BRCA (Breast cancer early onset)

P2, N=14, Completed, Yuan Yuan | Active, not recruiting --> Completed | Trial completion date: Aug 2026 --> Nov 2025

The combination of PARP inhibitors and platinum activates the cGAS-STING pathway, leading to increased infiltration of mature DCs and CD8+ T cells, thereby sensitizing NSCLC to anti-PD-L1 therapy. This study presents a promising strategy for treating patients with LUAD with low immunogenicity and poor prognosis.

Clinical implications are direct: SGTs in BRCA1 carriers should not be assumed eligible for PARP inhibitor therapy without HRD confirmation, and enhanced surveillance appears unwarranted. This case underscores that co-occurrence does not establish causation and highlights the critical importance of functional validation before expanding hereditary cancer spectra.

In addition, CellViT obtained R-squared values ¿ 0.1 in all five test folds. We also show that morphologically indicative cascades, such as the apoptosis cascade, provide significantly higher performance compared to the DDR cascade.

Despite patients with targetable molecular alterations identified, very few patients were treated with targeted therapy and/or included in a clinical trial. It is essential to increase SMA for advanced PA in routine clinical practice to increase the use of targeted therapy and inclusions in clinical trials.

SPECTAcolor has generated a clinical and molecular dataset with associated samples for >800 CRC patients for future academic research such as biomarker validation. Linking screening platforms to therapeutic trials and ensuring sustainability remain challenging.

P1/2, N=210, Recruiting, Shanghai SciBrunch Therapeutics Co., Ltd. | Not yet recruiting --> Recruiting

Mechanistically, compound 6 could increase DNA damage, induce cell cycle arrest in the G2/M phase, and promote MDA-MB-436 apoptosis. Overall, 6 is a potential hybrid molecule and can be a candidate compound for the treatment of BRCA-deficient TNBC.

CDKN2AIPNL expression positively correlated with CAF infiltration in ESCA, KICH, UVM, and other tumors, and interacted with MYC, XRN2, and CHAMP1 to regulate metabolic reprogramming, cell cycle, and immune suppression. Our findings systematically reveal CDKN2AIPNL's dual role in tumorigenesis and validate it as a potential pan-cancer prognostic biomarker, providing novel insights for cancer diagnosis and targeted therapy.

From a translational perspective, multiple clinical trials have confirmed the safety and preliminary efficacy of this combination strategy in solid tumors, particularly demonstrating synergistic antitumor activity in settings of PARPi resistance or in tumors with intact HRR function. The combinatorial approach of CDKi and PARPi, through multi-dimensional mechanistic integration, holds strong potential as a key strategy to overcome PARPi resistance and expand the population of patients who can benefit from this class of therapies.

In the PSM sensitivity analysis, the median PFS was not reached (95% CI, 19.55-NR) in the niraparib group and was 18.33 months (95% CI, 8.90-25.26) in the bevacizumab group (HR = 0.360, 95% CI, 0.176-0.736; P = .005).ConclusionThis analysis suggests that niraparib may provide a progression-free survival advantage compared with bevacizumab in BRCAwt AOC patients, with both regimens appearing to be generally well tolerated in the real-world setting. These findings offer preliminary reference value for maintenance treatment selection in patients with newly diagnosed BRCAwt AOC.

New primary breast cancer infrequently developed after PNSM in this study. Incidental breast cancer was identified on surgical pathology in a small subset of patients. PNSM may be associated with preventing breast cancer development.