About

Multiple myeloma (MM) is a fatal malignancy of plasma cells that accumulate in the bone marrow (BM). The interactions between the BM microenvironment and the MM cells promote disease progression and inhibit disease therapy. At present, treatment is provided to MM patients at their symptomatic stage while the pre-malignant stages (MGUS, SMM) usually go untreated. Indeed, there is dire need for better identification of subjects at risk to progress to MM.

The research in the Oncogenetic laboratory, headed by Prof. Liat Drucker, has demonstrated an active role of the BM resident mesenchymal stem cells (MSCs) in design of the malignant cells' phenotype. A distinct difference was observed between BM-MSCs of normal donors (MM suppressive) and those from MM patients (MM promoting). Indeed, accumulated data suggest that the MSCs are reprogrammed by the cancer cells.

MM cells as antibody producing plasma cells, are characterized with intense protein manufacture that is tightly regulated by internal and external cues. Therefore, Prof. Drucker and her team hypothesized that the rate limiting step of protein translation initiation (TI) may be targeted by the cancer microenvironment. In support of this conjecture, Drucker' team has shown that TI is manipulated by the BM-MSCs and responsible for many of the phenotypical alterations  observed in MM (in vivo and in vitro).

Prof. Drucker and her team are dedicated to identifying the signals involved in the communication between MM and BM-MSCs and devising ways to circumvent or manage this dialogue towards MM therapy. Particular attention is awarded to to BM-MSCs microvesicles, extracellular matrix and metabolic redesign. 

Using advanced state-of-the-art techniques the team aims to acquire the needed understanding of the crosstalk between MM cells and the BM-MSCs, identify clinically relevant biomarkers for progression and intercept the MM-MSCs support of MM.