Abstract
Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults with very poor prognosis and few advances in its treatment. Recently, fast-growing cancer immunotherapy provides a glimmer of hope for GBM treatment. Adoptive cell therapy (ACT) aims at infusing immune cells with direct anti-tumor activity, including tumor-infiltrating lymphocyte (TIL) transfer and genetically engineered T cells transfer. For example, complete regressions in patients with melanoma and refractory lymphoma have been shown by using naturally tumor-reactive T cells and genetically engineered T cells expressing the chimeric anti-CD19 receptor, respectively. Recently, the administration of ACT showed therapeutic potentials for GBM treatment as well. In this review, we summarize the success of ACT in the treatment of cancer and provide approaches to overcome some challenges of ACT to allow its adoption for GBM treatment.
Highlights
Gliomas, including astrocytoma, oligodendroglioma, mixed glioma, medulloblastoma, and ependymoma, are the most common primary central nervous system (CNS) tumors that arise from glial or its precursor cells [1]
Transfer of this mutant-reactive T cell receptor (TCR)-transgenic T cells notably inhibited the progression of diffuse intrinsic pontine glioma (DIPG) xenografts in mice and this provided laboratory evidence for evaluating TCR T-cell therapy targeting specific epitope in Glioblastoma multiforme (GBM), while brain inflammation during treatment should be concerned when translating into clinic [79]
Adoptive cell therapy (ACT) is a highly personalized therapy that possesses a significant potential for the treatment of different types of cancers
Summary
Gliomas, including astrocytoma, oligodendroglioma, mixed glioma, medulloblastoma, and ependymoma, are the most common primary central nervous system (CNS) tumors that arise from glial or its precursor cells [1]. A recent clinical trial (NCT02208362) showed that the regression of all intracranial and spinal lesions was observed in a patient with recurrent multifocal GBM who received CART cells targeting the interleukin-13 receptor alpha 2 (IL13Rα2) [66]. Recent research has identified a TCR that targeted histone 3 variant 3 K27M (H3.3K27M) mutation that was frequently expressed in DIPG with HLAA2 restriction Transfer of this mutant-reactive TCR-transgenic T cells notably inhibited the progression of DIPG xenografts in mice and this provided laboratory evidence for evaluating TCR T-cell therapy targeting specific epitope in GBM, while brain inflammation during treatment should be concerned when translating into clinic [79].
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