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Chromosomal aberrations in head and neck squamous cell carcinomas in Norwegian and Sudanese populations by array comparative genomic hybridization.

机译:阵列比较基因组杂交技术在挪威和苏丹人群的头颈部鳞状细胞癌中的染色体畸变。

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We used microarray-based comparative genomic hybridization to explore genome-wide profiles of chromosomal aberrations in 26 samples of head and neck cancers compared to their pair-wise normal controls. The samples were obtained from Sudanese (n=11) and Norwegian (n=15) patients. The findings were correlated with clinicopathological variables. We identified the amplification of 41 common chromosomal regions (harboring 149 candidate genes) and the deletion of 22 (28 candidate genes). Predominant chromosomal alterations that were observed included high-level amplification at 1q21 (harboring the S100A gene family) and 11q22 (including several MMP family members). Regions of copy number increase was also identified at 6p21 (p21), 7p12 (EGFR), 17p13 (p53) and 19p13.2 (p19INK4d), while regions showing deletion included among others 3p25.2 (RAF1) and 9p21 (p15, p16). We found genes from four common biological pathways (MAPK signaling, cytokine-cytokine receptor interaction, ECM-receptor interaction and Jak-STAT signaling) to be predominantly over-represented in areas of gain and loss. The current study provides valuable information on chromosomal aberrations likely to be involved in the pathogenesis of head and neck cancers. An increased copy number of the S100A and MMP gene family members, known to be involved in invasion and metastasis, may play an important role in the development of the tumors. Hierarchical clustering of the chromosomal alterations with clinicopathological parameters showed little correlation, suggesting an occurrence of gains/losses regardless of ethnic differences and clinicopathological status between the patients from the two countries. Our findings indicate the existence of common gene-specific amplifications/deletions in these tumors, regardless of the source of the samples or attributed carcinogenic risk factors.
机译:我们使用基于微阵列的比较基因组杂交技术研究了26个头颈癌样本与成对正常对照相比的染色体畸变全基因组分布。样本来自苏丹(n = 11)和挪威(n = 15)患者。这些发现与临床病理变量相关。我们确定了41个常见染色体区域的扩增(包含149个候选基因)和22个缺失(28个候选基因)。观察到的主要染色体改变包括在1q21(带有S100A基因家族)和11q22(包括几个MMP家族成员)的高水平扩增。还确定了拷贝数增加的区域为6p21(p21),7p12(EGFR),17p13(p53)和19p13.2(p19INK4d),而显示缺失的区域包括3p25.2(RAF1)和9p21(p15,p16) )。我们发现来自四种常见生物学途径(MAPK信号传导,细胞因子-细胞因子受体相互作用,ECM-受体相互作用和Jak-STAT信号传导)的基因在得失区域中主要被过度代表。当前的研究提供了可能与头颈癌发病机制有关的染色体畸变的有价值的信息。 S100A和MMP基因家族成员的拷贝数增加,已知与侵袭和转移有关,可能在肿瘤的发展中起重要作用。染色体改变与临床病理参数的分层聚类显示几乎没有相关性,表明两国患者之间种族差异和临床病理状况如何均会发生收益/损失。我们的发现表明,这些肿瘤中存在常见的基因特异性扩增/缺失,而与样品来源或致癌危险因素无关。

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