Multiple Myeloma is the second most frequently occurring blood cancer and accounts for approximately 10% of all newly diagnosed patients with hematological malignancies. Multiple Myeloma arises from clonal expansion of malignant plasma cells and is characterized by multi-organ damage including the bone marrow and kidneys. Despite significant improvement in the efficacy of anti-myeloma therapies over the past decade, most patients will at some point experience disease recurrence.

Genetics of malignant plasma cells

The tumor cells in Multiple Myeloma cells contain a diverse array of genetic lesions. Different genetic alterations are acquired during distinct phases of the disease, and can bestow Myeloma cells with highly specific properties. These genetic differences can be used to predict therapy responsiveness to commonly used anti-Myeloma drugs and ultimately design patient-specific targeting therapies.

Bone marrow environment

Multiple Myeloma cells are mainly localized in the bone marrow, where the tumor cells receive growth and survival factors from non-cancerous bone and bone marrow cells. The importance of this supportive environment for myeloma cell survival and resistance to therapy is well-established, and several drugs in current clinical practice are thought to function in part by affecting the bone marrow micro-environment.
Combined targeting of Multiple Myeloma cells and their supportive environment holds the promise of improving treatment efficacy and reducing disease recurrence.

Immune cell environment

Our immune system has the capacity to eliminate cancer cells. This notwithstanding, in many types of cancer immune function is inhibited leading to tumor growth. In Multiple Myeloma, alterations in the immune cell composition exist that negatively impact the ability of the immune system to target the malignant plasma cells.
Restoring immune cell homeostasis or activating specific immune cell subsets in Multiple Myeloma through targeted immuno therapy could increase anti-cancer immunity.