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首页> 外文期刊>The Journal of Urology >Re: Prostatic inflammation enhances basal-to-luminal differentiation and accelerates initiation of prostate cancer with a basal cell origin
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Re: Prostatic inflammation enhances basal-to-luminal differentiation and accelerates initiation of prostate cancer with a basal cell origin

机译：回复：前列腺炎症增强了基底到管腔的分化，并加速了基底细胞起源的前列腺癌的发作

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Editorial Comment: Chronic inflammation is a significant contributor to the initiation and progression of a wide spectrum of malignancies, including prostate cancer. The authors hypothesized that inflammation can accelerate the initiation of prostate cancer with a basal cell origin by stimulating basal to luminal differentiation. The hypothesis was tested using a mouse model of bacterial infection induced prostatitis. A reproducible mouse model of bacterial prostatitis has been established in which transurethral inoculation of uropathogenic strains of Escherichia coli into the prostate results in massive inflammation and reactive hyperplasia. The authors established this mouse model for prostatitis using a uropathogenic E. coli strain, CP9, that was isolated from the blood of a patient with pyelonephrititis. Using this model, it was demonstrated that acute inflammation induced by bacterial infection causes tissue damage and results in a tissue microenvironment that stimulates the differentiation of basal cells to luminal cells, and accelerates disease initiation in a mouse model for prostate cancer with a basal cell origin. The study suggests that inflammation also may accelerate tumor initiation by altering the tissue lineage differentiation program. Cells inclined to acquire oncogenic signaling within a tissue may be intrinsically resistant to transformation. However, tissue damage induced by various insults, including inflammation, may result in microenvironmental changes that are capable of stimulating the differentiation of these cells into other lineages. The prooncogenic signaling inherited by the daughter lineages may enhance their susceptibility to transformation induced by ensuing genetic changes.
机译：社论评论：慢性炎症是导致包括前列腺癌在内的各种恶性肿瘤发生和发展的重要因素。作者假设炎症可以通过刺激基底到管腔的分化来加速具有基底细胞起源的前列腺癌的发作。使用细菌感染引起的前列腺炎的小鼠模型测试了该假设。已经建立了可复制的细菌性前列腺炎小鼠模型，其中将尿道致病性大肠杆菌经尿道接种前列腺导致大量炎症和反应性增生。作者使用尿毒症性大肠杆菌CP9株建立了这种小鼠前列腺炎模型，该株是从肾盂肾炎患者的血液中分离出来的。使用该模型，已证明细菌感染引起的急性炎症会引起组织损伤，并导致组织微环境刺激基底细胞分化为腔细胞，并在具有基底细胞起源的前列腺癌小鼠模型中加速疾病的发生。研究表明，炎症也可能通过改变组织谱系分化程序来加速肿瘤的发生。倾向于在组织内获取致癌信号的细胞可能固有地对转化具有抗性。但是，由各种损伤（包括炎症）引起的组织损伤可能导致微环境变化，这种变化能够刺激这些细胞分化为其他谱系。子代谱系遗传的促癌信号可能增强其对随后发生的遗传变化诱导的转化的敏感性。

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    《The Journal of Urology》 |2014年第3期|共1页
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