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用化学致癌剂甲硝基亚硝胍（ＭＮＮＧ）对人类胃粘膜上皮细胞株ＧＥＳ－１进行不同方式处理，常规方法提取ＤＮＡ，经聚合酶链反应扩增Ｈ－ｒａｓ原癌基因后，以单链构象多态性检测Ｈ－ｒａｓ原癌基因，作者发现长期小剂量的ＭＮＮＧ打击ＧＥＳ－１可以诱导此细胞发生Ｈ－ｒａｓ基因改变，而大剂量短期处理的ＧＥＳ－１组未见Ｈ－ｒａｓ基因构型改变，提示化学致癌剂ＭＮＮＧ诱发Ｈ－ｒａｓ癌基因改变是一个缓慢、剂量叠加的过程，在ＭＮＮＧ诱发的胃癌中，Ｈ－ｒａｓ基因的改变不是首发事件。
Human gastric mucosal epithelial cell line GES-1 was treated by chemical carcinogen MNNG in different ways. The DNA was extracted by conventional method and the proto-oncogene H-ras was amplified by polymerase chain reaction Chain conformation polymorphism detection of H-ras proto-oncogene, the authors found that long-term low-dose MNNG against GES-1 can induce H-ras gene changes in this cell, while the high-dose short-term treatment of GES-1 group no H-ras The genetic conformational changes suggest that the chemosensitizer MNNG induced H-ras oncogene change is a slow, dose-superimposed process. The change of H-ras gene is not the first event in MNNG-induced gastric cancer.