BJC：特殊免疫标志物或可帮助预测卵巢癌患者对疗法的反应

  发表在国际杂志British Journal of Cancer上的一篇研究论文中，来自加拿大皇后大学的研究人员通过研究发现了一种生物标志物或许可以帮助较好地预测卵巢癌患者对化疗的反应，相关研究或为开发新型个体化疗法来治疗卵巢癌提供帮助。
  生物标志物是一种处于生物性状态的指示子，研究者Koti表示，近来有研究成功抑制了免疫系统来抵御癌症，这就表明癌症患者免疫系统在抵御癌症中扮演着非常重要的角色；很多研究的成功都是基于通过不同的疗法来增强机体抗癌免疫力来实现的，比如当有些疗法偶联一些可以预测患者对疗法产生反应的生物标志物时，其就会被证明是非常有效的。
  而本文中研究者进行的研究则是对超过200名卵巢癌患者进行的一项回顾性队列分析，文章中研究者利用了一种最尖端的已经建立的检测技术来进行目标标志物的检测，研究者在积累的肿瘤样本库中的冷冻肿瘤组织中对这些特殊的生物标志物进行了初期发现，这些肿瘤样本库包括安大略肿瘤样本库、渥太华健康研究所等处。
  如今研究者对来自样本库中超过500个卵巢癌患者的肿瘤组织进行分析研究，而且II期验证目前正处于回顾性队列研究中；这项研究最重要的就是这些生物标志物的发现，当其在特殊类型的卵巢癌患者中进行初期疗法使用后，其或许会帮助妇科肿瘤专家来决定是否患者需要进行额外的疗法治疗，从而来改善患者潜在的生存期。
  卵巢癌每年在全球引发大约15.2万人死亡，其目前已经成为引发女性个体患妇科癌症死亡的主要原因。（转化医学网360zhyx.com）
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转化医学网推荐的原文摘要：

A distinct pre-existing inflammatory tumour microenvironment is associated with chemotherapy resistance in high-grade serous epithelial ovarian cancer
British Journal of Cancer doi:10.1038/bjc.2015.81
M Koti, A Siu, I Clément, M Bidarimath, G Turashvili, A Edwards, K Rahimi, A-M M Masson and J A Squire
Background:
Chemotherapy resistance is a major determinant of poor overall survival rates in high-grade serous ovarian cancer (HGSC). We have previously shown that gene expression alterations affecting the NF-κB pathway characterise chemotherapy resistance in HGSC, suggesting that the regulation of an immune response may be associated with this phenotype.
Methods:
Given that intrinsic drug resistance pre-exists and is governed by both tumour and host factors, the current study was performed to examine the cross-talk between tumour inflammatory microenvironment and cancer cells, and their roles in mediating differential chemotherapy response in HGSC patients. Expression profiling of a panel of 184 inflammation-related genes was performed in 15 chemoresistant and 19 chemosensitive HGSC tumours using the NanoString nCounter platform.
Results:
A total of 11 significantly differentially expressed genes were found to distinguish the two groups. As STAT1 was the most significantly differentially expressed gene (P=0.003), we validated the expression of STAT1 protein by immunohistochemistry using an independent cohort of 183 (52 resistant and 131 sensitive) HGSC cases on a primary tumour tissue microarray. Relative expression levels were subjected to Kaplan–Meier survival analysis and Cox proportional hazard regression models.
Conclusions:
This study confirms that higher STAT1 expression is significantly associated with increased progression-free survival and that this protein together with other mediators of tumour–host microenvironment can be applied as a novel response predictive biomarker in HGSC. Furthermore, an overall underactive immune microenvironment suggests that the pre-existing state of the tumour immune microenvironment could determine response to chemotherapy in HGSC.