胃癌细胞因子变化规律与肿瘤相关性乏力关系研究

目的研究胃癌伴肿瘤相关性乏力患者细胞因子基因表达谱的变化规律,验证肿瘤相关性乏力的发病学机制可能是由TNF和TGF-β等细胞因子基因表达上调引起的理论研究结论。方法采用基因芯片技术检测胃癌伴乏力患者及胃癌不伴乏力患者的外周血单个核细胞的细胞因子基因表达谱的变化情况。结果胃癌伴有乏力患者较胃癌不伴乏力患者的TNF-α、TGF-β1等细胞因子基因表达上调。结论胃癌伴有乏力时TNF-α、TGF-β1等细胞因子基因表达上调,初步验证了肿瘤相关性乏力的发病学机制可能是由TNF及TGF-β等细胞因子基因表达上调引起的。

Human epidermal growth factor receptor-2 gene amplification in gastric cancer using tissue microarray technology

AIM:To assess human epidermal growth factor receptor-2 (HER2)-status in gastric cancer and matched lymph node metastases by immunohistochemistry (IHC) and chromogenic in situ hybridization (CISH).METHODS:120 cases of primary gastric carcinomas and 45 matched lymph node metastases from patients with full clinicopathological features were mounted onto multiple-punch and single-punch tissue microarrays,respectively,and examined for HER2 overexpression and gene amplification by IHC and CISH.RESULTS:Twenty-four tumors (20%) expressed HER2 immunohistochemically.An IHC score of ≥ 2+ was observed in 20 tumors (16.6%).HER2 amplification was detected by CISH in 19 tumors (15.8%) and in their matched lymph node metastases.A high concordancerate was found between HER2 positivity (as detected by IHC) and HER2 gene amplification (as detected by CISH),since 19 of the 20 IHC positive cases were amplified (95%).All amplified cases had 2+ or 3+ IHC results.Amplification was associated with intestinal phenotype (P < 0.05).No association with grading,staging or survival was found.CONCLUSION:In gastric cancer,HER2 amplification is the main mechanism for HER2 protein overexpression and is preserved in lymph node metastases.

Screening of the carcinogenesis associated gene in gastric mucosa by gene chip

Objective： To study the difference of gene expression and screen the carcinogenesis associated gene in gastric mucosa by oligonucleotide microarray. Methods： Using the U133A gene chip to detect the gene expression profile difference between pericancerous mucosa （mucosa inside nearly 2 cm by cancer） and normal section of gastric mucosa. Bioinformatics was used to analyze the detected result on their localization and function in chromosome. Results＂ （1） A total of 150 genes with a difference of more than 3 times in expression levels by comparing the pericancerous mucosa with normal gastric mucosa, of 130 genes were up-regulated （SLR〉I.5）, and 20 were down- regulated （SLR〈 -1.5）. From the gene expression difference was to do the function classification, among those 22 enzyme and 6 enzyme regular genes were most one （18.7%）. The next were 17 nucleic acid binding associated genes （11.3%）. The third were 15 signal transduction associated genes （10%）. Fourth, were 13 protein binding associated genes （8.7%）. Besides the 40 genes were unknown their function, above mentioned 4 groups were 48.7% of the gene total number; （2） The pericancerous mucosa （P） and gastric cancer （T） were simultaneously compared with normal gastric mucosa, which had 71 genes with the same expression difference, of 61 genes were up-regulated （pericancerous SLR〉I.5）, and other 10 genes were down-regulated （pericancerous SLR〈 -1.5）. From their localization on the chromosome, there was simultaneously 71 genes appearance both in the pericancerous mucosa and in gastric cancer. The most one was 11 abnormal genes on the No. 19 chromosome. The next was No. 1, 2, 16 and 17 chromosomes which had 6 genes, respectively. It was not finding an abnormal gene on the No. 5, 14, 22 and Y chromosome. Conclusion： It suggested those genes may be related to the promotion in early gastric carcinogenesis and their progress. Four main groups （enzyme and enzyme regular, nucleic acid binding, signal transduction, protein binding） that associated gene＇s abnormality be played an importance role in studying the carcinogenesis of gastric cancer. The No. 19 and No. 1, 2, 16, 17 chromosomes are important sites of the oncogene transformation.