【佳学基因检测】基因检测胃癌表皮生长因子受体结构改变

肿瘤基因检测多少钱一次—目标

小组讨论肿瘤基因学知识要点，《肿瘤致病基因突变位点的性质及影响分析》在消化科常见肿瘤这一节中引用了《BMC Cancer》在. 2008 Jan 16;8:10.发表了一篇题目为《胃癌表皮生长因子受体结构改变》肿瘤靶向药物治疗基因检测临床研究文章。该研究由Cátia Moutinho , Ana R Mateus, Fernanda Milanezi, Fátima Carneiro, Raquel Seruca, Gianpaolo Suriano等完成。促进了胃癌多种致病基因的基因检测及解读分析注意事项，为三甲医院医生通过基因检测与临床的结合发表科研成果的一个范例。

消化科肿瘤找到治疗药物的机构临床研究内容关键词：

胃癌,消化道,EGFR突变,靶向药物,FISH,基因检测

肿瘤靶向治疗基因检测临床应用结果

胃癌靶向用药基因检测研究背景：佳学基因检测已在人类的移种肿瘤中记录并析芝EGFR 的过度表达，这其中也包括胃癌。在非小细胞肺癌 NSCLC 患者中，蛋白质激酶结构域内的体细胞 EGFR 突变以及基因扩增与对 EGFR 抑制剂的良好临床反应相关。在胃肿瘤中，关于 EGFR 结构改变的数据仍然存在争议。鉴于其可能的治疗相关性，佳学基因解码旨在确定 EGFR 基因在一系列原发性胃癌中结构改变的频率和类型。消化道肿瘤靶向药物基因检测研究方法：在一系列 77 个原发性胃癌中对 EGFR 基因的激酶结构域进行直接测序基因测序。对 30 例进行了 FISH 基因检测分析。进行了EGFR改变与肿瘤临床病理特征之间的关联研究。胃癌基因检测与临床病理特征之间的关系研究结果：在77例原发性胃癌中，胃癌靶向药物治疗靶点研究发现了2个EGFR体细胞突变和几个存在于20号外显子EGFR多态性。还发现了6个不同的EGFR内含子序列变体。四种胃癌表现出平衡的多体性或EGFR基因扩增。肿瘤精准用药基因检测证实，与野生型 EGFR 癌相比，具有 EGFR 改变（体细胞突变或拷贝数变异）的胃癌显示出肿瘤大小显着增加（p = 0.0094）。肿瘤预后及基因突变特征研究结论：消化道肿瘤基因解码证明 EGFR 结构改变在胃癌中很少见，但只要存在，它就会导致肿瘤生长。肿瘤基因序列变化与胃癌的精准治疗认为寻找胃癌中的 EGFR 改变可能在临床上很重要，以识别对酪氨酸激酶抑制剂敏感的患者。

肿瘤发生与复发转移国际数据库描述：

Background: EGFR overexpression has been described in many human tumours including gastric cancer. In NSCLC patients somatic EGFR mutations, within the kinase domain of the protein, as well as gene amplification were associated with a good clinical response to EGFR inhibitors. In gastric tumours data concerning structural alterations of EGFR remains controversial. Given its possible therapeutic relevance, we aimed to determine the frequency and type of structural alterations of the EGFR gene in a series of primary gastric carcinomas.Methods: Direct sequencing of the kinase domain of the EGFR gene was performed in a series of 77 primary gastric carcinomas. FISH analysis was performed in 30 cases. Association studies between EGFR alterations and the clinical pathological features of the tumours were performed.Results: Within the 77 primary gastric carcinomas we found two EGFR somatic mutations and several EGFR polymorphisms in exon 20. Six different intronic sequence variants of EGFR were also found. Four gastric carcinomas showed balanced polysomy or EGFR gene amplification. We verified that gastric carcinoma with alterations of EGFR (somatic mutations or copy number variation) showed a significant increase of tumour size (p = 0.0094) in comparison to wild-type EGFR carcinomas.Conclusion: We demonstrate that EGFR structural alterations are rare in gastric carcinoma, but whenever present, it leads to tumour growth. We considered that searching for EGFR alterations in gastric cancer is likely to be clinically important in order to identify patients susceptible to respond to tyrosine kinase inhibitors.

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