MSI-H/dMMR可切除胃癌的异质性及辅助治疗方法:免疫疗法的新兴趋势。
Heterogeneity and Adjuvant Therapeutic Approaches in MSI-H/dMMR Resectable Gastric Cancer: Emerging Trends in Immunotherapy.
发表日期:2023 Sep 04
作者:
Hui Wu, Wenyuan Ma, Congfa Jiang, Ning Li, Xin Xu, Yongfeng Ding, Haiping Jiang
来源:
ANNALS OF SURGICAL ONCOLOGY
摘要:
胃癌(GC)仍然是全球常见和致命的恶性肿瘤之一。近年来,随着对分子分型的深入理解,微卫星不稳定性(MSI)成为胃癌的主要分子分型方法之一。在晚期GC的免疫治疗过程中,MSI因其重要作用而被广泛认可。然而,在可切除的胃癌中,其价值尚不清楚。关于可切除胃癌中微卫星不稳定性高(MSI-H)/缺乏错配修复(dMMR)的报道存在较大的差异,对于MSI-H/dMMR可切除GC患者术后辅助治疗的价值尚未达成共识。已知MSI-H/dMMR肿瘤细胞能够引起内源性免疫抗肿瘤反应,并广泛表达PD-1或PD-L1等免疫检查点配体。基于这些考虑,MSI-H/dMMR可切除GC患者对于辅助免疫治疗具有响应性,尽管迄今为止开展的研究有限。在本综述中,我们全面描述了MSI-H/dMMR可切除胃癌患者的地理分布和病理分期差异,并探讨了对MSI-H/dMMR的术后辅助化疗和免疫治疗的价值,以为该患者人群的个体化治疗提供依据。© 2023. 作者。
Gastric cancer (GC) remains one of the world's most common and fatal malignant tumors. With a refined understanding of molecular typing in recent years, microsatellite instability (MSI) has become a major molecular typing approach for gastric cancer. MSI is well recognized for its important role during the immunotherapy of advanced GC. However, its value remains unclear in resectable gastric cancer. The reported incidence of microsatellite instability-high (MSI-H)/deficient mismatch repair (dMMR) in resectable gastric cancer varies widely, with no consensus reached on the value of postoperative adjuvant therapy in patients with MSI-H/dMMR resectable GC. It has been established that MSI-H/dMMR tumor cells can elicit an endogenous immune antitumor response and ubiquitously express immune checkpoint ligands such as PD-1 or PD-L1. On the basis of these considerations, MSI-H/dMMR resectable GCs are responsive to adjuvant immunotherapy, although limited research has hitherto been conducted. In this review, we comprehensively describe the differences in geographic distribution and pathological stages in patients with MSI-H/dMMR with resectable gastric cancer and explore the value of adjuvant chemotherapy and immunotherapy on MSI-H/dMMR to provide a foothold for the individualized treatment of this patient population.© 2023. The Author(s).