Ovarian Cancer

This rational engineering strategy addresses multiple barriers simultaneously through molecular sequestration, offering a promising platform applicable to alternative checkpoint-cytokine combinations and other cellular therapeutics. Clinical translation represents a critical next step for extending CAR-T efficacy to solid malignancies.

The cooperative GOG 281/LOGS trial showed that trametinib, an MEK inhibitor (MEKi), was significantly more effective than standard-of-care options (including chemotherapy or hormonal therapy) in increasing progression-free survival (median PFS 13.0 months vs. 7.2 months; hazard ratio 0.48, p < 0.001)...Genomic and multi-omic profiling have revealed actionable vulnerabilities and precision oncology approaches. The advent of biomarker-directed trials, molecular subtyping incorporation, and innovative computational strategies is likely to gradually ameliorate therapy selection and, thereby, finally improve long-term outcomes for patients with this complex disease.

This study identifies, for the first time, a heritable processed transcript insertion as a pathogenic event in BRCA1. Such variants are undetectable by conventional diagnostic workflows lacking structural variant analysis, highlighting the importance of comprehensive approaches for accurate diagnosis and genetic counselling in hereditary cancer syndromes.

pDCs appear to exert a tumor-promoting, immune-evasive role, suggesting that DC function depends on their programming and tumor context. Selective targeting of DC subsets may offer novel therapeutic opportunities in TP53-mutated, low-TMB cancers.

For this reason, it is necessary to assess the influence of the tested compounds on cellular processes such as the cell cycle, epithelial-mesenchymal transition, autophagy, and apoptosis. This article summarizes available information on the effects of pentacyclic triterpenoids on the PI3K/AKT/mTOR, MAPK/ERK, NF-κB, JAK/STAT, Notch, HIF-1α, TGF-β, Wnt/β-catenin, Hippo, and Hedgehog signaling pathways in ovarian cancer cells.

Preclinical studies demonstrate that targeting growth factors and cytokine signaling, through monoclonal antibodies, receptor inhibitors, small molecules, or cytokine modulation, can reduce CSC frequency, restore chemosensitivity, and enhance immunotherapy efficacy. This review highlights the interplay between CSCs, growth factors, and cytokines as central to tumor progression and relapses, emphasizing their translational potential as therapeutic targets in precision oncology for gynecological cancers.

Imaging cytometry and single-cell transcriptomics revealed IFNγ-dependent macrophage reprogramming and IL-15 secretion, establishing a feed-forward loop that augments T cell functionality. A machine learning model trained on ex vivo cytotoxicity and transcriptomic data predicted patient responsiveness, supporting data-driven clinical stratification for solid tumour immunotherapy.

This interaction reduces global histone H4 acetylation and suppresses NF-κB transcriptional activity, ultimately altering epithelial migration. Our findings reveal a BRCA2-PCAF axis that modulates NF-κB signaling, a process co-opted by a recurrent BRCA2 pathogenic variant.

In summary, PDT exhibited comparable efficacy in both ferroptosis-sensitive and -resistant cells by triggering a combination of lipid peroxidation and ceramide upregulation, suggesting the activation of both ferroptosis and apoptosis pathways. Further studies are needed to explore the role of PDT-induced lipidomic changes in the initiation of various cell death pathways and in overcoming chemoresistance in HGSOC.

An in-depth analysis of the LacRGs data may yield valuable insights and enhance the molecular classification of OC. The identification of LRGS serves as a crucial factor in the early prognosis of patients and the selection of potential candidates for immunotherapy. The findings have significant implications for individual patients with OC.

Mechanistically, ATX020 blocks KIF18A's plus-end movement on spindle fibers, increasing spindle length, resulting in chromosomal mis-segregation, aneuploidy, and DNA damage. Our findings suggest that ATX020 inhibits CIN+ HGSOC cells mainly by inducing mitotic arrest and DNA damage, disrupting KIF18A's function crucial for mitosis.