細胞特性
上皮性卵巢癌發生於卵巢表面上皮(ovarian surface epithelium, OSE)。OSE由位於卵巢白膜的間充質細胞進行間葉細胞-上皮細胞轉化而成，同時表達上皮細胞和間葉細胞的標誌，從中可分離獲得表達早期胚胎髮育標誌SSEA-4、Oct-4、Nanog、Sox-2及C-kit的細胞，提示卵巢OSE中存在多能幹細胞。2005年首次分離鑑定了卵巢癌腫瘤幹細胞：他們從進展期卵巢漿液性腺癌患者的腹水中分離得到19個能夠不斷自我更新的細胞克隆，其中2個克隆可以在懸浮培養體系中形成細胞球，細胞球內有上皮細胞、顆粒細胞、生殖細胞特異性表面蛋白的腫瘤細胞。這兩個克隆表達了Nestin、Oct-4、Nanog等幹細胞標記，並且在小鼠體內實驗中可以形成與原發腫瘤相同的新生腫瘤。
EOCSCs的表面標記至今尚存爭議：側群細胞（side population, SP）中存在EOCSCs的富集，SP細胞較非SP細胞具有更強的增殖分化能力；卵巢癌CD133細胞亞群增殖性和克隆源性明顯強於CD133細胞亞群；CD44 CD117細胞亞群符合之前報導的所有CSCs的特性；CD44MYD88細胞亞群能夠產生細胞因子和趨化因子，修復能力強，對傳統的化療方案耐藥，能抵抗由TNFα介導的細胞凋亡，懸浮培養能夠形成細胞球，體內試驗可以形成原發腫瘤等。經對比多種標記，最近由Silva等提出ALDHCD133可以作為卵巢癌幹細胞的標誌。
相關研究發現Wnt/β-Catenin通路、Hedhog通路、Notch通路、PTEN/AKT通路等可能參與了EOCSCs及卵巢癌的發生髮展。對miRNAs的研究發現，EOCSCs的特點為低水平的miR-199a和miR-214，而成熟EOC細胞存在高水平的miR-199a和miR-214。且這些調控IKKβ/NF-κB和PTEN/AKT通路的miRNA由Twist1調控，並與EOCSCs的分化相關。
與腫瘤關係
EOCSCs已被證實與卵巢癌化療耐藥相關，使用含鉑類藥物化療造成了治療介導的選擇作用和耐藥性EOCSCs的富集，且CSCs的靜止為腫瘤細胞提供了保護機制，是臨床上腫瘤復發尤其是多重藥物耐藥的重要因素之一。EOCSC介導的化療耐藥可能由於特異性表達了藥物的膜轉運體。最近Ma等研究發現在含鉑類化療藥物的幹細胞培養體系中培養人EOC細胞系SKOV3，獲得了成球細胞並且該細胞亞群同時具有腫瘤幹細胞特性和化療耐藥特性。該細胞群具有自我更新和高成瘤能力，並且過表達Nanog、Oct-4、Sox-2及CD133等幹細胞相關標記。不但對選擇過程中套用的化療藥物耐藥，對其他藥物如氨甲喋呤等亦耐藥。
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