列斯特大學(xué)(University of Leicester)的科學(xué)家發(fā)現(xiàn)了兩個(gè)與乳癌治療相關(guān)的基因，能夠解釋為何有些人對(duì)于放射線治療的效果很差,，達(dá)到預(yù)先警告的目的,，以爭(zhēng)取時(shí)間尋求其它種治療方法。這是第一份對(duì)放射治療異常反應(yīng)作出的完整研究,。由Drs Paul Symonds以及Mark Plumb等科學(xué)家聯(lián)合完成,，研究成果發(fā)表于British Journal of Cancer期刊。
Dr Symonds說(shuō)：「放射線治療是乳癌治療很重要的一環(huán),，但卻有少部份的人會(huì)有很?chē)?yán)重的副作用,。」在進(jìn)行放射線治療時(shí),，病人的皮膚會(huì)發(fā)紅或脫皮,，乳房會(huì)皺縮，皮膚底下的組織會(huì)變硬,、變厚或纖維化,。研究人員詳細(xì)診察這些病人后，發(fā)現(xiàn)有兩個(gè)基因與上述征狀有強(qiáng)烈的關(guān)系,。
Dr. Symonds說(shuō)：「大約有8%的婦女帶有組織纖維化基因(fibrosis gene),，而有長(zhǎng)期慢性疼痛的人其組織纖維化的風(fēng)險(xiǎn)更比一般人高出15倍，而被鑒定出來(lái)的這兩個(gè)基因就是乳癌疼痛的標(biāo)記,，大約有50~60%的預(yù)測(cè)值,，若能同時(shí)再找出造成皮膚發(fā)紅或脫皮的基因，那么就能將預(yù)測(cè)值提高到100%,。未來(lái)也許能透過(guò)這些指標(biāo)基因,，來(lái)預(yù)測(cè)那些人對(duì)放射線治療是不適合的，而對(duì)于那些只能選擇放射性治療的人,，也能預(yù)告該病人是否會(huì)有組織纖維化的風(fēng)險(xiǎn),。」
（編譯/陳瑞娟） (資料來(lái)源 : Bio.com)
英文原文鏈接：
原始出處:
Genetics and Genomics
British Journal of Cancer (2007) 96, 1001-1007.
doi:10.1038/sj.bjc.6603637 Published online 27 February 2007
The late radiotherapy normal tissue injury phenotypes of telangiectasia, fibrosis and atrophy in breast cancer patients have distinct genotype-dependent causes
G Giotopoulos1, R P Symonds2, K Foweraker2, M Griffin3, I Peat2, A Osman2 and M Plumb1
1Department of Genetics, University of Leicester, Leicester LE1 7RH, UK
2Department of Cancer Studies and Molecular Medicine, University of Leicester, Level 2, Osborne Building, Leicester Royal Infirmary, Leicester LE1 5WW, UK
3Department of Oncology, Nottingham University Hospitals NHS Trust, CITY Hospital Campus, ICT Services, Hucknall Road, Nottingham, UK
Correspondence to: Dr RP Symonds, E-mail: [email protected]
Received 15 November 2006; revised 19 January 2007; accepted 23 January 2007; published online 27 February 2007
Abstract
The relationship between late normal tissue radiation injury phenotypes in 167 breast cancer patients treated with radiotherapy and: (i) radiotherapy dose (boost); (ii) an early acute radiation reaction and (iii) genetic background was examined. Patients were genotyped at single nucleotide polymorphisms (SNPs) in eight candidate genes. An early acute reaction to radiation and/or the inheritance of the transforming growth factor-1 (TGF1 -509T) SNP contributed to the risk of fibrosis. In contrast, an additional 15 Gy electron boost and/or the inheritance of X-ray repair cross-complementing 1 (XRCC1) (R399Q) SNP contributed to the risk of telangiectasia. Although fibrosis, telangiectasia and atrophy, all contribute to late radiation injury, the data suggest that they have distinct underlying genetic and radiobiological causes. Fibrosis risk is associated with an inflammatory response (an acute reaction and/or TGF1), whereas telangiectasia is associated with vascular endothelial cell damage (boost and/or XRCC1). Atrophy is associated with an acute response, but the genetic predisposing factors that determine the risk of an acute response or atrophy have yet to be identified. A combined analysis of two UK breast cancer patient studies shows that 8% of patients are homozygous (TT) for the TGF1 (C-509T) variant allele and have a 15-fold increased risk of fibrosis following radiotherapy (95% confidence interval: 3.76-60.3; P=0.000003) compared with (CC) homozygotes.
Keywords: breast cancer; radiation injury; TGF1; XRCC1; fibrosis; telangiectasia
