Multiple myeloma pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overveiw

Multiple myeloma develops in post-germinal center B lymphocytes.
A chromosomal translocation between the immunoglobulin heavy chain gene (on the fourteenth chromosome, locus 14q32) and an oncogene (often 11q13, 4p16.3, 6p21, 16q23 and 20q11^[1]) is frequently observed in patients with multiple myeloma.
This mutation results in dysregulation of the oncogene which is thought to be an important initiating event in the pathogenesis of myeloma.
The result is proliferation of a plasma cell clone and genomic instability that leads to further mutations and translocations.
The chromosome 14 abnormality is observed in about 50% of all cases of myeloma. Deletion of (parts of) the thirteenth chromosome is also observed in about 50% of cases.
Production of cytokines (especially IL-6) by the plasma cells causes much of their localised damage, such as osteoporosis, and creates a microenvironment in which the malignant cells thrive. Angiogenesis (the attraction of new blood vessels) is increased.
The produced antibodies are deposited in various organs, leading to renal failure, polyneuropathy and various other myeloma-associated symptoms.

Multiple Myeloma ^[2]
Bone marrow aspiration in multiple myeloma.
(Image courtesy of Melih Aktan M.D.)
Bone marrow biopsy in multiple myeloma.
(Image courtesy of Melih Aktan M.D.)
Bone marrow in multiple myeloma.
(Image courtesy of Melih Aktan M.D.)
Bone marrow in multiple myeloma.
(Image courtesy of Melih Aktan M.D.)