Healing of lytic lesions and restoration of bone health in multiple myeloma through sclerostin inhibition.

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Abstract

Conflict of interest statement: Declarations. Ethics approval and consent to participate: All procedures involving animals were performed in accordance with the guidelines issued by the University of Arkansas for Medical Sciences Institutional Animal Care and Use Committee (IACUC) (protocol #2022200000489). Collection and de-identification of human bone samples for ex vivo studies were coordinated by the UAMS Winthrop P. Rockefeller Cancer Institute TBAPS and approved by the UAMS IRB (protocol # 262940). All study procedures were approved by the University of Arkansas for Medical Sciences (IRB # 260312) and the Mayo Clinic (IRB # 23-012399) institutional review board with a waiver of informed consent owing to the retrospective nature of the data. Trephine iliac crest bone marrow biopsies from patients with MGUS or newly diagnosed MM were retrieved from Danish histopathological biobanks under approval from the Danish National Committee on Biomedical Research Ethics (S-20190110). All human samples were collected and processed in accordance with the Declaration of Helsinki. Competing interests: The authors declare no competing interests. 9. Cold Spring Harb Perspect Med. 2018 Aug 1;8(8):a031286. doi: 10.1101/cshperspect.a031286. Multiple Myeloma and Bone: The Fatal Interaction. Marino S(1), Roodman GD(1)(2). Author information: (1)Department of Medicine, Division Hematology Oncology, Indiana University School of Medicine, Indianapolis, Indiana 46202. (2)Roudebush VA Medical Center, Indianapolis, Indiana 46202. 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. Copyright © 2018 Cold Spring Harbor Laboratory Press; all rights reserved. DOI: 10.1101/cshperspect.a031286 PMCID: PMC6071546