英國科學(xué)家近日鑒別出了三個與室鼓膜瘤（ependymoma，兒童腦癌的常見形式）有關(guān)的基因,。這一研究對室鼓膜瘤遺傳學(xué)提出了更詳細的理解,，并將有助科學(xué)家開發(fā)出更有效的、副作用更少的藥物,。相關(guān)論文發(fā)表在《英國癌癥雜志》（British Journal of Cancer）上,。
研究人員分析了室鼓膜瘤基因組范圍的表達模式，鑒別出了三種具有獨特特征的基因,，并在74個室鼓膜瘤樣本中證實了這些基因的存在,。研究人員發(fā)現(xiàn)，基因SI00A4與幼兒的腫瘤強烈相關(guān),，基因SI00A6是大腦特殊部位腫瘤的標(biāo)記，而高水平的基因CHI3L1則在細胞大量死亡的癌癥中很常見,。
這些基因全部位于1號染色體的某個區(qū)域,，研究小組之前曾認(rèn)為這個區(qū)域與室鼓膜瘤的低存活率相關(guān)。
論文通訊作者,、英國諾丁漢大學(xué)兒童腦瘤研究中心的Richard Grundy說：“理解癌癥的生物學(xué)原因極為重要,，它將幫助我們開發(fā)出藥物標(biāo)靶癌細胞中的反常基因,，而非健康細胞,，這正是傳統(tǒng)化療所做的。更精確的標(biāo)靶治療將比傳統(tǒng)的化療更為有效,，且更少副作用。所以說這是一個重要的發(fā)現(xiàn),，我們希望它有助產(chǎn)生室鼓膜瘤新的治療手段。”
英國癌癥研究基金會臨床試驗主任Kate Law認(rèn)為：“我們對于兒童癌癥的成因了解的相對較少,，所以這是一項重要的研究。兒童癌癥的全部存活率正在大幅提升,，這要部分感謝國際臨床試驗,，不過進行此次這樣的研究以進一步改善治療也是至關(guān)重要的,。（生物谷Bioon.com）
生物谷推薦原始出處：
British Journal of Cancer，doi: 10.1038/sj.bjc.6604651,，V Rand,，R G Grundy
Investigation of chromosome 1q reveals differential expression of members of the S100 family in clinical subgroups of intracranial paediatric ependymoma
V Rand1, E Prebble2, L Ridley1, M Howard1, W Wei3, M-A Brundler4, B E Fee5, G J Riggins6, B Coyle1 and R G Grundy1 on behalf of the Children's Cancer and Leukaemia Group Biological Studies Committee
1Children's Brain Tumour Research Centre, University of Nottingham, Nottingham, NG7 2UH, UK
2West Midlands Regional Genetics Lab, BWH, Birmingham, B15 2TG, UK
3Cancer Research UK Institute for Cancer Studies, University of Birmingham, Birmingham, B15 2TT, UK
4Department of Pathology, Birmingham Children's Hospital, Birmingham, B4 6NH, UK
5Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
6Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
Gain of 1q is one of the most common alterations in cancer and has been associated with adverse clinical behaviour in ependymoma. The aim of this study was to investigate this region to gain insight into the role of 1q genes in intracranial paediatric ependymoma. To address this issue we generated profiles of eleven ependymoma, including two relapse pairs and seven primary tumours, using comparative genome hybridisation and serial analysis of gene expression. Analysis of 656 SAGE tags mapping to 1q identified CHI3L1 and S100A10 as the most upregulated genes in the relapse pair withde novo 1q gain upon recurrence. Moreover, three more members of the S100 family had distinct gene expression profiles in ependymoma. Candidates (CHI3L1, S100A10, S100A4, S100A6 and S100A2) were validated using immunohistochemistry on a tissue microarray of 74 paediatric ependymoma. In necrotic cases, CHI3L1 demonstrated a distinct staining pattern in tumour cells adjacent to the areas of necrosis. S100A6 significantly correlated with supratentorial tumours (P<0.001) and S100A4 with patients under the age of 3 years at diagnosis (P=0.038). In conclusion, this study provides evidence that S100A6 and S100A4 are differentially expressed in clinically relevant subgroups, and also demonstrates a link between CHI3L1 protein expression and necrosis in intracranial paediatric ependymoma.
