【佳學(xué)基因檢測】與甲狀腺癌相關(guān)的腫瘤抑制基因的甲基化

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比較腫瘤的基因組學(xué)特征與治療方案設(shè)計(jì)做了備注《Cancer Biomark》在.?2019;25(1):53-65.發(fā)表了一篇題目為《與甲狀腺癌相關(guān)的腫瘤抑制基因的甲基化》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由Anca Botezatu,?Iulia V Iancu,?Adriana Plesa,?Dana Manda,?Oana Popa,?Marinela Bostan,?Mirela Mihaila,?Adrian Albulescu,?Alina Fudulu,?Susana V Vladoiu,?Irina Huica,?Ruxandra Dobrescu,?Gabriela Anton,?Corin Badiu等完成。促進(jìn)了腫瘤的正確治療與個(gè)性化用藥的發(fā)展，進(jìn)一步強(qiáng)調(diào)了基因信息檢測與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究內(nèi)容關(guān)鍵詞：

腫瘤靶向治療基因檢測臨床應(yīng)用結(jié)果

基因解碼基因檢測的研究介紹：甲狀腺癌是全球賊常見的內(nèi)分泌惡性腫瘤。 DNA 甲基化的變化會(huì)導(dǎo)致正常活躍基因的沉默，尤其是腫瘤抑制基因 (TSG) 或正常沉默基因的激活?；蚪獯a基因檢測的研究目的：本研究的基因解碼基因檢測的研究目的是評(píng)估一組甲狀腺腫瘤標(biāo)志物的啟動(dòng)子甲基化程度和建立它們與甲狀腺腫瘤發(fā)生的關(guān)系?；蚪獯a基因檢測的研究方法：為了生成涉及甲狀腺腫瘤的 TSG 的全面 DNA 甲基化特征，基因解碼基因檢測使用 Human TSG EpiTect Methyl II Signature PCR Array-Qiagen 與正常樣本相比，對(duì) 24 個(gè)樣本（濾泡性腺瘤和乳頭狀甲狀腺癌）進(jìn)行了分析。甲狀腺組織?；蚪獯a基因檢測使用 qMS-PCR 擴(kuò)展了對(duì)三個(gè) TSG（TP73、WIF1、PDLIM4）的評(píng)估。使用 GraphPad Prism 進(jìn)行統(tǒng)計(jì)分析。基因解碼基因檢測的研究結(jié)果：基因解碼基因檢測注意到四個(gè)重要基因 NEUROG1、ESR1、RUNX3、MLH1，與正常相比，它們?cè)谀[瘤樣本中呈現(xiàn)甲基化啟動(dòng)子?；蚪獯a基因檢測發(fā)現(xiàn)了甲狀腺腫瘤的新特征：TP73、WIF1 和 PDLIM4 TSG 的甲基化，這可能導(dǎo)致甲狀腺腫瘤。 BRAF V600E突變與RET/PTC重排分別與TIMP3和CDH13、RARB甲基化顯著相關(guān)。基因解碼基因檢測的研究結(jié)論：TSGs啟動(dòng)子高甲基化是癌癥的標(biāo)志，采用甲基化定量基因解碼基因檢測的研究方法的檢測適用于甲狀腺的診斷和預(yù)后。癌癥。關(guān)鍵詞：甲狀腺癌；表觀遺傳學(xué)；啟動(dòng)子甲基化；抑癌基因。

腫瘤發(fā)生與反復(fù)轉(zhuǎn)移國際數(shù)據(jù)庫描述：

Background:?Thyroid carcinoma is the most common endocrine malignancy worldwide. Changes in DNA methylation can cause silencing of normally active genes, especially tumour suppressor genes (TSG) or activation of normally silent genes.Objective:?The aim of this study is to evaluate the degree of promoter methylation for a panel of markers for thyroid neoplasms and to establish their relationship with thyroid oncogenesis.Methods:?To generate a comprehensive DNA methylation signature of TSGs involved in thyroid neoplasia, we use Human TSG EpiTect Methyl II Signature PCR Array-Qiagen for 24 samples (follicular adenomas and papillary thyroid carcinomas) compared with normal thyroid tissue. We extended the evaluation for three TSGs (TP73, WIF1, PDLIM4) using qMS-PCR. Statistical analysis was performed with GraphPad Prism.Results:?We noted four important genes NEUROG1, ESR1, RUNX3, MLH1, which presented methylated promoter in tumour samples compared to normal. We found new characteristic of thyroid tumours: methylation of TP73, WIF1 and PDLIM4 TSGs, which can contribute to thyroid neoplasia. A significant correlation between BRAF V600E mutation and RET/PTC rearrangements with TIMP3 and CDH13, RARB methylation, respectively was observed.Conclusions:?TSGs promoter hypermethylation is a hallmark of cancer and a test that uses methylation quantification method is suitable for diagnosis and prognosis of thyroid cancer.Keywords:?Thyroid cancer; epigenetics; promoter methylation; tumour suppressor genes.