the American Society of Clinical Oncology

2001 Volume 19, Issue 15, Page(s) 3562–3571

Abstract: Bone is a frequent site of cancer metastasis. Bone metastases can result in bone destruction or new bone formation. Bone destruction is mediated by factors produced or induced by tumor cells that stimulate formation and activation of osteoclasts, the ... ...

Abstract	Bone is a frequent site of cancer metastasis. Bone metastases can result in bone destruction or new bone formation. Bone destruction is mediated by factors produced or induced by tumor cells that stimulate formation and activation of osteoclasts, the normal bone-resorbing cells. Local bone destruction also occurs in patients with osteoblastic metastases and may precede or occur simultaneously with increased bone formation. Several factors, including interleukin (IL)-1, IL-6, receptor activator of NF-kappaB (RANK) ligand, parathyroid hormone-related protein (PTHrP), and macrophage inflammatory protein-1-alpha (MIP-1alpha), have been implicated as factors that enhance osteoclast formation and bone destruction in patients with neoplasia. PTHrP seems to be the major factor produced by breast cancer cells that induces osteoclast formation through upregulation of RANK ligand. Enhanced RANK ligand expression also plays an important role in bone destruction in patients with myeloma. RANK ligand can act to enhance the effects of other factors produced by myeloma cells or in response to myeloma cells, such as MIP-1alpha and/or IL-6, to induce osteoclast formation. 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.
MeSH term(s)	Animals ; Bone Neoplasms/secondary ; Bone Resorption/complications ; Bone Resorption/pathology ; Cell Differentiation/physiology ; Humans ; Neoplasms/complications ; Neoplasms/pathology ; Osteoclasts/cytology ; Osteoclasts/pathology
Language	English
Publishing date	2001-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	604914-x
ISSN	1527-7755 ; 0732-183X
ISSN (online)	1527-7755
ISSN	0732-183X
DOI	10.1200/JCO.2001.19.15.3562
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Zs.A 1847: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 650: Show issues

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Article: Studies in Paget's disease and their relevance to oncology.

Roodman, G D

Seminars in oncology

2001 Volume 28, Issue 4 Suppl 11, Page(s) 15–21

Abstract: Paget's disease and bone metastases in cancer patients share many common properties. Both are characterized by a localized increase in osteoclast (OCL) formation leading to bone resorption. In both Paget's disease and bone metastases the increased OCL ... ...

Abstract	Paget's disease and bone metastases in cancer patients share many common properties. Both are characterized by a localized increase in osteoclast (OCL) formation leading to bone resorption. In both Paget's disease and bone metastases the increased OCL formation and the increased osteoclastogenic nature of the bone microenvironment are mediated by common factors, namely interleukin (IL)-6 and RANK ligand (RANKL). Available data suggest that in the case of Paget's disease there is increased RANKL and IL-6 production, and IL-6 enhances the responsivity of the OCL precursors to RANKL, contributing to the elevated numbers of OCLs. In patients with multiple myeloma, 95% to 100% of whom develop bone lesions, both IL-6 and RANKL levels are increased. Bisphosphonates bind locally to the surfaces of the bone undergoing osteoclastic resorption to inhibit this process. Paget's disease has in the past and will continue in the future to provide a model to test the efficacy of bisphosphonates in inhibiting bone resorption. 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.
MeSH term(s)	Bone Neoplasms/pathology ; Bone Neoplasms/physiopathology ; Bone Neoplasms/secondary ; Carrier Proteins/metabolism ; Diphosphonates/pharmacology ; Humans ; Interleukin-2/metabolism ; Membrane Glycoproteins/metabolism ; Osteitis Deformans/pathology ; Osteitis Deformans/physiopathology ; Osteoclasts ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B
Chemical Substances	Carrier Proteins ; Diphosphonates ; Interleukin-2 ; Membrane Glycoproteins ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B ; TNFRSF11A protein, human ; TNFSF11 protein, human
Language	English
Publishing date	2001-08-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	189220-4
ISSN	1532-8708 ; 0093-7754
ISSN (online)	1532-8708
ISSN	0093-7754
DOI	10.1016/s0093-7754(01)90227-1
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Zs.A 1348: Show issues

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Article: Mechanisms of abnormal bone turnover in Paget's disease.

Roodman, G D

Bone

1999 Volume 24, Issue 5 Suppl, Page(s) 39S–40S

MeSH term(s)	Bone and Bones/metabolism ; Humans ; Morbillivirus/physiology ; Morbillivirus Infections/metabolism ; Osteitis Deformans/metabolism ; Osteitis Deformans/virology ; Osteoclasts/metabolism ; Osteoclasts/virology ; RNA, Viral/genetics
Chemical Substances	RNA, Viral
Language	English
Publishing date	1999-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/s8756-3282(99)00045-9
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Zs.A 1571: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 332: Show issues

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Article: Osteoclast differentiation and activity.

Roodman, G D

Biochemical Society transactions

1998 Volume 26, Issue 1, Page(s) 7–13

MeSH term(s)	Cell Differentiation ; Cell Lineage ; Osteoclasts/cytology
Language	English
Publishing date	1998-02
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/bst0260007
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Zs.A 944: Show issues

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Article: Cell biology of the osteoclast.

Roodman, G D

Experimental hematology

1999 Volume 27, Issue 8, Page(s) 1229–1241

Abstract: The osteoclast is a hematopoietic cell derived from CFU-GM and branches from the monocyte-macrophage lineage early during the differentiation process. The marrow microenvironment appears critical for osteoclast formation due to production of RANK ligand, ...

Abstract	The osteoclast is a hematopoietic cell derived from CFU-GM and branches from the monocyte-macrophage lineage early during the differentiation process. The marrow microenvironment appears critical for osteoclast formation due to production of RANK ligand, a recently described osteoclast differentiation factor, by marrow stromal cells in response to a variety of osteotropic factors. In addition, factors such as osteoprotegerin, a newly described inhibitor of osteoclast formation, as well as secretory products produced by the osteoclast itself and other cells in the marrow enhance or inhibit osteoclast formation. The identification of the role of oncogenes such as c-fos and pp60 c-src in osteoclast differentiation and bone resorption have provided important insights in the regulation of normal osteoclast activity. Current research is beginning to delineate the signaling pathways involved in osteoclastic bone resorption and osteoclast formation in response to cytokines and hormones. 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.
MeSH term(s)	Animals ; Apoptosis ; Bone Marrow/metabolism ; Bone Resorption/physiopathology ; CHO Cells ; Carrier Proteins/metabolism ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cell Separation ; Cricetinae ; Cytokines/physiology ; Glycoproteins/physiology ; Hormones/physiology ; Humans ; Membrane Glycoproteins/metabolism ; Mice ; Organ Culture Techniques/methods ; Osteoclasts/cytology ; Osteoclasts/drug effects ; Osteoclasts/physiology ; Osteoprotegerin ; Proto-Oncogenes ; RANK Ligand ; Rats ; Receptor Activator of Nuclear Factor-kappa B ; Receptors, Cytoplasmic and Nuclear ; Receptors, Tumor Necrosis Factor ; Signal Transduction ; Stromal Cells/metabolism ; Transfection
Chemical Substances	Carrier Proteins ; Cytokines ; Glycoproteins ; Hormones ; Membrane Glycoproteins ; Osteoprotegerin ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B ; Receptors, Cytoplasmic and Nuclear ; Receptors, Tumor Necrosis Factor ; TNFRSF11A protein, human ; TNFRSF11B protein, human ; TNFSF11 protein, human ; Tnfrsf11a protein, mouse ; Tnfrsf11b protein, mouse ; Tnfrsf11b protein, rat ; Tnfsf11 protein, mouse
Language	English
Publishing date	1999-08
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	185107-x
ISSN	1873-2399 ; 0301-472X ; 0531-5573
ISSN (online)	1873-2399
ISSN	0301-472X ; 0531-5573
DOI	10.1016/s0301-472x(99)00061-2
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Zs.A 922: Show issues

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Article ; Online: Osteoclast-derived IGF1 is required for pagetic lesion formation in vivo.

Miyagawa, Kazuaki / Ohata, Yasuhisa / Delgado-Calle, Jesus / Teramachi, Jumpei / Zhou, Hua / Dempster, David D / Subler, Mark A / Windle, Jolene J / Chirgwin, John M / Roodman, G David / Kurihara, Noriyoshi

JCI insight

2020 Volume 5, Issue 6

Abstract: We report that transgenic mice expressing measles virus nucleocapsid protein (MVNP) in osteoclasts (OCLs) (MVNP mice) are Paget's disease (PD) models and that OCLs from patients with PD and MVNP mice express high levels of OCL-derived IGF1 (OCL-IGF1). To ...

Abstract	We report that transgenic mice expressing measles virus nucleocapsid protein (MVNP) in osteoclasts (OCLs) (MVNP mice) are Paget's disease (PD) models and that OCLs from patients with PD and MVNP mice express high levels of OCL-derived IGF1 (OCL-IGF1). To determine OCL-IGF1's role in PD and normal bone remodeling, we generated WT and MVNP mice with targeted deletion of Igf1 in OCLs (Igf1-cKO) and MVNP/Igf1-cKO mice, and we assessed OCL-IGF1's effects on bone mass, bone formation rate, EphB2/EphB4 expression on OCLs and osteoblasts (OBs), and pagetic bone lesions (PDLs). A total of 40% of MVNP mice, but no MVNP/Igf1-cKO mice, had PDLs. Bone volume/tissue volume (BV/TV) was decreased by 60% in lumbar vertebrae and femurs of MVNP/Igf1-cKO versus MVNP mice with PDLs and by 45% versus all MVNP mice tested. Bone formation rates were decreased 50% in Igf1-cKO and MVNP/Igf1-cKO mice versus WT and MVNP mice. MVNP mice had increased EphB2 and EphB4 levels in OCLs/OBs versus WT and MVNP/Igf1-cKO, with none detectable in OCLs/OBs of Igf1-cKO mice. Mechanistically, IL-6 induced the increased OCL-IGF1 in MVNP mice. These results suggest that high OCL-IGF1 levels increase bone formation and PDLs in PD by enhancing EphB2/EphB4 expression in vivo and suggest OCL-IGF1 may contribute to normal bone remodeling.
MeSH term(s)	Animals ; Bone Remodeling/physiology ; Disease Models, Animal ; Humans ; Insulin-Like Growth Factor I/metabolism ; Mice ; Mice, Transgenic ; Nucleocapsid Proteins ; Osteitis Deformans/metabolism ; Osteitis Deformans/pathology ; Osteoclasts/metabolism
Chemical Substances	Nucleocapsid Proteins ; measles virus nucleocapsid protein ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2020-03-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.133113
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