Ovarian Cancer

P=N/A, N=25, Recruiting, Fred Hutchinson Cancer Center | Initiation date: Jul 2026 --> Feb 2026

Our findings provide a reliable independent prognostic tool for OC and elucidate the intricate interplay between metabolic reprogramming and the immunosuppressive microenvironment. These results offer critical mechanistic insights for prognostic stratification and the development of personalized combinatorial immunotherapies in OC.

Niraparib exhibits antitumor effects and promotes ferroptosis by inhibiting TM4SF1 expression through ALKBH1-mediated 6mA modification in BRCAwt OC. These findings emphasize the potential application of niraparib in BRCAwt OC and reveal the important role of epigenetic regulation in cancer treatment.

In the SKOV3 xenograft model, primed CAR-NK cells achieved superior tumor control and increased intratumoral infiltration compared with non-primed CAR-NK cells, while maintaining a favorable safety profile. Collectively, these findings demonstrate that chemical priming enhances CAR-NK cell function and provides a promising non-genetic strategy to improve CAR-NK cell activity against solid tumor models.

Economic analysis revealed a significant correlation between AL and hospital stay, hospital costs, and time to chemotherapy.DiscussionEarly postoperative inflammatory and nutritional biomarkers, particularly CRP and albumin, demonstrated significant predictive value for anastomotic leakage, providing an early warning for risk stratification and intervention. The investigation also bolstered the evidence supporting the restrictive surgical scope approach advocated in clinical guidelines.

Functional validation confirmed that: (1) secretomes from Tex cells-but not effector T cells-significantly promoted M2 polarization in both THP-1 and bone marrow-derived macrophages (CD206⁺ THP-1: 83.8% vs. 51.4%, p < 0.001; CD206⁺ BMDM: 72.4% vs. 41.5%, p < 0.001); and (2) recombinant CCL3 acted synergistically with IL-4/IL-10 to further enhance M2 polarization (59.2% vs. 37.7%, p = 0.008). Collectively, our findings unveil a previously unrecognized immunoregulatory axis whereby exhausted CD8⁺ T cells drive immunosuppression via CCL3-CCR1-mediated communication with M2 macrophages, presenting a promising therapeutic target to reverse the immune-cold TME in HGSOC.

Scanning electron microscopy, immunofluorescence, Western Blot, and other molecular functional assays show that the ERRα/LDHA axis drives lactate accumulation, downregulates inflammasome-related proteins (NLRP3, caspase-1, GSDMD and GSDMD-N), thereby suppressing pyroptosis and promoting resistance to cisplatin, carboplatin, and paclitaxel in ovarian cancer cells. Created in BioRender. Ren, Y. (2025) https://BioRender.com/qeh0dw8.

Three ADCs are currently approved for previously treated gynaecological cancers: mirvetuximab soravtansine for folate receptor-α-positive ovarian cancer, trastuzumab deruxtecan for solid tumours expressing HER2 (defined as a staining intensity on immunohistochemistry of 3+) and tisotumab vedotin for cervical cancer (independent of tissue factor expression). Moreover, rational combinations could reinforce and extend the clinical potential of these agents, as has already been demonstrated with the addition of ADCs to immune checkpoint inhibitors in an effort to amplify antitumour immunity and prolong the durability of clinical responses. In this Review, we provide an overview of the current landscape of ADCs in gynaecological malignancies, highlighting key advances and future opportunities.

These TNBC cells were significantly more sensitive to cisplatin than wild-type TNBC cells, consistent with our clinical data. In conclusion, RAD51D-deficient tumors were shown to have a phenotype similar to that of BRCA1-deficient tumors, and further investigation of responses to DNA-damaging agents, particularly platinum-based chemotherapy, is warranted.

P2/3, N=175, Recruiting, GE Healthcare | Initiation date: May 2026 --> Oct 2026

P2, N=135, Recruiting, MetaFines | Not yet recruiting --> Recruiting | Trial completion date: Jul 2027 --> Jun 2028 | Initiation date: Sep 2025 --> May 2026 | Trial primary completion date: Mar 2026 --> Apr 2028

P=N/A, N=112, Recruiting, Dana-Farber Cancer Institute | Trial completion date: Dec 2026 --> Apr 2027 | Trial primary completion date: May 2026 --> Dec 2026