Bakgrunn og aktiviteter
Research focus: TGF-β family signaling in multiple myeloma
Our research is focused on understanding the role of transforming growth factor (TGF)-ß family signaling pathways in multiple myeloma. This includes ligands such as TGF-ß, activins, BMPs and GDFs. There is extensive redundancy in this family of ligands and receptors, and the effects of a given molecule will always depend on the context. Activation of the SMAD1/5 transcription factors by TGF-ß family ligands induces apoptosis in myeloma cells by downregulating the oncogene c-MYC. Potentiaion of SMAD1/5 activity represents therefore a possible treatment option for myeloma patients. We are also interested in the role of TGF-ß signaling in the context of the tumor microenvironment, particularly in relation to angiogenesis and dissemination. For this part we collaborate with the Bjørkøy group.
We welcome students that want to study regulation of signaling in the TGF-ß family.
Our group, Fall 2020: Lu Bai (master student), Toril Holien (group leader, PhD), Ingrid Quist-Løkken (MSc, medical research student), Clara Andersson-Rusch (MSc, PhD candidate) and Megan Anne Vik (master student).
Medical Students' Research Programme: Ingrid Quist-Løkken
PhD student: Clara Andersson-Rusch
PhD student (Bjørkøy group, cosupervised): Camilla Wolowczyk
Master students (molecular medicine): Megan Anne Vik and Lu Bai
Post doctor (2017-2020): Oddrun Elise Olsen
PhD (2012-2017): Oddrun Elise Olsen
Biotechnology (2019/20, cosupervised): Jenny Malm Rasmussen
Pharmacy (2018/19): Martin Haugrud Kastnes, Nerissa Rae Booc
Pharmacy (2017/18): Thi Le, Fartun Hussein Ali
Molecular Medicine (2016/17): Samah Elsaadi, Fekadu Alemu Atire
Biotechnology (2013/15): Anette Skjærvik
Cell biology (2012/14): Kine Husteli Kristiansen
Biotechnology (2011/12): Oddrun Elise Olsen
Erasmus trainee students: Alexander Stockhammer (2018), Marie-Thérèse Henke (2017), Meenu Sankar (2015/16), Sarah Nevens (2013/14)
Vitenskapelig, faglig og kunstnerisk arbeid
Viser et utvalg av aktivitet. Se alle publikasjoner i databasen
- (2020) Activins as Dual Specificity TGF-β Family Molecules: SMAD-Activation via Activin- and BMP-Type 1 Receptors. Biomolecules. vol. 10 (4).
- (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).
- (2019) GREM1 is associated with metastasis and predicts poor prognosis in ER-negative breast cancer patients. Cell Communication and Signaling. vol. 17.
- (2018) BMPR2 inhibits activin and BMP signaling via wild-type ALK2. Journal of Cell Science. vol. 131 (11).
- (2017) TGF-β contamination of purified recombinant GDF15. PLOS ONE. vol. 12:e0187349 (11).
- (2016) VOLIN and KJON—Two novel hyperdiploid myeloma cell lines. Genes, Chromosomes and Cancer. vol. 55 (11).
- (2015) Activin A inhibits BMP-signaling by binding ACVR2A and ACVR2B. Cell Communication and Signaling. vol. 13:27.
- (2015) Growth differentiation factor 15 (GDF15) promotes osteoclast differentiation and inhibits osteoblast differentiation and high serum GDF15 levels are associated with multiple myeloma bone disease. Haematologica. vol. 100 (12).
- (2014) The role of bone morphogenetic proteins in myeloma cell survival. Cytokine & growth factor reviews. vol. 25 (3).
- (2014) Bone morphogenetic protein-9 suppresses growth of myeloma cells by signaling through ALK2 but is inhibited by endoglin. Blood Cancer Journal. vol. 4.
- (2012) Bone morphogenetic proteins induce apoptosis in multiple myeloma cells by Smad-dependent repression of MYC. Leukemia. vol. 26.
- (2012) Addiction to c-MYC in multiple myeloma. Blood. vol. 120 (12).
- (2010) CpG-Oligodeoxynucleotide Inhibits Smad-Dependent Bone Morphogenetic Protein Signaling: Effects on Myeloma Cell Apoptosis and In Vitro Osteoblastogenesis. Journal of Immunology. vol. 185 (6).