New Target Discovered for Treating Acute Myeloid Leukemia
Researchers at Lund University have discovered a new target for treating acute myeloid leukemia (AML). The protein SLAMF6, present in around 60% of AML cases, acts as an immune-suppressive shield on leukemia cells. Blocking this protein with an engineered antibody has shown promising results in restoring T cell activity and reactivating the immune system's ability to fight AML.
The human SLAMF6 antibody, TNC-1, binds the homodimerization interface with high affinity and disrupts the SLAMF6-SLAMF6 interaction. Preclinical validation and safety studies are ongoing before clinical trials. The discovery explains the limited effects of immunotherapy in AML and opens up new avenues for immunotherapies. The SLAMF protein family, including SLAMF6, plays a role in various immunological processes. Strategies to block immune-suppressive mechanisms, such as checkpoint molecules, are being explored to rejuvenate T cell activity and enhance the immune response against cancer cells. This includes antibody-based therapies, peptide or molecule therapies, and gene editing techniques like CRISPR/Cas9.
Lund University's discovery of SLAMF6's role in AML and the successful blocking of this protein using an engineered antibody offer hope for improved immunotherapies. Further preclinical studies are underway to validate these findings and ensure safety before clinical trials. This breakthrough could significantly impact the treatment of AML, which currently has limited response to immune-based treatments.
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