Immune Cell Therapy Promises More Effective Cure for Medulloblastoma.
This review discusses immune checkpoint inhibition, CAR T and CAR NK therapies, molecular subgrouping, proteomics, and liquid biopsy as emerging approaches for medulloblastoma while emphasizing resistance, target-antigen scarcity, heterogeneity, and treatment toxicities.
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This review discusses immune checkpoint inhibition, CAR T and CAR NK therapies, molecular subgrouping, proteomics, and liquid biopsy as emerging approaches for medulloblastoma while emphasizing resistance, target-antigen scarcity, heterogeneity, and treatment toxicities.
Research significance
The supplied record reports that CAR-based therapies and immune checkpoint strategies are being studied in medulloblastoma and that CAR NK therapy may be less prone to some limitations; it is an inference—not demonstrated here—that subgroup-informed antigen selection, checkpoint modulation, and proteomic or liquid-biopsy monitoring could improve efficacy or safety.
Source abstract
Medulloblastoma is one of the most prevalent pediatric brain tumors. Currently, existing therapies for this devastating type of cancer can only prolong survival time with severe side-effects and relapse. These therapies are not curative for almost a third of treated patients, while most survivors are condemned to a poor quality of life. The addition of immune checkpoint inhibitors (ICIs) to immune therapy has given some hope to those suffering from this type of cancer. Although ICIs provide a valuable contribution to immunotherapy, the exploitation of immune checkpoint inhibition within existing therapeutic strategies to cure Medulloblastoma remains understudied. However, the identification of the main molecular subgroups of medulloblastoma is considered one of the success stories of oncology. This advancement in molecular profiling of MB paved the way to subgroup-directed clinical trials, which may lead to efficacious immune-targeted therapy. However, this relatively new development is still hampered by a substantial biological heterogeneity of the disease and the absence of a full understanding of the various mechanisms behind its resistance to existing therapeutic modalities. The inclusion of chimeric antigen receptor (CAR) T and CAR NK cell therapy within various therapeutic strategies and ongoing clinical trials has given fresh hope those suffering from this fatal disease. However, ongoing clinical trials suggest that this highly promising therapy can be impaired by a number of serious limitations, including cytokine release syndrome, Graft-versus-host disease, the scarcity of target antigens, and severe adverse events. Some of the ongoing clinical trials also suggest that CAR NK is less prone to some of these limitations. This review also highlights the contribution of mass spectrometry-based proteomics, and the increasing role of liquid biopsy rather than tissue biopsy.