Repairing bone damage caused by multiple myeloma

Background

Multiple myeloma is a cancer of the blood that grows in the bone, forming painful bone lesions which fracture easily having a devastating impact on quality of life. Current treatments which prevent bone further destruction cannot rebuild bone, therefore lesions are not repaired and fractures still occur. Further current tumour targeted treatments are only effective temporarily as myeloma cells develop resistance to these anti-cancer drugs.

In the early stages of the disease, myeloma cells move to bone and stay dormant until activated to grow. Even after active myeloma cells are treated with chemotherapy, some tumour cells can resist treatment and return to a dormant state. They are then reactivated during disease relapse, forming new tumours and bone lesions

This incurable blood cancer is expected to be diagnosed in around 2,000 Australians this year. With a five-year survival rate of only 50%, due to high rates of relapse, new treatment options that can both stop myeloma from returning and rebuild damaged bone are urgently needed.

The research

In a previous project funded by Cancer Council NSW, Professor Peter Croucher and his team developed a world-first technique to see single myeloma cells in living bone. By studying the disease in its early stages, the team advanced our knowledge about what makes dormant myeloma cells awaken in bone marrow causing a relapse.

In the current study, the team has been investigating ways to rebuild bone and repair lesions caused by Myeloma. They explored the effects of a new drug called anti-sclerostin, or anti-Scl. This potent bone forming drug has recently been approved by the FDA for the prevention of bone loss and fractures in patients with osteoporosis. The team has demonstrated that anti-Scl can also prevent bone loss and damage in myeloma. When combined with another commonly used bone drug, the team achieved further increases in bone mass and strength. Therefore this new bone rebuilding agent is likely to improve fracture prevention in patients with myeloma.

Using their unique technique for watching myeloma, Professor Croucher and his team also tracked the impact of these drugs on the myeloma cells to ensure they don’t exacerbate the disease. They found that despite the increased bone formation, anti-Sci does not activate myeloma cells or stimulate tumour growth.

The team also tested the effectiveness of anti-Scl when used in combination with chemotherapy, finding that the bone strengthening effects of anti-Scl can also be achieved during active tumour treatment.