Department of Obstetrics, Gynecology and Reproductive Sciences, Reproductive Immunology Unit, Yale University School of Medicine, New Haven, Connecticut.
Cancer Med. 2013 Dec;2(6):751-62. doi: 10.1002/cam4.115. Epub 2013 Aug 27.
Epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy. Despite initial responsiveness, 80% of EOC patients recur and present with chemoresistant and a more aggressive disease. This suggests an underlying biology that results in a modified recurrent disease, which is distinct from the primary tumor. Unfortunately, the management of recurrent EOC is similar to primary disease and does not parallel the molecular changes that may have occurred during the process of rebuilding the tumor. We describe the characterization of unique in vitro and in vivo ovarian cancer models to study the process of recurrence. The in vitro model consists of GFP+/CD44+/MyD88+ EOC stem cells and mCherry+/CD44-/MyD88- EOC cells. The in vivo model consists of mCherry+/CD44+/MyD88+ EOC cells injected intraperitoneally. Animals received four doses of Paclitaxel and response to treatment was monitored by in vivo imaging. Phenotype of primary and recurrent disease was characterized by quantitative polymerase chain reaction (qPCR) and Western blot analysis. Using the in vivo and in vitro models, we confirmed that chemotherapy enriched for CD44+/MyD88+ EOC stem cells. However, we observed that the surviving CD44+/MyD88+ EOC stem cells acquire a more aggressive phenotype characterized by chemoresistance and migratory potential. Our results highlight the mechanisms that may explain the phenotypic heterogeneity of recurrent EOC and emphasize the significant plasticity of ovarian cancer stem cells. The significance of our findings is the possibility of developing new venues to target the surviving CD44+/MyD88+ EOC stem cells as part of maintenance therapy and therefore preventing recurrence and metastasis, which are the main causes of mortality in patients with ovarian cancer.
上皮性卵巢癌 (EOC) 是最致命的妇科恶性肿瘤。尽管最初有反应,但 80%的 EOC 患者会复发,并表现出化疗耐药和更具侵袭性的疾病。这表明存在一种潜在的生物学机制,导致复发性疾病发生改变,与原发性肿瘤不同。不幸的是,复发性 EOC 的治疗方法与原发性疾病相似,与肿瘤重建过程中可能发生的分子变化并不平行。我们描述了用于研究复发过程的独特体外和体内卵巢癌模型的特征。体外模型由 GFP+/CD44+/MyD88+ EOC 干细胞和 mCherry+/CD44-/MyD88- EOC 细胞组成。体内模型由注射到腹腔内的 mCherry+/CD44+/MyD88+ EOC 细胞组成。动物接受了四剂紫杉醇治疗,并通过体内成像监测治疗反应。通过定量聚合酶链反应 (qPCR) 和 Western blot 分析对原发性和复发性疾病的表型进行了特征描述。使用体内和体外模型,我们证实化疗富集了 CD44+/MyD88+ EOC 干细胞。然而,我们观察到存活的 CD44+/MyD88+ EOC 干细胞获得了更具侵袭性的表型,表现为化疗耐药和迁移能力。我们的研究结果强调了可能解释复发性 EOC 表型异质性的机制,并强调了卵巢癌干细胞显著的可塑性。我们研究结果的意义在于有可能开发新的途径来靶向存活的 CD44+/MyD88+ EOC 干细胞作为维持治疗的一部分,从而预防复发和转移,这是卵巢癌患者死亡的主要原因。