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ｇｓｐ癌基因是肢端肥大症患者发生垂体肿瘤的重要原因，这是由于编码刺激性Ｇ蛋白α亚基（Ｇｓα）的基因存在突变，导致细胞内ｃＡＭＰ水平持速升高所致。令人惊讶的是，来自日本的报导ｇｓｐ癌基因的发病率（４～９％）明显低于西方（４０％），推测为种族差异所至。为了进一步观察，我们检测了ｇｓｐ癌基因在我国肢端肥大患者中的表达率。材料与方法：检测了１０例国人肢端肥大患者（男６例，女４例，年龄２３～５４岁，其中３例表现有巨人症，肿瘤直径为１１～４０ｍｍ，６例肿瘤有侵袭性）。从肿瘤组织中提取ＤＮＡ，经ＰＣＲ扩增Ｇｓα基因，ＰＣＲ－ＤＮＡ直接进行序列分析来检测ｇｓｐ癌基因突变位点。结果：４例（４０％）肿瘤ｇａｓ癌基因为阳性，３例突变位点位于编码Ｇｓα基因的２０１号密码子上，精氨酸被替换为半胱氨酸（ＣＧＴ→ＴＧＴ），１例位于２２７号密码子，甘氨酸被替换为亮氨酸（ＣＡＧ→ＣＴＧ）。讨论：结果显示，ｇｓｐ癌基因在中国肢端肥大症患者中的发病率与西方一致，其与日本研究结果的差异似乎不是种族不同所致
The gsp oncogene is an important cause of pituitary tumors in patients with acromegaly due to mutations in the gene encoding the stimulatory G protein α subunit (Gsα), resulting in a sustained increase in intracellular cAMP levels. Surprisingly, the incidence of gsp oncogene (4 to 9%) from Japan was significantly lower than in the West (40%), presumably due to ethnic differences. For further observation, we examined the expression of gsp oncogene in patients with acromegaly in our country. MATERIALS AND METHODS: Totally 10 patients with acromegaly (6 males and 4 females, aged 23-54 years, including 3 gigantic tumors, 11-40 mm in diameter and 6 invasive tumors) were examined. . DNA was extracted from the tumor tissue, Gsα gene was amplified by PCR and sequenced directly by PCR-DNA to detect the site of gsp oncogene mutation. Results: Gastrinogene was positive in 4 cases (40%) of the tumors, 3 sites were located on codon 201 encoding Gsα gene, arginine was replaced by cysteine (CGT → TGT) and 1 At codon 227, glycine is replaced by leucine (CAG → CTG). Discussion: The results show that the incidence of gsp oncogene in Chinese patients with acromegaly is in line with that in the West, and the difference with the Japanese study does not appear to be due to race differences