Therese Standal
Background and activities
Research activity
Multiple myeloma is a cancer caused by accumulation of malignant plasma cells within the bone marrow. Almost all myeloma patients suffer from an osteolytic bone disease, caused by increased numbers of cells degrading bone (osteoclasts) and reduced numbers of cells producing bone (osteoblasts). Bone destruction is also common in inflammtory diseases such as rheumatoid arthritis.
My research focus is on how myeloma cells, myeloma derived factors and inflammation affects the activity and differentiation of osteoblast and osteoclasts. My research group consists of one researcher, two post docs, four PhD students and one technician. Currently main research projects are on the importance of cross talks between adipocytes, immune cells and myeloma cells for disease progression and on the role of the pro-inflammatory cytokine IL-32 for disease progression.
Scientific, academic and artistic work
A selection of recent journal publications, artistic productions, books, including book and report excerpts. See all publications in the database
Journal publications
- (2021) Intracellular IL-32 regulates mitochondrial metabolism, proliferation, and differentiation of malignant plasma cells. iScience. vol. 25 (1).
- (2021) Smac-mimetics reduce numbers and viability of human osteoclasts. Cell death discovery. vol. 7:36.
- (2021) Bystander memory T cells and IMiD/checkpoint therapy in multiple myeloma: A dangerous tango?. Frontiers in Immunology. vol. 12:636375.
- (2021) Revealing the influence of electron beam melted Ti-6Al-4V scaffolds on osteogenesis of human bone marrow-derived mesenchymal stromal cells. Journal of materials science. Materials in medicine. vol. 32 (97).
- (2020) Molecular interactions and functions of IL-32. Journal of Leukocyte Biology.
- (2020) Bone Morphogenetic Protein 4 Gene Therapy in Mice Inhibits Myeloma Tumor Growth, But Has a Negative Impact on Bone. JBMR Plus. vol. 4 (1).
- (2020) Monoclonal immunoglobulins promote bone loss in multiple myeloma. Blood. vol. 136 (23).
- (2020) Conversion of ATP to adenosine by CD39 and CD73 in multiple myeloma can be successfully targeted together with adenosine receptor A2A blockade. Journal for ImmunoTherapy of Cancer (JITC).
- (2019) Why do myeloma patients have bone disease? A historical perspective. Blood reviews. vol. 00:100646.
- (2019) N-glykosylering av serumproteiner endres ved myelomatose. Bestpractice Onkologi/Hematologi.
- (2019) Serum protein N-glycosylation changes in multiple myeloma. Biochimica et Biophysica Acta - General Subjects. vol. 1863 (5).
- (2018) BMP4 Gene Therapy Inhibits Myeloma Tumor Growth, but Has a Negative Impact on Bone. Blood. vol. 132.
- (2018) PD1 is expressed on exhausted T cells as well as virus specific memory CD8+ T cells in the bone marrow of myeloma patients. OncoTarget. vol. 9 (62).
- (2018) Myelomatose - bein i ubalanse. Bestpractice Onkologi/Hematologi.
- (2018) Chemerin is elevated in multiple myeloma patients and is expressed by stromal cells and pre-adipocytes. Biomarker Research. vol. 6 (21).
- (2017) Monitoring multiple myeloma by quantification of recurrent mutations in serum. Haematologica. vol. 102 (7).
- (2017) Hypoxia promotes IL-32 expression in myeloma cells, and high expression is associated with poor survival and bone loss. Blood Advances. vol. 27 (1).
- (2016) Caspase-8 regulates the expression of pro- and anti-inflammatory cytokines in human bone marrow-derived mesenchymal stromal cells. Immunity,Inflammation and Disease. vol. 4 (3).
- (2015) The proportion of CD16+CD14dim monocytes increases with tumor cell load in bone marrow of patients with multiple myeloma. Immunity,Inflammation and Disease. vol. 3 (2).
- (2015) PDL1 expression on plasma and dendritic cells in myeloma bone marrow suggests benefit of targeted anti PD1-PDL1 therapy. PLOS ONE. vol. 10:e0139867 (10).