【佳學(xué)基因檢測(cè)】YAP/TAZ在角囊性牙源性腫瘤中的表達(dá)及其與增殖行為的可能關(guān)聯(lián)

人體基因檢測(cè)需要多少錢(qián)—比較

開(kāi)會(huì)學(xué)習(xí)基因?qū)嶒?yàn)室人員知識(shí)更新《腫瘤靶向藥物選擇的基因突變標(biāo)準(zhǔn)》《Biomed Res Int》在.?2017;2017:4624890.發(fā)表了一篇題目為《YAP/TAZ在角囊性牙源性腫瘤中的表達(dá)及其與增殖行為的可能關(guān)聯(lián)》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Qi-Wen Man?,?Yan-Qi Ma?,?Jin-Yuan Liu?,?Yi Zhao?,?Bing Liu?,?Yi-Fang Zhao?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(cè)與分析的重要性。

腫瘤遺傳的可能性分析臨床研究?jī)?nèi)容關(guān)鍵詞：

角囊性牙源性腫瘤,KCOT,口腔科腫瘤,YAP,TAZ

腫瘤靶向治療基因檢測(cè)臨床應(yīng)用結(jié)果

口腔科腫瘤基因檢測(cè)研究的目的是闡明 YAP/TAZ 是否參與角囊性牙源性腫瘤 (KCOT) 的發(fā)病機(jī)制和增殖性生長(zhǎng)，以便優(yōu)化口腔癌腫瘤基因檢測(cè)的基因及基因位點(diǎn)的選擇及結(jié)果解讀。通過(guò)免疫組化和實(shí)時(shí)定量PCR檢測(cè)和比較正?？谇火つぃ∣M）和角囊性牙源性腫瘤 (KCOT)中YAP/TAZ及下游蛋白和基因的表達(dá)水平。腫瘤基因檢測(cè)結(jié)果表明，與口腔黏膜（OM）相比，角囊性牙源性腫瘤 (KCOT) 中 YAP/TAZ 和下游蛋白（Cyr61、CTGF）的表達(dá)顯著上調(diào)，Ki-67 上調(diào)。重要的是，與轉(zhuǎn)錄共激活因子 YAP/TAZ 相互作用的轉(zhuǎn)錄因子（TEAD1、TEAD4 和 RUNX2）和細(xì)胞周期相關(guān)基因（CDK2、PCNA）的 mRNA 水平也在 KCOT 中上調(diào)。此外，Spearman 秩相關(guān)檢驗(yàn)的結(jié)果揭示了 YAP/TAZ 和 Ki-67 之間的密切關(guān)系，雙標(biāo)記免疫熒光進(jìn)一步證明了這一點(diǎn)，揭示了 KCOT 樣品中 YAP/TAZ 與 Ki-67 的同步分布。所有數(shù)據(jù)表明 YAP/TAZ 可能與角囊性牙源性腫瘤 (KCOT) 的增殖行為有關(guān)。

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

The aim of this study is to clarify whether YAP/TAZ is involved in the pathogenesis and proliferative growth of keratocystic odontogenic tumor (KCOT). The expression levels of YAP/TAZ and downstream proteins and genes in normal oral mucosa (OM) and KCOT were determined and compared by immunohistochemistry and real-time quantitative PCR. The results showed that the expression of YAP/TAZ and downstream proteins (Cyr61, CTGF) was significantly upregulated in KCOT with upregulation of Ki-67 compared to OM. Importantly, the mRNA levels of transcription factors (TEAD1, TEAD4, and RUNX2) and cell cycle related genes (CDK2, PCNA), which interact with the transcriptional coactivators YAP/TAZ, are also upregulated in the KCOT. In addition, the results from Spearman rank correlation test revealed the close relationship between YAP/TAZ and Ki-67, which was further evidenced by double-labelling immunofluorescence that revealed a synchronous distribution for YAP/TAZ with Ki-67 in KCOT samples. All the data suggested YAP/TAZ might be involved in the proliferative behavior of KCOT.