Targeting RAS in neuroblastoma: Is it possible?

Abstract

Neuroblastoma is a common solid tumor in children and a leading cause of cancer death in children. Neuroblastoma exhibits genetic, morphological, and clinical heterogeneity that limits the efficacy of current monotherapies. With further research on neuroblastoma, the pathogenesis of neuroblastoma is found to be complex, and more and more treatment therapies are needed. The importance of personalized therapy is growing. Currently, various molecular features, including RAS mutations, are being used as targets for the development of new therapies for patients with neuroblastoma. A recent study found that RAS mutations are frequently present in recurrent neuroblastoma. RAS mutations have been shown to activate the MAPK pathway and play an important role in neuroblastoma. Treating RAS mutated neuroblastoma is a difficult challenge, but many preclinical studies have yielded effective results. At the same time, many of the therapies used to treat RAS mutated tumors also have good reference values for treating RAS mutated neuroblastoma. The success of KRAS-G12C inhibitors has greatly stimulated confidence in the direct suppression of RAS. This review describes the biological role of RAS and the frequency of RAS mutations in neuroblastoma. This paper focuses on the strategies, preclinical, and clinical progress of targeting carcinogenic RAS in neuroblastoma, and proposes possible prospects and challenges in the future.

Keywords: Cancer; Drug discovery; Neuroblastoma; RAS.