Department of Urology, Stanford University, Stanford, California.
Department of Radiology, Stanford University, Stanford, California; Canary Center at Stanford for Cancer Early Detection, Stanford University, Stanford, California.
Lab Invest. 2024 Oct;104(10):102129. doi: 10.1016/j.labinv.2024.102129. Epub 2024 Aug 31.
Benign prostatic hyperplasia (BPH) is a common condition marked by the enlargement of the prostate gland, which often leads to significant urinary symptoms and a decreased quality of life. The development of clinically relevant animal models is crucial for understanding the pathophysiology of BPH and improving treatment options. This study aims to establish a patient-derived xenograft (PDX) model using benign prostatic tissues to explore the molecular and cellular mechanisms of BPH. PDXs were generated by implanting fresh BPH (transition zone) and paired normal (peripheral zone) prostate tissue from 8 patients under the renal capsule of immunodeficient male mice. Tissue weight, architecture, cellular proliferation, apoptosis, prostate-specific marker expression, and molecular profiles of PDXs were assessed after 1 week and 1, 2, or 3 months of implantation by immunohistochemistry, enzyme-linked immunosorbent assay, transcriptomics, and proteomics. Responses to finasteride, a standard-of-care therapy, were evaluated. PDXs maintained histologic and molecular characteristics of the parental human tissues. BPH, but not normal PDXs, demonstrated significant increases in weight and cellular proliferation, particularly at 1 month. Molecular profiling revealed specific gene and protein expression patterns correlating with BPH pathophysiology. Specifically, an increased immune and stress response was observed at 1 week, followed by increased expression of proliferation markers and BPH-specific stromal signaling molecules, such as BMP5 and CXCL13, at 1 month. Graft stabilization to preimplant characteristics was apparent between 2 and 3 months. Treatment with finasteride reduced proliferation, increased apoptosis, and induced morphologic changes consistent with therapeutic responses observed in human BPH. Our PDX model recapitulates the morphologic, histologic, and molecular features of human BPH, offering a significant advancement in modeling the complex interactions of cell types in BPH microenvironments. These PDXs respond to therapeutic intervention as expected, providing a valuable tool for preclinical testing of new therapeutics that will improve the well-being of BPH patients.
良性前列腺增生(BPH)是一种常见病症,其特征为前列腺腺体增大,常导致严重的尿路症状和生活质量下降。建立具有临床相关性的动物模型对于理解 BPH 的病理生理学并改善治疗选择至关重要。本研究旨在建立一种使用良性前列腺组织的患者来源异种移植(PDX)模型,以探索 BPH 的分子和细胞机制。通过将 8 名患者的新鲜 BPH(移行带)和配对的正常(外周带)前列腺组织植入免疫缺陷雄性小鼠的肾包膜下,生成 PDX。在植入后 1 周以及 1、2 或 3 个月,通过免疫组织化学、酶联免疫吸附试验、转录组学和蛋白质组学评估 PDX 的组织重量、结构、细胞增殖、细胞凋亡、前列腺特异性标志物表达和分子谱,并评估对非那雄胺(一种标准治疗药物)的反应。PDX 保持了供体人类组织的组织学和分子特征。BPH 而不是正常 PDX 显示出显著的重量和细胞增殖增加,特别是在 1 个月时。分子谱分析显示出与 BPH 病理生理学相关的特定基因和蛋白表达模式。具体而言,在第 1 周观察到免疫和应激反应增加,随后在第 1 个月观察到增殖标志物和 BPH 特异性基质信号分子(如 BMP5 和 CXCL13)的表达增加。在第 2 至 3 个月期间,移植物的特征稳定。非那雄胺治疗减少了增殖,增加了凋亡,并诱导了与人类 BPH 中观察到的治疗反应一致的形态变化。我们的 PDX 模型再现了人类 BPH 的形态、组织学和分子特征,为在 BPH 微环境中模拟细胞类型的复杂相互作用提供了重要进展。这些 PDX 对治疗干预的反应如预期的那样,为新治疗方法的临床前测试提供了有价值的工具,将改善 BPH 患者的生活质量。