EGFR, HLA-G, CD70, c-MET, and NY-ESO1 as potential biomarkers in high grade epithelial ovarian carcinoma.

IF 2.2 4区 医学 Q3 ONCOLOGY
Duc Vo, Yan Liu, Anil K Sood, Katy Rezvani, Amir A Jazaeri, Jinsong Liu
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引用次数: 0

Abstract

High grade epithelial ovarian carcinoma is an aggressive tumor. Treatment includes platinum therapy, however it recurs in most patients due to therapy resistance. In this project, we study the immunohistochemical (IHC) expression of five potential biomarkers/prognostic markers in high grade epithelial ovarian carcinoma: EGFR, HLA-G, CD70, c-MET, and NY-ESO1. A cohort of 274 patients is used. We compare the IHC expression with age, stage, ascites status, family history of cancer, disease free survival (DFS) and overall survival (OS). EGFR expression is significantly correlated with family history and worse OS. HLA-G is associated with worse OS. To confirm the results of EGFR and HLA-G, a second separated cohort of 248 patients is used. Positive EGFR expression again shows worse OS, while HLA-G expression has worse prognostic trend. CD70 has a worse OS trend. C-MET and NY-ESO1 do not have any clinical correlations. EGFR can potentially serve as target in future clinical immune therapy trials.

表皮生长因子受体、HLA-G、CD70、c-MET 和 NY-ESO1 作为高级别上皮性卵巢癌的潜在生物标记物。
高级别上皮性卵巢癌是一种侵袭性肿瘤。治疗方法包括铂类疗法,但大多数患者会因耐药性而复发。在该项目中,我们研究了高级别上皮性卵巢癌中五种潜在生物标记物/预后标志物的免疫组化(IHC)表达:表皮生长因子受体(EGFR)、HLA-G、CD70、c-MET 和 NY-ESO1。我们使用了 274 例患者的队列。我们将 IHC 表达与年龄、分期、腹水状况、癌症家族史、无病生存期(DFS)和总生存期(OS)进行了比较。表皮生长因子受体(EGFR)的表达与家族史和较差的 OS 有明显相关性。HLA-G与较差的OS相关。为了证实表皮生长因子受体(EGFR)和 HLA-G 的结果,研究人员又对 248 名患者进行了分组。表皮生长因子受体(EGFR)阳性表达再次显示出更差的OS,而HLA-G表达则有更差的预后趋势。CD70 的 OS 趋势更差。C-MET和NY-ESO1没有任何临床相关性。表皮生长因子受体有可能成为未来临床免疫疗法试验的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cancer Biomarkers
Cancer Biomarkers ONCOLOGY-
CiteScore
5.20
自引率
3.20%
发文量
195
审稿时长
3 months
期刊介绍: Concentrating on molecular biomarkers in cancer research, Cancer Biomarkers publishes original research findings (and reviews solicited by the editor) on the subject of the identification of markers associated with the disease processes whether or not they are an integral part of the pathological lesion. The disease markers may include, but are not limited to, genomic, epigenomic, proteomics, cellular and morphologic, and genetic factors predisposing to the disease or indicating the occurrence of the disease. Manuscripts on these factors or biomarkers, either in altered forms, abnormal concentrations or with abnormal tissue distribution leading to disease causation will be accepted.
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