In 2025, gynecological cancers are projected to account for approximately 10% of cancer-related deaths in women. High-grade serous ovarian carcinoma (HGSC) and serous endometrial carcinoma (SEC) are the most lethal gynecological cancer subtypes. Both malignancies commonly haveTP53mutations, alterations of the RB1 pathway, and numerous secondary mutations. Both carcinoma types consist of poorly differentiated and highly heterogeneous cell populations at the time of detection. Latent development and rapid progression of HGSC and SEC impede the identification of definitive cells of origin and genetic drivers. Here, we review our current knowledge about cancer-prone cell states and genetic drivers. We also discuss how emerging transcriptomic and genetic tools applied to contemporary model systems may facilitate the identification of novel targets for timely detection and therapeutic intervention.
预计到2025年,妇科恶性肿瘤将占女性癌症相关死亡病例的10%左右。高级别浆液性卵巢癌(HGSC)与浆液性子宫内膜癌(SEC)是致死率最高的妇科恶性肿瘤亚型。这两种癌症通常存在TP53基因突变、RB1通路改变及大量继发性突变。在检出时,两类癌组织均由分化程度低且高度异质性的细胞群构成。HGSC与SEC的潜伏性发展及快速进展特性,阻碍了对其确切起源细胞与遗传驱动因素的鉴定。本文综述了当前关于易癌变细胞状态与遗传驱动因素的认知,并探讨如何通过新兴转录组学与遗传学工具应用于现代模型系统,以促进发现用于早期检测与治疗干预的新靶点。