New Hope for AML: Protein Shield Discovery Leads to Immunotherapy Breakthrough
Researchers at Lund University have discovered a protein, SLAMF6, that acts as a shield for acute myeloid leukemia (AML) cells, helping them evade the immune system. This finding, published in the journal Nature, could pave the way for new immunotherapies for AML, a type of cancer with limited response to current immune-based treatments.
AML cells express SLAMF6 in about 60% of cases, while normal blood cells do not. This protein acts as an immune-suppressive shield, protecting AML cells from immune attack. The research team, led by Professor Carl Blomqvist, confirmed the role of SLAMF6 using CRISPR/Cas9 gene editing, which showed that removing SLAMF6 from AML cell lines activated T cells to destroy the leukemia cells.
To translate this discovery into clinical applications, a spin-off company called Lead Biologics has been launched. The company is developing an antibody, TNC-1, that binds to the SLAMF6 protein and disrupts its interaction with other SLAMF6 molecules. This blocks the protein's immune-suppressive function, restoring the immune system's ability to recognize and destroy AML cells. Preclinical validation and safety studies are ongoing to prepare for clinical trials.
The discovery of SLAMF6's role in AML immune evasion and the development of the TNC-1 antibody offer new hope for treating this aggressive blood cancer. Further research is needed to confirm the safety and efficacy of this approach in clinical trials.
