來(lái)自瑞典哥特堡大學(xué)的研究人員首次識(shí)別了12種與侵略性乳癌相關(guān)的基因,。這項(xiàng)發(fā)現(xiàn)將有助于開(kāi)發(fā)更可靠的疾病預(yù)測(cè)和治療方法。
研究結(jié)果發(fā)布在Clinical Cancer Research雜志上,，是基于97位乳癌患者得出的結(jié)論,。在這些患者中,，將近一般的患者在診斷出乳癌后的8年內(nèi)已經(jīng)死亡，而其他患者都存活超過(guò)8年。
乳癌由多種不同的腫瘤細(xì)胞構(gòu)成的,，從基因和生物特性上來(lái)說(shuō),，這些細(xì)胞具有顯著差異性。研究人員使用微陣列技術(shù)分析每個(gè)腫瘤中DNA和基因產(chǎn)物（RNA）的量,，以探究遺傳改變和臨床特征之間的關(guān)系,，比如腫瘤性狀和對(duì)療法的應(yīng)答。
"我們已經(jīng)成功識(shí)別了12個(gè)基因,，這些基因的表達(dá)與侵略性乳癌有關(guān),。"腫瘤學(xué)系在讀博士Toshima Parris表示，"相對(duì)于那些還存活的患者,，這12個(gè)基因在那些已經(jīng)死亡的患者中表達(dá)十分顯著,。"
另外，在侵略性乳癌中,，3個(gè)基因的產(chǎn)物表現(xiàn)出更高的水平,。而剩下的9個(gè)基因在侵略性乳癌中表達(dá)水平更低。
據(jù)Parris介紹,，這些基因會(huì)影響細(xì)胞生長(zhǎng),，運(yùn)動(dòng)，發(fā)育,，從而影響腫瘤的發(fā)展,。在未來(lái)或能通過(guò)含有腫瘤細(xì)胞的血液樣本測(cè)試這些標(biāo)記,，確定是否患者能從特定的療法或藥物中獲益,。（生物谷Bioon.com）
【生物谷會(huì)議推薦：
2010細(xì)胞治療研究進(jìn)展與臨床應(yīng)用前沿研討會(huì) 2010.09.23-2010.09.25
會(huì)議官方網(wǎng)址：www.Cell-therapies.net 】
生物谷推薦原始出處：
Clinical Cancer Research, DOI: 10.1158/1078-0432.CCR-10-0889
Expand+Clinical Implications of Gene Dosage and Gene Expression Patterns in Diploid Breast Carcinoma
Toshima Z. Parris1, Anna Danielsson1, Szilárd Nemes1, Anikó Kovács2, Ulla Delle1, Ghita Fallenius1, Elin M?llerstr?m1, Per Karlsson1, and Khalil Helou1
Purpose: Deregulation of key cellular pathways is fundamental for the survival and expansion of neoplastic cells. In cancer, regulation of gene transcription can be mediated in a variety of ways. The purpose of this study was to assess the impact of gene dosage on gene expression patterns and the effect of other mechanisms on transcriptional levels, and to associate these genomic changes with clinicopathologic parameters.
Experimental Design: We screened 97 invasive diploid breast tumors for DNA copy number alterations and changes in transcriptional levels using array comparative genomic hybridization and expression microarrays, respectively.
Results: The integrative analysis identified an increase in the overall number of genetic alterations during tumor progression and 15 specific genomic regions with aberrant DNA copy numbers in at least 25% of the patient population, i.e., 1q22, 1q22-q23.1, 1q25.3, 1q32.1, 1q32.1-q32.2, 8q21.2-q21.3, 8q22.3, 8q24.3, and 16p11.2 were recurrently gained, whereas 11q25, 16q21, 16q23.3, and 17p12 were frequently lost (P < 0.01). An examination of the expression patterns of genes mapping within the detected genetic aberrations identified 47 unique genes and 1 Unigene cluster significantly correlated between the DNA and relative mRNA levels. In addition, more malignant tumors with normal gene dosage levels displayed a recurrent overexpression of UBE2C, S100A8, and CBX2, and downregulation of LOC389033, STC2, DNALI1, SCUBE2, NME5, SUSD3, SERPINA11, AZGP1, and PIP.
Conclusions: Taken together, our findings suggest that the dysregulated genes identified here are critical for breast cancer initiation and progression, and could be used as novel therapeutic targets for drug development to complement classical clinicopathologic features. Clin Cancer Res; 16(15); 3860–74. ?2010 AACR.
