Group Leader:
A/Prof Andrew ZannettinoChief Medical Scientist
Associate Member, Hanson Institute
Associate Professor (Affiliate), Department of Medicine, University of Adelaide
Contact Details:
Bone and Cancer Laboratories,
Department of Haematology,
Level 3, Hanson Institute, IMVS
Frome Road, Adelaide, SA 5000
| Tel (Office) | +61-8-8222-3455 |
| Tel (Lab) | +61-8-8222-3735 |
| Fax | +61-8-8222-3162 |
| email: andrew.zannettino@imvs.sa.gov.au | |
Lab Members
| Postdoctoral Fellows | |
|---|---|
| Andrea Dewar | andrea.dewar@imvs.sa.gov.au |
| Peter Diamond | peter.diamond@imvs.sa.gov.au |
| Stephen Fitter | stephen.fitter@imvs.sa.gov.au |
| Sharon Hampton-Smith | sharon.hampton@imvs.sa.gov.au |
| Research Assistants | |
| Jenny Drew | jenny.drew@imvs.sa.gov.au |
| Amanda Farrugia | amanda.farrugia@imvs.sa.gov.au |
| Penny Kostakis | penny.kostakis@imvs.sa.gov.au |
| PhD students | |
| Sally Martin | sally.martin@imvs.sa.gov.au |
| Kate Vandyke | kate.vandyke@imvs.sa.gov.au |
Research Focus
Multiple myeloma is an incurable but treatable haematological (blood) cancer of antibody-producing plasma cell. Plasma cells are an important part of the immune system that produce immunoglobulins (antibodies) to help fight infection and disease. The estimated frequency of this disease in our community is estimated to be 5-6 new cases per 100,000 persons per year.
Multiple myeloma is unique amongst haematological malignancies in its capacity to cause massive destruction of the skeleton. The focal osteolytic lesions result in a range of debilitating clinical symptoms including bone pain, pathological fractures, spinal cord compression, hypercalcemia and renal failure. Whilst the precise molecular mechanism(s) responsible for this bone loss remain to be determined, histological and histomorphometric studies suggest that the process of normal bone remodeling are perturbed. The destructive osteolytic lesions associated with MM are characterised by a marked increase in both osteoclast (OC) formation and activity, with a reduced or absent coupled osteoblast (OB)-mediated osteogenic response. Active myeloma disease is also associated with increased bone marrow (BM) angiogenesis, as evidenced by an increase in microvessel density (MVD). Whilst increased MVD in MM correlates with poor prognosis and survival, the precise mechanisms responsible for the elevated angiogenesis requires further elucidation.
The Myeloma Research Laboratory (MRL) was established in January 2000 with the express aim of identifying the molecular and cellular mechanisms responsible for the bone destruction seen in individuals with MM, in particular, the role of CXCL12/CXCR4 in angiogenesis and osteolytic bone disease. Recently, MMRL has commenced studies to investigate the use of protein tyrosine kinase inhibition (TKI) as a modality to treat osteolytic bone diseases, such as MM. This follows our observation that administration of the TKI, imatinib, inhibits bone resorption by osteoclasts and promotes mineral formation by osteoblasts, and that treatment of patients with imatinib results in increased trabecular bone volume.
Research Projects
- The Role Of CXCL12/CXCR4 In Pathological Angiogenesis And Osteolytic Bone Disease In Multiple Myeloma
- Modulation Of Bone Remodelling By Tyrosine Kinase Inhibitors
Recent Publications (2000-2007)
Student Projects
The MMRL currently has two PhD students working in the field of CXCL12 and tyrosine kinase inhibition. There is further scope within these areas for prospective PhD and honours students. Interested parties should contact A/Prof Andrew Zannettino.
Scholarships are available through a number of sources, including:
- University of Adelaide Scholarships
- University of South Australia
- Royal Adelaide Hospital Scholarships
- Cancer Council SA
Funding
The MMRL is funded by research grants from the NHMRC, Novartis Pharmaceuticals International, Mesoblast Ltd. and Johnson and Johnson.
