In the case of multiple myeloma, what cellular change occurs as a result of chemotherapy with proteasome inhibitors?

In multiple myeloma, chemotherapy with proteasome inhibitors leads to increased apoptosis of malignant plasma cells. Proteasome inhibitors work by disrupting the proteasome's function, which is essential for degrading ubiquitinated proteins that regulate various cellular processes, including the cell cycle and apoptosis.

By inhibiting the proteasome, these drugs cause an accumulation of pro-apoptotic factors and other regulatory proteins within the cell. This build-up disrupts normal cellular functions and promotes programmed cell death, particularly in cancer cells that are overly reliant on the proteasome for survival.

In multiple myeloma, the malignant plasma cells are especially sensitive to this disruption because they already have an increased level of protein production due to their role in producing antibodies. The additional stress from proteasome inhibition can tip the balance toward apoptosis, leading to a reduction in these harmful cells. This is why proteasome inhibitors are considered a valuable treatment option in the management of multiple myeloma.