The Bone Disease Group

The Bone Disease Group

– The Bone Disease Group studies how cancer and inflammation influence bone

photo_Bone Disease

The Bone Disease Group, CEMIR. Photo: Janne Østvang / NTNU

Bone Disease Group_txt

Loss of bone is a common feature of different inflammatory diseases as well as for cancers metastasizing to or located within bone.

Multiple myeloma is a cancer of plasma cells, located within the bone marrow. The bone disease of multiple myeloma is highly aggressive, and is the cause of pain and reduced quality of life for the myeloma patients. Hypoxic and ER stress and a low grade, chronic inflammation characterizes the myeloma bone marrow.

Our research is centered on identifying inflammatory factors present in the bone marrow microenvironment that influence differentiation or activation of bone cells. The underlying hypothesis is that the causes of bone loss associated with inflammatory diseases and cancer might be common.

Research projects

  • Effect of cancer cell-derived cytokines on osteoclast and osteoblast differentiation and function.
  • The role of bone marrow mesenchymal stromal cells in multiple myeloma disease pathogenesis.
  • The role of inflammatory cells, inflammation and intracellular stress-signaling for bone health and myeloma disease progression.

Research documentation

Research documentation

  1. Zahoor M, Westhrin M, Moen SH, Aass KR, MisundK, Psonka-Antonczyk KM, Giliberto M, Buene G, Sundan A, Waage A, Sponaas AM and Standal T. Hypoxia promotes IL-32 expression in myeloma cells, and high expression is associated with poor survival and bone loss. Blood Adv. 2017 Dec 13;1(27):2656-2666. doi: 10.1182/bloodadvances.2017010801.
  2. Westhrin M, Moen SH, Holien H, Mylin AK, Heickendorff L, Olsen OE, Sundan A, Turesson I, Gimsing P, Waage A, Standal T. GDF15 promotes osteoclast differentiation, inhibits osteoblast differentiation and high serum GDF15 levels are associated with multiple myeloma bone disease. Haematologica. 2015 Dec;100(12):e511-4. doi: 0.3324/haematol.2015.
  3. Standal T, Johnson RW, McGregor NE, Poulton IJ, Ho PW, Martin TJ, Sims NA. gp130 in late osteoblasts and osteocytes is required for PTH-induced osteoblast differentiation. J Endocrinol. 2014 Nov;223(2):181-90
  4. Johnson RW, Brennan HJ, Poulton IJ, McGregor NE, Standal T, Walker EC, Vrahnas C, Koh T, Nguyen H, Walsh NC, Forwood MR, Martin TJ, Sims NA. The Primary Function of gp130 Signaling in Osteoblasts is to Maintain bone Formation and Strength, Rather than Promote Osteoclast Formation. J Bone Miner Res. 2014 Jun;29(6):1492-505
  5. Holien T, Våtsveen T, Hella H, Rampa C, Brede G, Grøseth LA, Rekvig M, Børset M, Standal T, Waage A, Sundan A. Bone morphogenetic proteins induce apoptosis in multiple myeloma cells by Smad-dependent repression of MYC. Leukemia. 2012;26:1073-1080
  6. Grandaunet B, Syversen S, Hoff M, Haugeberg G, Sundan A, van der Heijde D, Kvien T and Standal T. Association between high plasma levels of hepatocyte growth factor and progression of radiographic damage in the joints of patients with rheumatoid arthritis. Arthritis Rheum. 2011;63:662-669
  7. Nørgaard N, Holien T, Jönsson S, Hella H, Espevik T, Sundan A and Standal T. CpG-oligodeoxynucleotide inhibits Smad-dependent bone morphogenetic protein signaling: effects on myeloma cell apoptosis and in vitro osteoblastogenesis.  J Immunol. 2010 ;185:3131-3139.
  8. Jönsson S, Hjorth-Hansen H, Olsson B, Wadenvik H, Sundan A and Standal T. Second-generation TKI dasatinib inhibits proliferation of mesenchymal stem cells and osteoblast differentiation in vitro. Leukemia 2010;24:1357-1359
  9. Standal T, Abildgaard N, Fagerli UM, Stordal B, Hjertner O, Borset M and Sundan A. HGF inhibits BMP-induced osteoblastogenesis: possible implications for the bone disease of multiple myeloma. Blood. 2007; 109:3024-3030
  10. Standal T, Seidel C, Hjertner Ø, Plesner T, Sanderson R, Waage A, Borset B and Sundan A. Osteoprotegerin is bound, internalized, and degraded by multiple myeloma cells. Blood. 2002;100:3002-3007


22 Jun 2017

People_Bone Disease



  • Manfred Wuhrer, Leiden University Medical Center (LUMC), The Netherlands
  • Niels Abildgaard, University of Southern Denmark (SDU), Denmark
  • Unni Syversen, Norwegian University of Science and Technology (NTNU)
  • Berit Strand, Norwegian University of Science and Technology (NTNU)