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中华普通外科学文献(电子版) ›› 2023, Vol. 17 ›› Issue (05) : 376 -379. doi: 10.3877/cma.j.issn.1674-0793.2023.05.012

综述

甲胎蛋白在胃肝样腺癌中的作用机制及诊断预后研究进展
兰青, 熊枝繁(), 杨盛力   
  1. 430077 武汉,华中科技大学同济医学院附属梨园医院消化内科
    430022 武汉,华中科技大学同济医学院附属协和医院肿瘤中心
  • 收稿日期:2023-03-28 出版日期:2023-10-01
  • 通信作者: 熊枝繁

Progress on the role mechanism, diagnostic value and prognosis of alpha fetoprotein in hepatoid adenocarcinoma of the stomach

Qing Lan, Zhifan Xiong(), Shengli Yang   

  1. Department of Gastroenterology,Liyuan Hospital of Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430077, China
    Cancer Center of Xiehe Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430022, China
  • Received:2023-03-28 Published:2023-10-01
  • Corresponding author: Zhifan Xiong
引用本文:

兰青, 熊枝繁, 杨盛力. 甲胎蛋白在胃肝样腺癌中的作用机制及诊断预后研究进展[J/OL]. 中华普通外科学文献(电子版), 2023, 17(05): 376-379.

Qing Lan, Zhifan Xiong, Shengli Yang. Progress on the role mechanism, diagnostic value and prognosis of alpha fetoprotein in hepatoid adenocarcinoma of the stomach[J/OL]. Chinese Archives of General Surgery(Electronic Edition), 2023, 17(05): 376-379.

胃肝样腺癌(HAS)是一种罕见的恶性肿瘤,属于胃癌的特殊亚型,兼具腺癌和肝细胞癌样分化特征,且大部分患者血清甲胎蛋白(AFP)升高。作为肝癌的肿瘤标志物,AFP被广泛应用于临床,但其对于HAS的作用和价值还不明确。为进一步加深AFP在HAS中的认识并了解其临床意义,现就AFP在该病中的作用机制、诊断价值及预后关系等方面进行综述,以帮助临床医师准确诊治。

Hepatoid adenocarcinoma of the stomach (HAS) is a special subtype of gastric cancer, which is a rare malignant tumor with both adenocarcinoma and hepatocellular carcinoma-like differentiation, and most patients have elevated serum alpha fetoprotein (AFP). However, the value of AFP in HAS is still unclear. In order to further deepen the comprehensive understanding of AFP in HAS and to understand its clinical significance, the role mechanism, diagnostic value and prognosis of AFP are reviewed for accurate diagnosis and treatment of HAS in clinics.

表1 各文献中报道的AFP在胃肝样腺癌中的表达阳性率(%)
图1 AFP促进HAS发生发展可能的作用机制 左上部分:AFP通过抑制PTEN活性,激活PI3K/AKT/mTOR通路,促进src和ras表达,AFP还可作用于肿瘤细胞AFPR激活cAMP-PKA通路,Ca2+内流增多,进一步促进癌基因c-fos、c-jun和n-ras的表达,从而刺激肿瘤细胞增殖;右上部分:Wnt与细胞表面特异性受体作用激活DVL,DVL下调糖原合成激酶-3蛋白和轴蛋白复合体的降解活性,引起β-catenin堆积,β-catenin进入细胞核,调节基因表达,导致肿瘤发生;下半部分:AFP通过抑制效应T细胞的分化,同时激活调节T细胞扩增,还可抑制树突状细胞分泌IL-12,从而下调自然杀伤细胞的表达,进而抑制细胞免疫
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