Department of Medicine,University of Washington, Seattle, WA 98195-8056, USA.
Anticancer Res. 2011 Apr;31(4):1189-95.
Erythropoietin (EPO) was shown to reduce tumor survival in recent trials, however, its mechanisms of action are unclear. Efforts to measure tumor EPO receptor (EPOR) are limited by the promiscuity of EPOR antibodies, and concerns as to whether EPOR mRNA measurements are confounded by heterogeneity of tumor vasculature, a known EPOR source.
This study compared mRNA levels of EPOR and JAK2 in 11 breast tumor epithelial versus endothelial dissections.
In nine tumors EPOR mRNA was 2.6 (1.2-5.7)-fold lower in the epithelial fraction, however, this reduction was less than the reduction of endothelial markers. In two tumors, EPOR mRNA was 2.9 (1.7-4.0)-fold higher in the epithelial fraction. The inter-tumor variation in EPOR levels exceeded the intra-tumor variation between fractions. Similar results were obtained for JAK2.
Tumor vasculature is not the sole source of EPOR and JAK2, and tumors can be segregated by EPOR and JAK2 levels for correlative analysis with clinical outcomes.
促红细胞生成素（EPO）在最近的试验中被证明可以减少肿瘤的存活，但它的作用机制尚不清楚。由于 EPOR 抗体的混杂性，以及 EPOR mRNA 测量是否受到肿瘤血管异质性的影响，人们对测量肿瘤 EPO 受体（EPOR）的努力存在疑虑，而肿瘤血管是已知的 EPOR 来源。
本研究比较了 11 例乳腺肿瘤上皮与内皮分离物中 EPOR 和 JAK2 的 mRNA 水平。
在 9 例肿瘤中，上皮部分的 EPOR mRNA 水平降低了 2.6（1.2-5.7）倍，但这种降低小于内皮标志物的降低。在 2 例肿瘤中，上皮部分的 EPOR mRNA 水平升高了 2.9（1.7-4.0）倍。肿瘤之间 EPOR 水平的变异性超过了肿瘤内各部分之间的变异性。JAK2 也得到了类似的结果。
肿瘤血管不是 EPOR 和 JAK2 的唯一来源，肿瘤可以根据 EPOR 和 JAK2 水平进行分类，以便与临床结果进行相关分析。
