An unusual characteristic of multiple myeloma is exactly which chemotherapy drugs it will respond to. The usual suspects, like bleomycin, carboplatin and cyclophosphamide are nearly useless. What is effective, though, is the steroid dexamethasone. Now, dexamethasone is used in many other chemotherapy regimens, like ABVD or AC+T, but there it's used as an antiemetic, or to enhance the effectiveness of other antiemetics like ondansetron or palonosetron. In multiple myeloma, however, it's used to directly kill off cancer cells. It's usually combined with thalidomide, and sometimes melphalan.
Treatment with dexamethasone, thalidomide and oral melphalan is very rarely curative, however. The only therapy that's curative with any significant rate of success is a bone marrow transplant, usually an allogenic one. This consists of first ablating, that is destroying, the patient's bone marrow with very high doses of chemotherapy. The drugs usually used are carmustine (or BCNU, its trade name), etoposide, cytarabine (also called ARA-C), and melphalan. When doing this, the melphalan is administered by IV at very high doses, rather than the small doses orally used in maintenance therapy. Bone marrow transplants carry severe risks. Once the BEAM chemotherapy has been administered, the immune system is almost completely obliterated, leaving the patient vulnerable to bacterial and fungal infections. Patients often receive amphotericin B or voriconazole and vancomyicn prophylactically, since any infection that develops could kill within hours if left unchecked. Since ARA-C also interferes with most viruses, viral infection is less of a risk, but potentially more serious if it does occur. Once the patient's blood counts drop to their nadir, the donor bone marrow is injected. Often shots of Neupogen or Neulasta are administered at this time to speed regeneration of the bone marrow. If all goes well, the donor bone marrow 'takes', and begins producing immune cells. These immune cells should attack any remaining cancer and destroy it, called the graft versus tumor effect.
Dangerous as that is, it's the best hope for long-term cancer-free survival for multiple myeloma patients. Work is being done on new drugs to treat it with less risk, though. Among these are bortezomib (or Velcade), and sunitinib (Sutent), which are tyrosine kinase inhibitors, and also monoclonal antibodies. Unfortunately, progress is slow, but the next ten years should bring significant improvements in multiple myeloma treatment. Hopefully, it will become as treatable as Hodgkin's Disease and testicular cancer, but that's a long way off.