Gene Mutations in the FGF-MAPK Signaling Pathway and Targeted Therapy in Ameloblastoma

Nattanit Boonsong, Kittipong Laosuwan, N. Kitkumthorn, P. Lapthanasupkul, Wacharaporn Thosaporn, A. Iamaroon
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Abstract

Abstract Ameloblastoma is one of the most common odontogenic tumors in Asia. In the past decade, many studies have shown gene mutations in the mitogen-activated protein kinase (MAPK) signaling pathway, especially on an extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. Mutations of fibroblast growth factor receptor 2 (FGFR2), rat sarcoma virus (RAS), and B-rapidly accelerated fibrosarcoma (BRAF) are able to cause a continuous activation of the ERK1/2 signaling pathway, hence uncontrolled tumor cell proliferation. Due to the ERK1/2 signaling pathway role in cell growth and cell survival, upregulation of this pathway can cause approximately one-third of human tumors including ameloblastoma. After the discovery of gene mutations in several cancers, many inhibitors have been designed to target these mutations. We, here, reviewed the alteration of the FGF-MAPK signaling pathway in ameloblastoma and targeted treatment used as an adjuvant or neoadjuvant therapy for ameloblastoma especially in cases where wide surgical resection is needed. Keywords: Genetic, Growth factor, Mutation, Targeted therapy
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成釉细胞瘤FGF-MAPK信号通路的基因突变及靶向治疗
摘要成釉细胞瘤是亚洲最常见的牙源性肿瘤之一。在过去的十年中,许多研究表明有丝分裂原活化蛋白激酶(MAPK)信号通路,特别是细胞外信号调节激酶1/2(ERK1/2)信号通路的基因突变。成纤维细胞生长因子受体2(FGFR2)、大鼠肉瘤病毒(RAS)和B快速加速纤维肉瘤(BRAF)的突变能够引起ERK1/2信号通路的持续激活,从而导致肿瘤细胞增殖失控。由于ERK1/2信号通路在细胞生长和细胞存活中的作用,该通路的上调可导致约三分之一的人类肿瘤,包括成釉细胞瘤。在发现几种癌症的基因突变后,许多抑制剂被设计用于靶向这些突变。在此,我们综述了成釉细胞瘤中FGF-MAPK信号通路的改变,以及作为成釉细胞癌辅助或新辅助治疗的靶向治疗,特别是在需要广泛手术切除的情况下。关键词:遗传,生长因子,突变,靶向治疗
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来源期刊
Chiang Mai University journal of natural sciences
Chiang Mai University journal of natural sciences Health Professions-Health Professions (miscellaneous)
CiteScore
1.70
自引率
0.00%
发文量
67
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