Helena Jernberg Wiklund – The control of survival and apoptosis in human multiple myeloma

    Photo: Axel Henriksson

Our research focuses on multiple myeloma (MM). This is an incurable tumour where malignant plasma cells with complex genetic alterations grow in the bone marrow. Recent treatment improvements have proven successful in selected sub-fractions of MM patients. However, due to large intra-tumoural heterogeneity the identification of common causative alterations for MM has been hampered. Further understanding of the biology of MM is of primary importance in order to be able to tackle the disease complexity.

Using multiple myeloma models to find new treatment possibilities

The long-term goal of our research is to identify targets essential for tumour cell survival and explore in models of MM whether their function can be blocked in parallel survival pathways. To study the molecular mechanisms and therapeutic use of target proteins in survival pathways of MM, a prerequisite has been to select and implement relevant models in vitro and in vivo.

We are presently using a highly clinically relevant model of human MM. This consists of immunocompetent syngeneic murine models of MM in vivo and in vitro, a large well characterized authenticated panel of cell lines representing all common genetic subtypes of MM, and primary patient cells and normal age-matched counterpart cells.

Previously accomplished results in our MM model has generated proof-of-principle that the IGF-1R is an attractive target for intervention, and that survival circuits act via gene silencing by epigenetic mechanisms. The hypothesis that tumour stemness may lie within a novel tumour associated epigenetically silenced gene signature by the Polycomb complex (PcG) is an attractive idea since it may be reverted and genes reactivated by pharmacological intervention.


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