【佳學(xué)基因檢測(cè)】染色體穩(wěn)定性基因檢測(cè)揭示致癌過程及腫瘤致死率抑制

醫(yī)生推薦做基因檢測(cè)合理嗎

挖掘腫瘤基因組學(xué)個(gè)性化藥物選擇記錄，在基因檢測(cè)技術(shù)相關(guān)章節(jié)中引用并參考了《J Cell Biochem》在. 2008 Dec 15;105(6):1327-41.發(fā)表了一篇題目為《染色體穩(wěn)定性基因檢測(cè)揭示致癌過程及腫瘤致死率抑制》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Changxian Shen , Yonggang Zhou, Jun Zhan, Sven N Reske, Andreas K Buck等完成?；驒z測(cè)揭示突變的存在、種類與數(shù)量，而基因解碼則是將這種信息轉(zhuǎn)化為臨床應(yīng)用指導(dǎo)的核心。清晰地闡述了基因檢測(cè)們息應(yīng)用的不同不節(jié)的實(shí)際價(jià)值。

腫瘤三甲醫(yī)院主任醫(yī)師共識(shí)性方法臨床研究內(nèi)容關(guān)鍵詞：

染色體不穩(wěn)定性,基因組完整性,腫瘤抑制,耐藥性,靶向藥物,新靶點(diǎn)

腫瘤靶向治療基因檢測(cè)臨床應(yīng)用結(jié)果

每個(gè)生物體的維持和生存取決于其基因組的完整性。必需基因的改變或異常的染色體數(shù)目和結(jié)構(gòu)會(huì)導(dǎo)致細(xì)胞死亡。但是腫瘤的基因解碼發(fā)現(xiàn)癌細(xì)胞，特別是在實(shí)體瘤中，含有體細(xì)胞基因突變并且是染色體不穩(wěn)定性（CIN），這表明癌細(xì)胞已經(jīng)獲得了抑制致命突變和/或染色體不穩(wěn)定性（CIN）的機(jī)制。在腫瘤的發(fā)生與演變的領(lǐng)域里，佳學(xué)基因解碼討論基于酵母遺傳相互作用和轉(zhuǎn)基因小鼠研究的腫瘤殺傷力抑制概念。在腫瘤發(fā)生的多步驟過程的早期階段，早期癌細(xì)胞可能已經(jīng)采用遺傳和表觀遺傳改變來耐受隨后發(fā)生的其他基因的致命突變，以及更大程度的染色體不穩(wěn)定性（CIN）。反過來，染色體不穩(wěn)定性（CIN）介導(dǎo)的大量基因獲得和丟失為進(jìn)一步的基因重組提供了更廣泛的緩沖，導(dǎo)致癌細(xì)胞異質(zhì)性、耐藥性和逃避癌基因成癮，因此染色體不穩(wěn)定性（CIN）可能既是腫瘤發(fā)生的效應(yīng)物，也是誘導(dǎo)物。因此，通過基因檢測(cè)后干擾腫瘤殺傷力抑制可能導(dǎo)致癌細(xì)胞死亡或生長缺陷，從而提供新的藥物治療靶點(diǎn)。進(jìn)一步驗(yàn)證腫瘤殺傷力抑制概念將有助于闡明染色體不穩(wěn)定性（CIN）在腫瘤發(fā)生中的作用、染色體不穩(wěn)定性（CIN）與體細(xì)胞基因突變之間的關(guān)系，并將影響抗癌藥物開發(fā)的設(shè)計(jì)。

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

The maintenance and survival of each organism depends on its genome integrity. Alterations of essential genes, or aberrant chromosome number and structure lead to cell death. Paradoxically, cancer cells, especially in solid tumors, contain somatic gene mutations and are chromosome instability (CIN), suggesting a mechanism that cancer cells have acquired to suppress the lethal mutations and/or CIN. Herein we will discuss a tumor lethality suppression concept based on the studies of yeast genetic interactions and transgenic mice. During the early stages of the multistep process of tumorigenesis, incipient cancer cells probably have adopted genetic and epigenetic alterations to tolerate the lethal mutations of other genes that ensue, and to a larger extent CIN. In turn, CIN mediated massive gain and loss of genes provides a wider buffer for further genetic reshuffling, resulting in cancer cell heterogeneity, drug resistance and evasion of oncogene addiction, thus CIN may be both the effector and inducer of tumorigenesis. Accordingly, interfering with tumor lethality suppression could lead to cancer cell death or growth defects. Further validation of the tumor lethality suppression concept would help to elucidate the role of CIN in tumorigenesis, the relationship between CIN and somatic gene mutations, and would impact the design of anticancer drug development.