Differing leukocyte gene expression profiles associated with fatigue in patients with prostate cancer versus chronic fatigue syndrome.
Differing leukocyte gene expression profiles associated with fatigue in patients with prostate cancer versus chronic fatigue syndrome.
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DOI：
10.1016/j.psyneuen.2013.08.008
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发表时间：
2013-12
影响因子：
3.7
通讯作者：
Light, Alan R.
中科院分区：
文献类型：
--
作者：
Light, Kathleen C.;Agarwal, Neeraj;Lacob, Eli;White, Andrea T.;Kinney, Anita Y.;VanHaitsma, Timothy A.;Aizad, Hannah;Hughen, Ronald W.;Bateman, Lucinda;Light, Alan R.
关键词：
雄激素剥夺疗法（ADT）通常会加重前列腺癌患者的疲劳，产生类似慢性疲劳综合征（CFS）的症状。比较adt治疗的前列腺癌患者、慢性疲劳综合症患者和健康对照组中许多疲劳相关基因的表达（mRNA），以及mRNA与疲劳严重程度的相关性，可能阐明这些疾病中疲劳的不同途径。对30例疲劳、adt治疗的前列腺癌患者（PCF）、39例CFS患者和22例年龄在40-79岁的对照组的白细胞进行了实时荧光定量PCR检测，并对疲劳和疼痛严重程度进行了评分。来自这些途径的46个基因包括：1)肾上腺素能/单胺/神经肽，2)免疫，3)代谢检测，4)线粒体/能量，5)转录因子。PCF患者的2个免疫转录基因（NR3C1和TLR4）、趋化因子CXCR4和线粒体基因SOD2的表达高于对照组或CFS。2种血管舒张相关基因（ADRB2和VIPR2）、2种细胞因子（TNF和LTA）和2种代谢物检测受体（ASIC3和P2RX7）的表达均较低。与对照组和PCF相比，CFS患者的P2RX7较高，HSPA2较低。仅GABA-A受体调节剂DBI在PCF和CFS中与疲劳程度的相关性相似（r= - 0.50, p<0.005和r= - 0.34, p<0.05）。嘌呤能P2RY1仅与PCF疲劳和疼痛严重程度相关（r= +0.43和+0.59,p=0.025和p=0.001）。PCF患者在5种途径中10个基因的平均表达量与对照组和CFS不同。与疲劳严重程度的相关性涉及两组患者的DBI和PCF的P2RY1。这些途径可能为减少疲劳的干预提供新的目标。
Androgen deprivation therapy (ADT) often worsens fatigue in patients with prostate cancer, producing symptoms similar to Chronic Fatigue Syndrome (CFS). Comparing expression (mRNA) of many fatigue-related genes in patients with ADT-treated prostate cancer versus with CFS versus healthy controls, and correlating mRNA with fatigue severity may clarify the differing pathways underlying fatigue in these conditions. Quantitative real-time PCR was performed on leukocytes from 30 fatigued, ADT-treated prostate cancer patients (PCF), 39 patients with CFS and 22 controls aged 40–79, together with ratings of fatigue and pain severity. 46 genes from these pathways were included: 1) adrenergic/monoamine/neuropeptides, 2) immune, 3) metabolite-detecting, 4) mitochondrial/energy, 5) transcription factors. PCF patients showed higher expression than controls or CFS of 2 immune transcription genes (NR3C1 and TLR4), chemokine CXCR4, and mitochondrial gene SOD2. They showed lower expression of 2 vasodilation-related genes (ADRB2 and VIPR2), 2 cytokines (TNF and LTA), and 2 metabolite-detecting receptors (ASIC3 and P2RX7). CFS patients showed higher P2RX7 and lower HSPA2 versus controls and PCF. Correlations with fatigue severity were similar in PCF and CFS for only DBI, the GABA-A receptor modulator (r=−0.50, p<0.005 and r=−0.34, p<0.05). Purinergic P2RY1 was correlated only with PCF fatigue and pain severity (r= +0.43 and +0.59, p=0.025 and p=0.001). PCF patients differed from controls and CFS in mean expression of 10 genes from all 5 pathways. Correlations with fatigue severity implicated DBI for both patient groups and P2RY1 for PCF only. These pathways may provide new targets for interventions to reduce fatigue.
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