【佳學(xué)基因檢測(cè)】模擬癌癥基因檢測(cè)中的非隨機(jī)缺失:基因解碼的驗(yàn)證機(jī)制
腫瘤基因檢測(cè)費(fèi)用熱點(diǎn)
與同行交流腫瘤檢測(cè)的時(shí)間與空間對(duì)治療效果的影響知道《Semin Cancer Biol》在 2007 Feb;17(1):19-30發(fā)表了一篇題目為《模擬癌癥中的非隨機(jī)缺失》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Maria Kost-Alimova, Stefan Imreh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。
项目名称 | 检测价格 | 优惠价格 |
---|---|---|
肿瘤基因检测 | 3500 | 3500 |
眼睛近视基因检测 | 750 | 750 |
注意力基因检测 | 750 | 750 |
糖尿病基因检测 | 750 | 750 |
高血压基因检测 | 1500 | 1500 |
心脏病基因检测 | 1500 | 1500 |
猝死基因检测 | 3500 | 3500 |
心脏衰竭基因检测 | 3500 | 3500 |
腫瘤靶向藥物及正確治療臨床研究?jī)?nèi)容關(guān)鍵詞:
模擬,基因檢測(cè),缺失突變,節(jié)段性損失,基因解碼,驗(yàn)證
腫瘤靶向治療基因檢測(cè)臨床應(yīng)用結(jié)果
染色體缺失在癌癥中確實(shí)比比皆是,并且在某些區(qū)域以非隨機(jī)方式檢測(cè)到。盡管它們的相關(guān)性仍然難以捉摸,但普遍認(rèn)為節(jié)段性損失為細(xì)胞提供了選擇性生長(zhǎng)優(yōu)勢(shì)。因此,這些可能包含控制正常生長(zhǎng)和抑制惡性腫瘤的基因和/或調(diào)節(jié)序列?!痘蚪獯a創(chuàng)新技術(shù)團(tuán)隊(duì)》開(kāi)發(fā)了一種基于單染色體雜合體的實(shí)驗(yàn)?zāi)P?,用于基因檢測(cè)中缺失的產(chǎn)生和功能分析,稱為“消除測(cè)試”(Et)。專注于人類 3 號(hào)染色體——已知它攜帶多個(gè) 3p 缺失——預(yù)計(jì) Et 將 3p 腫瘤抑制區(qū)域限制在一個(gè)足夠小的片段上,從而允許選擇一個(gè)至關(guān)重要的候選基因。令人驚訝的是,基因解碼創(chuàng)新技術(shù)團(tuán)隊(duì)檢測(cè)到三個(gè)區(qū)域在全部或大部分腫瘤中丟失:CER1 (3p21.3, Mb: 43.32-45.74)、CER2 (3p22, Mb: 37.83-39.06) 和 FER (3p14.3-p21.2, mb:50.12-58.03)。相比之下,定期保留 3q26-qter 區(qū)域 (CRR)。 CER1 - 基因解碼創(chuàng)新技術(shù)團(tuán)隊(duì)的主要關(guān)注點(diǎn) - 包含多個(gè)可能抑制腫瘤生長(zhǎng)的基因,但 RIS1、LF (LTF) 和 LIMD1 這 3 個(gè)基因已經(jīng)獲得了必要的實(shí)驗(yàn)支持,被認(rèn)為是真正的腫瘤抑制因子。腫瘤抑制區(qū)域邊界顯示出不穩(wěn)定特征,包括:(1)它們?cè)谶M(jìn)化和腫瘤中斷裂,(2)它們水平進(jìn)化,(3)它們富含假基因插入。斷點(diǎn)簇區(qū)域賊顯著的特征是驅(qū)動(dòng)水平進(jìn)化并導(dǎo)致癌癥相關(guān)不穩(wěn)定性的節(jié)段性重復(fù)。
腫瘤發(fā)生與反復(fù)轉(zhuǎn)移國(guó)際數(shù)據(jù)庫(kù)描述:
Chromosome deletions do abound in cancer and are detected in certain regions in a non-random manner. Although their relevance remains elusive, it is a general agreement that segmental losses provide the cell with selective growth advantage. Consequently these may contain genes and/or regulatory sequences that control normal growth and inhibit malignancy. We have developed a monochromosomal hybrid based experimental model for the generation and functional analysis of deletions, that is called "elimination test" (Et). Focused on human chromosome 3 - that was known to carry multiple 3p deletions - the Et was expected to restrict a 3p tumor suppressor region to a sufficiently small segment that permits the selection of a critically important candidate gene. Surprisingly, we detected three regions that were lost in all or majority of tumors: CER1 (3p21.3, Mb: 43.32-45.74), CER2 (3p22, Mb: 37.83-39.06) and FER (3p14.3-p21.2, Mb: 50.12-58.03). In contrast a 3q26-qter region (CRR) was regularly retained. CER1 - our main focus - contains multiple genes that may inhibit tumor growth, but 3 genes, RIS1, LF (LTF) and LIMD1 have already the necessary experimental support to be considered bona fide tumor suppressors. Tumor suppressor region borders display instability features including: (1) they break in evolution and in tumors, (2) they evolve horizontally, and (3) they are enriched with pseudogene insertions. The most remarkable features at the breakpoint cluster regions were segmental duplications that drive horizontal evolution and contribute to cancer associated instability.
(責(zé)任編輯:佳學(xué)基因)