Plasmacytoma in patients with multiple myeloma: morphology and immunohistochemistry

Abstract

Background: To study the histological structure and immunohistochemical (IHC) parameters of the plasmacytoma tumour substrate in patients with multiple myeloma (MM). Methods: The study included 21 patients (10 men/11 women) aged 23 to 73 years old with newly diagnosed MM complicated by plasmacytoma. Bone plasmacytoma was diagnosed in 14 patients, and extramedullary plasmacytoma was diagnosed in 7 patients. Plasmacytoma tissue specimens were examined using a LEICA DM4000B microscope. Anti-CD56, anti-CD166, anti-CXCR4, anti-Ki-67, and anti-c-MYC antibodies were used for IHC study of plasmacytoma biopsies. Results: When comparing the morphology of bone and extramedullary plasmacytoma, no significant differences were revealed; however, the substrate of extramedullary plasmacytoma was more often represented by tumour cells with an immature morphology than was the bone plasmacytoma substrate (57.1% vs. 28.6%, respectively). We revealed a significant difference in the expression of CD166 between bone and extramedullary plasmacytoma. The mean values of CD166 expression in bone plasmacytoma cells were significantly higher (36.29 ± 7.61% versus 9.57 ± 8.46%, respectively; p = 0.033) than those in extramedullary plasmacytoma cells. We noticed that in extramedullary plasmacytoma cells, there were higher values for the Ki-67 index than in bone plasmacytoma cells, and this result was independent of cell morphology. Conclusion: The mechanisms involved in the dissemination of tumour plasma cells are currently unexplored. Even in such a small sample, some differences in expression could be identified, which may indicate that different mechanisms lead to the formation of bone and extramedullary plasmacytomas. Specifically, the expression of CD166 in extramedullary plasmacytoma cells was almost 4 times lower than that in bone plasmacytoma cells, which may indicate the involvement of CD166 in the mechanisms of bone destruction. The proliferative activity of extramedullary plasmacytoma cells was shown to be higher than that of bone plasmacytoma cells.

A Rare Case of Extra-Medullary Portacaval Plasmacytoma in a Patient With Relapsed Multiple Myeloma

“…Some of the proposed and commonly accepted theories include a downregulation of adhesion molecules (VLA-4, CD44, and CD56) that normally function to anchor tumor cells to the endothelial basement membrane, chemokine receptors (CCR1, CCR2), and factors that play a critical role in basement membrane homing of myeloma cells (CXCR4 and its ligand, SDF-1alpha). Some research even suggests that increased angiogenesis is culpable for metastatic myeloma cells [ 12 , 13 ]. In these ways, either through direct extension from the bone tumor or hematogenous spread, myeloma cells disseminate leading to EMP.…”

Elotuzumab for the treatment of extramedullary myeloma: a retrospective analysis of clinical efficacy and SLAMF7 expression patterns

“…Myeloma cells that are capable of surviving outside the bone marrow have previously undergone a biological evolution, including chromosomal aberrations, mutations of individual genes, and epigenetic changes [ 3 ]. Furthermore, they demonstrate an increased proliferative index compared to bone marrow myeloma cells [ 13 , 31 ]. Therefore, it is plausible that the therapeutic efficacy of elotuzumab may be limited by the overall more aggressive nature of the disease in this setting.…”

The Cancer-Immunity Cycle in Multiple Myeloma

“…The immune microenvironment of EMM has not been fully characterized. Given that malignant plasma cells in extramedullary lesions frequently show high Ki-67 expression, 42 highly proliferative myeloma cells might overwhelm T-cell infiltration, leading to the generation of immunologically “cold” EMM. Genetically modified CAR-T cell therapies with enhanced migration capacities are being developed to treat solid malignancies, 43 which might provide a clue to improve control of EMM.…”