【佳學(xué)基因檢測(cè)】Onc 基因和其他癌癥化療的新靶點(diǎn)的基因檢測(cè)

基因治療腫瘤要多少錢—爭(zhēng)論

與同行交流時(shí)腫瘤啟動(dòng)預(yù)防及反復(fù)抑制基因檢測(cè)發(fā)現(xiàn)《J Cancer Res Clin Oncol》在. 1984;107(1):1-14.發(fā)表了一篇題目為《Onc 基因和其他癌癥化療的新靶點(diǎn)的基因檢測(cè)》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由H Busch等完成。詳細(xì)討論了原癌基因、癌變基因與腫瘤致病基因與普通看家基因檢測(cè)中的區(qū)別，列出了基因檢測(cè)機(jī)構(gòu)基因檢測(cè)項(xiàng)目選擇的一個(gè)參考意見(jiàn)。

腫瘤靶向藥物及正確治療臨床研究?jī)?nèi)容關(guān)鍵詞：

Onc基因,化療,新靶點(diǎn),生存關(guān)聯(lián)性,基因檢測(cè)

腫瘤靶向治療基因檢測(cè)臨床應(yīng)用結(jié)果

分子生物學(xué)的賊新進(jìn)展庫(kù)腫瘤科癌癥患者帶來(lái)了希望，即對(duì)人類癌癥的理解可能會(huì)迅速發(fā)展，并且可能會(huì)導(dǎo)致治療的改進(jìn)。隨著基因克隆、DNA序列分析和改進(jìn)的雜交方法的發(fā)展，尤其是基因解碼技術(shù)在確解基因突變序列方面的突出優(yōu)勢(shì)，有可能評(píng)估癌癥是否由基因劑量的改變、基因的點(diǎn)或多重突變、易位、缺失、插入、倒位、順式或反式改變的啟動(dòng)子引起，或者是由擴(kuò)增和各種其他遺傳因素，包括改變特定 mRNA 種類讀出率的增強(qiáng)子元素。 “Onc 基因”正在深入研究，因?yàn)樗鼈兲峁┝丝晒芾淼奶结榿?lái)評(píng)估這些各種可能性，還因?yàn)閷?duì)其細(xì)胞類似物的研究可能會(huì)進(jìn)一步了解正常胎兒和惡性細(xì)胞的分子生物學(xué)。盡管該領(lǐng)域的一些支持者過(guò)于熱情，批評(píng)者也持否定態(tài)度，但很明顯，分析工具和新信息將在進(jìn)一步研究實(shí)驗(yàn)性癌癥時(shí)具有價(jià)值，無(wú)論是否細(xì)胞癌基因（c-onc 基因）是否與人類癌癥有關(guān)。與此同時(shí)，對(duì)參與生長(zhǎng)過(guò)程的酶、蛋白質(zhì)和表位的研究，為通過(guò)定量減少生物合成反應(yīng)來(lái)抑制人類癌癥開(kāi)辟了新途徑。

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

Recent advances in molecular biology have raised the hope that understanding of human cancer might progress rapidly and that improvements in therapy might result (Bishop 1983a, b; Busch 1962; Busch 1976; Duesberg 1983). With the development of gene cloning, DNA sequence analysis and improved hybridization methods, it became possible to evaluate whether cancer results from alteration in gene dosage, point or multiple mutation of genes, translocations, deletions, insertions, inversions, cis or trans altered promoters, amplification, and a variety of other genetic factors, including enhancer elements that alter rates of readouts of particular mRNA species. "Onc genes" are under intensive study because they offer manageable probes for evaluation of these various possibilities and also because the study of their cellular analogs may further understanding of the molecular biology of normal fetal and malignant cells. Despite the excessive enthusiasm of some proponents of this field and the negativism of its critics (Bishop 1983 a, b; Duesberg 1983), it is clear that analytical tools and new information will be of value in further studies on experimental cancer, regardless of whether cellular oncogenes (c-onc genes) have anything to do with human cancer or not. In the meantime, studies on enzymes, proteins and epitopes involved in growth processes, have opened new avenues for inhibition of human cancer by quantitative reduction of biosynthetic reactions.