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  1. Book: Myeloma bone disease

    Roodman, G. David

    (Current clinical oncology)

    2010  

    Author's details ed. by G. David Roodman
    Series title Current clinical oncology
    Language English
    Size X, 252 S. : Ill., graph. Darst., 24 cm
    Publisher Humana Press
    Publishing place Pittsburgh, Pa
    Publishing country United States
    Document type Book
    HBZ-ID HT016427771
    ISBN 978-1-60761-553-8 ; 1-60761-553-3 ; 9781607615545 ; 1607615541
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: Deciphering Cancer and Bone Interactions for Therapeutic Benefits.

    Roodman, G David

    JBMR plus

    2019  Volume 3, Issue 3, Page(s) e10137

    Language English
    Publishing date 2019-03-15
    Publishing country England
    Document type Editorial
    ISSN 2473-4039
    ISSN (online) 2473-4039
    DOI 10.1002/jbm4.10137
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Doubling Down on Wnt Signaling to Overcome Myeloma Bone Disease.

    Delgado-Calle, Jesús / Roodman, G David

    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    2023  Volume 38, Issue 6, Page(s) 812–813

    MeSH term(s) Humans ; Wnt Signaling Pathway ; Multiple Myeloma ; Wnt Proteins ; Bone Diseases ; Cell Line, Tumor
    Chemical Substances Wnt Proteins
    Language English
    Publishing date 2023-06-05
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 632783-7
    ISSN 1523-4681 ; 0884-0431
    ISSN (online) 1523-4681
    ISSN 0884-0431
    DOI 10.1002/jbmr.4863
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Osteocytes and Paget's Disease of Bone.

    Tenshin, Hirofumi / Delgado-Calle, Jesus / Windle, Jolene J / Roodman, G David / Chirgwin, John M / Kurihara, Noriyoshi

    Current osteoporosis reports

    2024  Volume 22, Issue 2, Page(s) 266–272

    Abstract: Purpose of review: To describe the contributions of osteocytes to the lesions in Paget's disease, which are characterized by locally overactive bone resorption and formation.: Recent findings: Osteocytes, the most abundant cells in bone, are altered ... ...

    Abstract Purpose of review: To describe the contributions of osteocytes to the lesions in Paget's disease, which are characterized by locally overactive bone resorption and formation.
    Recent findings: Osteocytes, the most abundant cells in bone, are altered in Paget's disease lesions, displaying increased size, decreased canalicular length, incomplete differentiation, and less sclerostin expression compared to controls in both patients and mouse models. Pagetic lesions show increased senescent osteocytes that express RANK ligand, which drives osteoclastic bone resorption. Abnormal osteoclasts in Paget's disease secrete abundant IGF1, which enhances osteocyte senescence, contributing to lesion formation. Recent data suggest that osteocytes contribute to lesion formation in Paget's disease by responding to high local IGF1 released from abnormal osteoclasts. Here we describe the characteristics of osteocytes in Paget's disease and their role in bone lesion formation based on recent results with mouse models and supported by patient data.
    MeSH term(s) Osteitis Deformans/metabolism ; Osteitis Deformans/pathology ; Osteocytes/metabolism ; Osteocytes/pathology ; Humans ; Animals ; Osteoclasts/metabolism ; RANK Ligand/metabolism ; Bone Resorption/metabolism ; Mice ; Insulin-Like Growth Factor I/metabolism ; Disease Models, Animal ; Cellular Senescence
    Chemical Substances RANK Ligand ; Insulin-Like Growth Factor I (67763-96-6)
    Language English
    Publishing date 2024-03-08
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2186581-4
    ISSN 1544-2241 ; 1544-1873
    ISSN (online) 1544-2241
    ISSN 1544-1873
    DOI 10.1007/s11914-024-00863-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: The acid-sensing nociceptor TRPV1 controls breast cancer progression in bone via regulating HGF secretion from sensory neurons.

    Okui, Tatsuo / Hiasa, Masahiro / Hata, Kenji / Roodman, G David / Nakanishi, Masako / Yoneda, Toshiyuki

    Research square

    2023  

    Abstract: Cancers showing excessive innervation of sensory neurons (SN) in their microenvironments are associated with poor outcomes due to promoted growth, increased tumor recurrence, metastasis, and cancer pain, suggesting SNs play a regulatory role in cancer ... ...

    Abstract Cancers showing excessive innervation of sensory neurons (SN) in their microenvironments are associated with poor outcomes due to promoted growth, increased tumor recurrence, metastasis, and cancer pain, suggesting SNs play a regulatory role in cancer aggressiveness. Using a preclinical model in which mouse 4T1 breast cancer (BC) cells were injected into the bone marrow of tibiae, we found 4T1 BC cells aggressively colonized bone with bone destruction and subsequently spread to the lung. Of note, 4T1 BC colonization induced the acidic tumor microenvironment in bone in which SNs showed increased innervation and excitation with elevated expression of the acid-sensing nociceptor transient receptor potential vanilloid-1 (TRPV1), eliciting bone pain (BP) assessed by mechanical hypersensitivity. Further, these excited SNs produced increased hepatocyte growth factor (HGF). Importantly, the administration of synthetic and natural TRPV1 antagonists and genetic deletion of TRPV1 decreased HGF production in SNs and inhibited 4T1 BC colonization in bone, pulmonary metastasis from bone, and BP induction. Our results suggest the TRPV1 of SNs promotes BC colonization in bone and lung metastasis via up-regulating HGF production in SNs. The SN TRPV1 may be a novel therapeutic target for BC growing in the acidic bone microenvironment and for BP.
    Language English
    Publishing date 2023-07-05
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-3105966/v1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: CCN1: a sticky issue in myeloma.

    Roodman, G David

    Blood

    2014  Volume 124, Issue 13, Page(s) 2006–2008

    MeSH term(s) Animals ; Bone Diseases/etiology ; Cysteine-Rich Protein 61/genetics ; Gene Expression ; Humans ; Multiple Myeloma/complications ; Multiple Myeloma/genetics ; Tumor Microenvironment/genetics
    Chemical Substances Cysteine-Rich Protein 61
    Language English
    Publishing date 2014-09-24
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2014-08-592303
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Editor's Note: Targeting Akt and Heat Shock Protein 90 Produces Synergistic Multiple Myeloma Cell Cytotoxicity in the Bone Marrow Microenvironment.

    Huston, Alissa / Leleu, Xavier / Jia, Xiaoying / Moreau, Anne-Sophie / Ngo, Hai T / Runnels, Judith / Anderson, Judy / Alsayed, Yazan / Roccaro, Aldo / Vallet, Sonia / Hatjiharissi, Evdoxia / Tai, Yu-Tsu / Sportelli, Peter / Munshi, Nikhil / Richardson, Paul / Hideshima, Teru / Roodman, David G / Anderson, Kenneth C / Ghobrial, Irene M

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2024  Volume 30, Issue 4, Page(s) 922

    Language English
    Publishing date 2024-02-16
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-24-0181
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Multiple Myeloma and Bone: The Fatal Interaction.

    Marino, Silvia / Roodman, G David

    Cold Spring Harbor perspectives in medicine

    2018  Volume 8, Issue 8

    Abstract: Multiple myeloma (MM) is the second-most-common hematologic malignancy and the most frequent cancer to involve bone. MM bone disease (MMBD) has devastating consequences for patients, including dramatic bone loss, severe bone pain, and pathological ... ...

    Abstract Multiple myeloma (MM) is the second-most-common hematologic malignancy and the most frequent cancer to involve bone. MM bone disease (MMBD) has devastating consequences for patients, including dramatic bone loss, severe bone pain, and pathological fractures that markedly decrease the quality of life and impact survival of MM patients. MMBD results from excessive osteoclastic bone resorption and persistent suppressed osteoblastic bone formation, causing lytic lesions that do not heal, even when patients are in complete and prolonged remission. This review discusses the cellular and molecular mechanisms that regulate the uncoupling of bone remodeling in MM, the effects of MMBD on tumor growth, and potential therapeutic approaches that may prevent severe bone loss and repair damaged bone in MM patients.
    MeSH term(s) Bone Diseases/etiology ; Bone Diseases/physiopathology ; Bone Marrow Cells/cytology ; Bone Marrow Cells/pathology ; Bone Remodeling/physiology ; Bone Resorption/pathology ; Humans ; Multiple Myeloma/complications ; Multiple Myeloma/mortality ; Multiple Myeloma/physiopathology ; Osteoblasts/physiology ; Osteoclasts/physiology ; Osteogenesis/physiology
    Language English
    Publishing date 2018-08-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a031286
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Therapeutic targets in myeloma bone disease.

    Marino, Silvia / Petrusca, Daniela N / Roodman, G David

    British journal of pharmacology

    2020  Volume 178, Issue 9, Page(s) 1907–1922

    Abstract: Multiple myeloma (MM) is the second most common haematological malignancy and is characterized by a clonal proliferation of neoplastic plasma cells within the bone marrow. MM is the most frequent cancer involving the skeleton, causing osteolytic lesions, ...

    Abstract Multiple myeloma (MM) is the second most common haematological malignancy and is characterized by a clonal proliferation of neoplastic plasma cells within the bone marrow. MM is the most frequent cancer involving the skeleton, causing osteolytic lesions, bone pain and pathological fractures that dramatically decrease MM patients' quality of life and survival. MM bone disease (MBD) results from uncoupling of bone remodelling in which excessive bone resorption is not compensated by new bone formation, due to a persistent suppression of osteoblast activity. Current management of MBD includes antiresorptive agents, bisphosphonates and denosumab, that are only partially effective due to their inability to repair the existing lesions. Thus, research into agents that prevent bone destruction and more importantly repair existing lesions by inducing new bone formation is essential. This review discusses the mechanisms regulating the uncoupled bone remodelling in MM and summarizes current advances in the treatment of MBD. LINKED ARTICLES: This article is part of a themed issue on The molecular pharmacology of bone and cancer-related bone diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.9/issuetoc.
    MeSH term(s) Bone Density Conservation Agents/therapeutic use ; Humans ; Multiple Myeloma/drug therapy ; Osteoblasts ; Osteolysis ; Quality of Life
    Chemical Substances Bone Density Conservation Agents
    Language English
    Publishing date 2020-02-03
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.14889
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Pharmacologic targeting of the p62 ZZ domain enhances both anti-tumor and bone-anabolic effects of bortezomib in multiple myeloma.

    Marino, Silvia / Petrusca, Daniela N / Bishop, Ryan T / Anderson, Judith L / Sabol, Hayley M / Ashby, Cody / Layer, Justin H / Cesarano, Annamaria / Davé, Utpal P / Perna, Fabiana / Delgado-Calle, Jesus / Chirgwin, John M / Roodman, G David

    Haematologica

    2024  Volume 109, Issue 5, Page(s) 1501–1513

    Abstract: Multiple myeloma (MM) is a malignancy of plasma cells whose antibody secretion creates proteotoxic stress relieved by the N-end rule pathway, a proteolytic system that degrades N-arginylated proteins in the proteasome. When the proteasome is inhibited, ... ...

    Abstract Multiple myeloma (MM) is a malignancy of plasma cells whose antibody secretion creates proteotoxic stress relieved by the N-end rule pathway, a proteolytic system that degrades N-arginylated proteins in the proteasome. When the proteasome is inhibited, protein cargo is alternatively targeted for autophagic degradation by binding to the ZZ-domain of p62/ sequestosome-1. Here, we demonstrate that XRK3F2, a selective ligand for the ZZ-domain, dramatically improved two major responses to the proteasome inhibitor bortezomib (Btz) by increasing: i) killing of human MM cells by stimulating both Btz-mediated apoptosis and necroptosis, a process regulated by p62; and ii) preservation of bone mass by stimulating osteoblast differentiation and inhibiting osteoclastic bone destruction. Co-administration of Btz and XRK3F2 inhibited both branches of the bimodal N-end rule pathway exhibited synergistic anti-MM effects on MM cell lines and CD138+ cells from MM patients, and prevented stromal-mediated MM cell survival. In mice with established human MM, co-administration of Btz and XRK3F2 decreased tumor burden and prevented the progression of MM-induced osteolytic disease by inducing new bone formation more effectively than either single agent alone. The results suggest that p62-ZZ ligands enhance the anti- MM efficacy of proteasome inhibitors and can reduce MM morbidity and mortality by improving bone health.
    MeSH term(s) Bortezomib/pharmacology ; Bortezomib/therapeutic use ; Multiple Myeloma/drug therapy ; Multiple Myeloma/pathology ; Multiple Myeloma/metabolism ; Humans ; Animals ; Mice ; Cell Line, Tumor ; Sequestosome-1 Protein/metabolism ; Apoptosis/drug effects ; Xenograft Model Antitumor Assays ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Protein Domains ; Proteasome Inhibitors/pharmacology ; Proteasome Inhibitors/therapeutic use ; Disease Models, Animal
    Chemical Substances Bortezomib (69G8BD63PP) ; Sequestosome-1 Protein ; Antineoplastic Agents ; Proteasome Inhibitors
    Language English
    Publishing date 2024-05-01
    Publishing country Italy
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2023.283787
    Database MEDical Literature Analysis and Retrieval System OnLINE

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