Multiple myeloma results from an interplay between the manoclonal mali
gnant plasma cells and supporting nonmalignant cells in the bone marro
w. Recent studies suggest that the final transforming event in this B
cell disorder occurs at a late stage of B cell differentiation based o
n the characteristics of the immunoglobulin genes expressed by the mal
ignant clone as well as surface markers present on the tumor cells. Re
cently, an increasing pathogenic role in this malignancy by the nonmal
ignant cells in the bone marrow has been suggested by several studies.
Specific infection of these supporting cells by the recently identifi
ed Kaposi's sarcoma-associated herpes virus (KSHV) suggests a novel me
chanism by which this nonmalignant population may lead to the developm
ent of this B cell malignancy and support its growth.