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【佳學(xué)基因檢測(cè)】WNT抑制因子-1的啟動(dòng)子甲基化基因檢測(cè)與多種腫瘤的發(fā)病風(fēng)險(xiǎn)

【佳學(xué)基因檢測(cè)】WNT抑制因子-1的啟動(dòng)子甲基化基因檢測(cè)與多種腫瘤的發(fā)病風(fēng)險(xiǎn)。腫瘤基因檢測(cè)回扣機(jī)會(huì),參加學(xué)術(shù)會(huì)議時(shí),討論了成人腫瘤與兒童腫瘤基因檢測(cè)序列的異同點(diǎn),并在《腫瘤治療

佳學(xué)基因檢測(cè)】WNT抑制因子-1的啟動(dòng)子甲基化基因檢測(cè)與多種腫瘤的發(fā)病風(fēng)險(xiǎn)

腫瘤基因檢測(cè)回扣機(jī)會(huì)


參加學(xué)術(shù)會(huì)議時(shí),討論了成人腫瘤與兒童腫瘤基因檢測(cè)序列的異同點(diǎn),并在《腫瘤治療效果與基因檢測(cè)結(jié)果的相關(guān)性》的報(bào)告中得知《J Cancer Res Ther》在 2018 Jun;14(Supplement):S381-S387發(fā)表了一篇題目為《WNT抑制因子-1的啟動(dòng)子甲基化可能與多種人類腫瘤的發(fā)病機(jī)制有關(guān)》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Yong Zhou, Zhaohua Li, Yinlu Ding, Peng Zhang, Jinqing Wang, Jianliang Zhang, Hao Wang 等完成。為腫瘤風(fēng)險(xiǎn)基因檢測(cè)增加了新的檢測(cè)位點(diǎn),選擇多腫瘤風(fēng)險(xiǎn)基因解碼的全面性再次向前邁進(jìn)一步。


腫瘤風(fēng)險(xiǎn)基因檢測(cè)位點(diǎn)的選擇及驗(yàn)證關(guān)鍵詞:


隊(duì)列研究, WNT抑制因子-1,薈萃分析,甲基化。


腫瘤風(fēng)險(xiǎn)基因檢測(cè)的位點(diǎn)選擇和驗(yàn)證臨床應(yīng)用結(jié)果


多腫瘤風(fēng)險(xiǎn)基因檢測(cè)位點(diǎn)增加團(tuán)隊(duì)的研究目的:多腫瘤風(fēng)險(xiǎn)基因檢測(cè)位點(diǎn)增加團(tuán)隊(duì)使用基于薈萃分析的方法研究了 WNT 抑制因子-1 (WIF-1) 基因甲基化與多種人類腫瘤發(fā)病機(jī)制的關(guān)聯(lián)。多腫瘤風(fēng)險(xiǎn)基因檢測(cè)位點(diǎn)增加團(tuán)隊(duì)的研究材料和方法:另外采用電子數(shù)據(jù)庫(kù)和手動(dòng)搜索來(lái)檢索相關(guān)的發(fā)表的基因解碼數(shù)據(jù)。根據(jù)預(yù)定義的選擇標(biāo)準(zhǔn)篩選與腫瘤和 WIF-1 相關(guān)的隊(duì)列研究,并通過(guò) STATA 軟件分析從所選研究中提取的所有數(shù)據(jù)。多腫瘤風(fēng)險(xiǎn)基因檢測(cè)位點(diǎn)增加團(tuán)隊(duì)的研究結(jié)果:多腫瘤風(fēng)險(xiǎn)基因檢測(cè)位點(diǎn)增加團(tuán)隊(duì)的研究賊終納入了 16 項(xiàng)研究的原始數(shù)據(jù),涉及 1112 個(gè)腫瘤樣本和 612 個(gè)相鄰正常樣品。研究結(jié)果表明,腫瘤組織中WIF-1基因甲基化水平明顯高于鄰近/正常組織。種族亞組分析結(jié)果顯示,在高加索人、亞洲人和非洲人中,腫瘤組織中WIF-1基因的甲基化狀態(tài)高于鄰近/正常組織。對(duì)疾病類型的進(jìn)一步亞組分析顯示,WIF-1 基因甲基化狀態(tài)是一種普遍現(xiàn)象,即在患有多個(gè)人類腫瘤的患者的腫瘤組織中與鄰近/正常組織相比觀察到。有趣的是,WIF-1基因甲基化基因檢測(cè)在肺癌、胃癌、星形細(xì)胞瘤和鄰近/正常組織患者的腫瘤組織之間沒有顯著差異,表明WIF-1基因甲基化不是一般的非特異性現(xiàn)象。多腫瘤風(fēng)險(xiǎn)基因檢測(cè)位點(diǎn)增加團(tuán)隊(duì)的研究結(jié)論:WIF-與鄰近正常組織相比,腫瘤組織中的1基因甲基化明顯更頻繁,表明WIF-1基因甲基化可能是多種人類腫瘤發(fā)病機(jī)制中的重要事件。可以做為多腫瘤風(fēng)險(xiǎn)基因檢測(cè)的位點(diǎn)。


腫瘤發(fā)生與反復(fù)轉(zhuǎn)移國(guó)際數(shù)據(jù)庫(kù)描述:


Aim: We investigated the association of WNT inhibitory factor-1 (WIF-1) gene methylation with the pathogenesis of multiple human tumors, using a meta-analysis based approach.Materials and methods: Electronic databases and manual search was additionally employed to retrieve relevant published literature. The cohort studies relating to tumor and WIF-1 were screened based on predefined selection criteria, and all extracted data from the selected studies were analyzed through STATA software.Results: Sixteen studies were finally enrolled in our study involved 1112 tumor samples and 612 adjacent normal samples. The study result showed that WIF-1 gene methylations in tumor tissues were significantly higher compared with adjacent/normal tissues. The result of subgroup analysis on ethnicity revealed that in the Caucasians, Asians, and Africans, the methylation status of WIF-1 gene in tumor tissues was higher than adjacent/normal tissues. Further subgroup analysis on disease types revealed that WIF-1 gene methylation status is a widespread phenomenon that is, observed in tumor tissues of patients with multiple human tumors compared with that in adjacent/normal tissues. Interestingly, there was no significant difference in WIF-1 gene methylation between tumor tissues among patients with lung cancer, gastric cancer, astrocytoma, and adjacent/normal tissues, indicating the WIF-1 gene methylation not a general nonspecific phenomenon.Conclusion: WIF-1 gene methylation in tumor tissues was significantly more frequent as compared to that in adjacent normal tissues, indicating that WIF-1 gene methylation may be an important event in the pathogenesis of multiple human tumors.



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