BRCA2 mutation

P3, N=420, Not yet recruiting, K-Group, Beta, Inc., a wholly owned subsidiary of Zentalis Pharmaceuticals, Inc

Preoperative breast cancer imaging before GACMS identified malignancies that significantly influenced surgical planning, preventing additional procedures postoperatively. Implementing a decision-making algorithm could guide and standardize breast imaging before GACMS.

Using cell line-derived xenograft, patient-derived organoid, and patient-derived xenograft models, we discovered that IPA-3 potentiated the therapeutic efficacy of olaparib both in vivo and ex vivo. Collectively, our findings suggest that targeting PAK1 might offer a new avenue for increasing the sensitivity of olaparib and improving the outcomes of ovarian cancer patients.

The 2025 Swedish prostate cancer guidelines introduce multiple new recommendations and differ in several aspects from the European guidelines.

In this review, we critically evaluate the clinical relevance of molecular, metabolic, and microenvironmental determinants of PDAC progression and therapeutic resistance. We focus on translational bottlenecks that have limited clinical success to date and highlight biomarker-driven strategies, ongoing clinical trials, and emerging technologies poised to shift treatment from uniform algorithms toward biologically informed, patient-specific therapeutic approaches in pancreatic cancer.

P3, N=700, Recruiting, AstraZeneca

P4, N=43, Active, not recruiting, AstraZeneca | Completed --> Active, not recruiting | Trial completion date: Jul 2025 --> Dec 2026

Combining eprenetapopt with carboplatin shows promising preclinical efficacy by enhancing cytotoxicity in olaparib-resistant models and demonstrating synergistic interaction; these data support the combination as a potential strategy to mitigate PARPi resistance and carboplatin cross-resistance in TP53 mutant HGSOC and TNBC cell lines. Although further studies are needed to elucidate the molecular mechanisms underlying the synergistic effect, here we point out the combination of eprenetapopt and carboplatin as a potential therapeutic strategy to address olaparib resistance in HGSOC and TNBC patients.

Actionable genomic mutations such as PIK3CA, ESR1, ERBB2, BRCA1/2, and AKT/PTEN are reviewed in relation to their corresponding therapeutic agents. Implementation challenges, pre-analysis pitfalls, uncertain sampling cadence, cost barriers, and disparities in access are discussed, along with potential solutions.

Prognosis appears to be driven primarily by tumor biology, stage, and surgical outcome rather than the presence of endometriosis itself. The online version contains supplementary material available at 10.1186/s12885-026-15980-w.

GGT prevalence has increased at RPCCC and informed treatment decisions. Universal point-of-care testing is being implemented with the goal of completing testing for all patients with PDAC seen at RPCCC.

Subsequently, we explore how olaparib treatment itself can alter the expression profile of ncRNAs, creating a dynamic feedback loop that may influence therapeutic outcome. By consolidating these findings across various cancers, including ovarian, breast, prostate, and hepatocellular carcinoma, this review highlights the potential of ncRNAs as both predictive biomarkers and therapeutic targets to overcome PARPi resistance and enhance patient outcomes.