Abstract
Chimeric antigen receptors (CARs) are among the curative immunotherapeutic approaches that exploit the antigen specificity and cytotoxicity function of potent immune cells against cancers. Neuroblastomas, the most common extracranial pediatric solid tumors with diverse characteristics, could be a promising candidate for using CAR therapies. Several methods harness CAR-modified cells in neuroblastoma to increase therapeutic efficiency, although the assessment has been less successful. Regarding the improvement of CARs, various trials have been launched to overcome insufficient capacity. However, the reasons behind the inadequate response against neuroblastoma of CAR-modified cells are still not well understood. It is essential to update the present state of comprehension of CARs to improve the efficiency of CAR therapies. This review summarizes the crucial features of CARs and their design for neuroblastoma, discusses challenges that impact the outcomes of the immunotherapeutic competence, and focuses on devising strategies currently being investigated to improve the efficacy of CARs for neuroblastoma immunotherapy.
Highlights
Neuroblastoma, an extracranial solid tumor that initiates from the sympathetic nervous system’s neuroendocrine tissue, is one of the most common causes of death in pediatric cancers [1,2]
Significant factors derived from tumor microenvironment (TME) in neuroblastomas include immunosuppressive cells like tumor-associated macrophages (TAMs), Type 2 regulatory T cells (Tregs), and myeloid-derived suppressor cells (MDSCs), which contributed to poor results of Chimeric antigen receptors (CARs) therapy [16]
The strategies to improve CARs for use in neuroblastomas are mostly concerned with increasing the antitumor activity and persistence of the infused CAR cells
Summary
Neuroblastoma, an extracranial solid tumor that initiates from the sympathetic nervous system’s neuroendocrine tissue, is one of the most common causes of death in pediatric cancers [1,2] It is often diagnosed during the perinatal period, which accounts for 8% in patients under 15 years. One such approach is treatment with anti-GD2 monoclonal antibody, which has already been assessed in a Phase III clinical trial. The use of this antibody-based therapy was compiled into a therapeutic protocol for high-risk neuroblastoma patients and revealed promising results [9,10]. Defining these strategies would suggest an attractive route of improving the potency of CAR immunotherapy
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