Recently, several advances have been made in understanding the pathogenesis
of multiple myeloma. Increasing evidence favours a pre-switched, but somat
ically mutated B-cell as myeloma stem cell to give rise to the malignant cl
one. Deletions of the p53-gene, partial or total loss of chromosome 13 and
rearrangements of band 14q32 and 11q13 are frequently found in multiple mye
loma, and were shown to harbour prognostic significance. Presence or absenc
e of distinct chromosomal aberrations may guide selection of treatment stra
tegies in the future.
Although melphalan/prednisolone remains the standard of myeloma treatment i
n elderly patients, significant improvement has been achieved in antimyelom
a and in supportive therapy. High dose therapy with autologous stem cell tr
ansplantation enhances survival in younger patients and several trials are
ongoing to substantiate these results. The effect of interferon maintenance
treatment on overall survival is significant in metaanalysis, although the
gain achieved is limited. Newer treatment strategies - targeting the molec
ular level - have just entered clinical trials, and may further improve out
come of myeloma patients.