Most high grade serous ovarian cancers (HGSOC) originate in the fallopian tube but spread to the ovary and peritoneal cavity, highlighting the need to understand antitumor immunity across HGSOC sites. Using spatial analyses, we discover that tertiary lymphoid structures (TLSs) within ovarian tumors are less developed compared with TLSs in fallopian tube or omental tumors. We reveal transcriptional differences across a spectrum of lymphoid structures, demonstrating that immune cell activity increases when residing in more developed TLSs and produce a prognostic, spatially derived TLS signature from HGSOC tumors. We interrogate TLS-adjacent stroma and assess how normal mesenchymal stem cells MSCs (nMSCs) may support B cell function and TLS, contrary to cancer-educated MSCs (CA-MSCs) which negate the prognostic benefit of our TLS signature, suggesting that pro-tumorigenic stroma could limit TLS formation.

中文翻译：

---

高级别浆液性卵巢癌中三级淋巴结构的活动受部位、基质和细胞相互作用的控制


大多数高级别浆液性卵巢癌 （HGSOC） 起源于输卵管，但扩散到卵巢和腹膜腔，这凸显了了解 HGSOC 部位抗肿瘤免疫的必要性。使用空间分析，我们发现与输卵管或网膜肿瘤中的 TLS 相比，卵巢肿瘤内的三级淋巴结构 （TLS） 发育较少。我们揭示了一系列淋巴结构的转录差异，证明当驻留在更发达的 TLS 中时，免疫细胞活性会增加，并从 HGSOC 肿瘤产生预后、空间衍生的 TLS 特征。我们询问 TLS 相邻的基质并评估正常的间充质干细胞 MSC （nMSC） 如何支持 B 细胞功能和 TLS，这与癌症教育的 MSC （CA-MSC） 相反，后者否定了我们的 TLS 签名的预后益处，表明促肿瘤基质可以限制 TLS 的形成。