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目的检测微卫星位点 TP53、RPS6在口腔鳞癌浸润前沿、中心及癌间质细胞中的基因变化,揭示口腔鳞癌的生物学行为。方法运用激光捕获显微切割分别获取同一肿瘤浸润前沿、中心及癌间质足量的细胞,提取 DNA,PCR-变性 PAGE 电泳检测 TP53和 RPS6位点的基因变化。结果浸润前沿、中心和癌间质中 TP53和 RPS6存在杂合性缺失(loss of heterozygosity,LOH)和微卫星不稳定(microsatellite instability,MI),发生率从23.5%(4/17)到64.7%(11/17),且 LOH 和(或)MI 的模式存在不同。上皮 TP53和 RPS6的 LOH 和 MI 发生率分别为70.6%(12/17)和64.7%(11/17),间质为43.8%(7/16)和23.5%(4/17),癌实质较间质发生率高,差异有统计学意义(P<0.05)。浸润前沿 TP53的 LOH 发生率为64.7%(11/17),中心为60.0%(9/15)。RPS6在浸润前沿的 LOH 和 MI为58.8%(10/17),中心为29.4%(5/17)。两位点总发生率分别为62.5%(20/32)和44.1%(15/34),差异有统计学意义(P<0.05)。结论部分口腔鳞癌样本浸润前沿、中心和肿瘤间质的基因变化不同,癌实质基因变化率与肿瘤分化程度有关。
Objective To detect the gene changes of microsatellite loci TP53 and RPS6 in the frontal, central and stromal cells of oral squamous cell carcinoma, and to reveal the biological behavior of oral squamous cell carcinoma. Methods Laser capture microdissection was used to obtain the cells with the same tumor infiltration front, center and interstitial cells, respectively. DNA was extracted and the gene changes of TP53 and RPS6 were detected by PCR-denaturing PAGE. Results There was loss of heterozygosity (LOH) and microsatellite instability (MI) between TP53 and RPS6 in the infiltration front, center and in the interstitial mesenchyme. The incidence rates ranged from 23.5% (4/17) to 64.7% (11/17), and the pattern of LOH and / or MI is different. The incidences of LOH and MI in epithelial TP53 and RPS6 were 70.6% (12/17) and 64.7% (11/17), respectively. The interstitial masses were 43.8% (7/16) and 23.5% (4/17) Interstitial high incidence, the difference was statistically significant (P <0.05). The incidence of LOH in invasive frontal TP53 was 64.7% (11/17) and 60.0% (9/15) in the center. The frontal LOH and MI of RPS6 were 58.8% (10/17) at the infiltration front and 29.4% (5/17) at the center. The total incidence of the two sites were 62.5% (20/32) and 44.1% (15/34), respectively, with significant difference (P <0.05). Conclusion Some samples of oral squamous cell carcinoma have different gene changes in the frontier, center and tumor stroma, and the rate of change of cancer parenchyma gene is related to the degree of tumor differentiation.