B-cell maturation antigen (BCMA)

BCMA is expressed by malignant and normal plasma cells with some mature B cells.

BCMA and its ligands result in activation and proliferation of plasma cells and BCMA signaling, is responsible for harmful effects of malignant plasma cells.

Serum BCNA levels a higher among patients with active myeloma, than those with smoldering disease, and are higher among those with smoldering myeloma, than among those with MGUS.

As multiple myeloma progresses it involves BCMA over expression on multiple myeloma cells, leading to increase up regulation of survival, growth, and immunosuppressive genes.

Among patients with smoldering myeloma and those with MGUS, higher levels of serum BCMA predict a higher risk of transformation to active myeloma.

Among patients starting treatment for myeloma, baseline serum, BCMA levels, predict, both progression free and overall survival.

Changes in serum BCMA levels during treatment correlate with changes in traditional multiple myeloma markers, but occur more rapidly, allowing the opportunity to identify worsening disease more rapidly.

BCMA can be used to follow patients with non-signatory disease.

Levels of seum BCMA are not impacted by renal function.

BCMA Is a universally expressed plasma cell membrane antigen that is a major target of T-cell therapy in multiple myeloma.

Expressed on the surface of mature B cells, but not native B cells or or other hematopoietic cells.

It is thought to promote the survival of plasma cells in the bone marrow.

Serum BCMA levels are higher in patients with myeloma compared with those without myeloma.

A protein that in humans is encoded by the TNFRSF17 gene.

Chromosome 16.

TNFRSF17 is a cell surface receptor of the TNF receptor superfamily which recognizes B-cell activating factor (BAFF).

The protein is a member of the TNF-receptor superfamily.

This receptor is expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response.

BCMA receptor has been shown to bind to the tumor necrosis factor and to lead to NF-kappaB and MAPK8/JNK activation.

It also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation.

TNFRSF17 has been shown to interact with the B-cell activating factor TNFSF13B.

A conserved domain at the N-terminus, BCMA TALL-1 binding domain, is required for binding to the TNFSF13B.

TNFRSF17 is implicated in leukemia, lymphomas, and multiple myeloma.

A phase 1 clinical trial employed a CAR-T therapy that targeted BCMA02 in multiple myeloma.

Side-effects seen include cytokine release syndrome and mild neurotoxicity.

BCMA direct therapies have been approved for the treatment of patients with myeloma who have received immunomodulatory agentsm proteosome inhibitors, and anti-CD 38 antibodies.