The poor outcome of second primary oral squamous cell carcinoma is attributed to Bmi1 upregulation.

The poor outcome of second primary oral squamous cell carcinoma is attributed to Bmi1 upregulation.
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第二原发性口腔鳞状细胞癌的不良预后归因于 Bmi1 上调

DOI:
10.1002/cam4.1348
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发表时间:
2018-04
期刊:
影响因子:
4
通讯作者:
Cheng B
Cheng B
中科院分区:
医学3区
文献类型:
--
作者:
Hu Q;Wu T;Chen X;Li H;Du Z;Hao Y;Peng J;Tai S;Song M;Cheng B

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据报道,鼻咽癌的放射治疗会导致第二原发性口腔鳞状细胞癌(s-OSCC)。 s-OSCC 的预后和病理特征很大程度上未知。 Bmi1 与辐射引起的 DNA 损伤的修复相关,表明它可能参与 s-OSCC 的病理过程。在此,我们比较了 s-OSCC 和原发性 OSCC (p-OSCC) 的预后,并探讨了 Bmi1 在 s-OSCC 发展中的参与。在这项回顾性研究中,s-OSCC 和 p-OSCC 患者通过倾向评分进行匹配。通过单变量和多变量分析比较他们的结果。通过免疫组织化学(IHC)检测Bmi1在s-OSCC和p-OSCC中的表达。在大鼠模型和 HaCaT 细胞中探索了辐射诱导的早期 Bmi1 改变。匹配后,纳入116对特征高度均衡的患者。在单变量分析中,s-OSCC 的总生存期(OS)、疾病特异性生存期(DSS)和局部无复发生存期(LRFS)均低于 p-OSCC(P < 0.05),而区域无转移生存期(RMFS)则相似(P = 0.112)。多变量分析进一步显示,放疗史是 OS、DSS 和 LRFS 的独立危险因素(P < 0.05)。 IHC 结果显示,Bmi1 在 s-OSCC 中的阳性率较高(P = 0.0027)。在放疗引起的粘膜炎大鼠模型中,放疗后 8 天观察到 Bmi1 上调。一致的是,照射后 1 小时,HaCaT 细胞中 Bmi1 上调,并且其上调与 X 射线暴露时间一致。总之,与 p-OSCC 相比,s-OSCC 的预后较差,这可能归因于 Bmi1 上调。
Radiotherapy for nasopharyngeal carcinoma has been reported to cause second primary oral squamous cell carcinoma (s‐OSCC). The prognosis and pathologic characteristic of s‐OSCC are largely unknown. Bmi1 was associated with the repair of radiation‐induced DNA damage, suggesting its possible involvement in the pathologic process of s‐OSCC. Herein, we compared the prognosis between s‐OSCC and primary OSCC (p‐OSCC) and explored the involvement of Bmi1 in s‐OSCC development. In this retrospective study, s‐OSCC and p‐OSCC patients were matched by propensity scores. Their outcomes were compared by univariate and multivariate analyses. The expression of Bmi1 in s‐OSCC and p‐OSCC was detected by immunohistochemistry (IHC). Radiation‐induced Bmi1 alteration in early‐stage was explored in a rat model and HaCaT cells. After matching, 116 pairs of patients with highly balanced characteristics were included. In univariate analysis, the overall survival (OS), disease‐specific survival (DSS), and local recurrence‐free survival (LRFS) were poorer in s‐OSCC than in p‐OSCC (P < 0.05), while their regional metastasis‐free survival (RMFS) was parallel (P = 0.112). Multivariate analysis further revealed that radiotherapy history was an independent risk factor for OS, DSS, and LRFS (P < 0.05). IHC results showed that the positive rate of Bmi1 was higher in s‐OSCC (P = 0.0027). In a rat model of radiotherapy‐induced mucositis, Bmi1 upregulation was observed 8 days after irradiation. Consistently, Bmi1 was upregulated in HaCaT cells 1 h after irradiation, and its upregulation was in accord with X‐ray exposure duration. In conclusion, the prognosis of s‐OSCC is poorer as compared to p‐OSCC, which may be attributed to Bmi1 upregulation.
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