EGFR mutation

This study provides a regional molecular profile of advanced CRC in Bulgaria, highlighting a high prevalence of KRAS mutations and dMMR status, while underrepresentation of rare targetable alterations, likely due to limited use of broad molecular profiling. The association between stromal features and MMR status supports their potential role as surrogate markers in settings with constrained testing resources. Findings underscore the urgent need for equitable access to molecular diagnostics and targeted therapies to close the survival gap between Eastern and Western Europe.

P2/3, N=174, Active, not recruiting, SWOG Cancer Research Network | Trial completion date: Nov 2025 --> Dec 2026

P2, N=33, Recruiting, Fondazione Ricerca Traslazionale

The interpretable DeepSurv model, integrating multimodal features, enables quantitative survival prediction and risk stratification in advanced NSCLC, facilitating personalized decision-making.

PRMT5 inhibitor activity is independent of TKI exposure, driver alteration, and SDMA expression and enhanced by addition of TKI. These findings support clinical evaluation of PRMT5 inhibitor + TKI combinations for advanced NSCLC.

Patients with non-small-cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations who experience disease progression after treatment with an EGFR-tyrosine kinase inhibitor (EGFR-TKI) often receive subsequent treatment with either platinum-based chemotherapy (Chemo) or a combination regimen of atezolizumab, bevacizumab, carboplatin, and paclitaxel (ABCP). After propensity score matching, among patients who responded to prior EGFR-TKIs for ≥10 months, the ABCP group had a significantly longer PFS than the Chemo group (8.6 versus 5.3 months; log-rank test, P = 0.008). The efficacy of prior EGFR-TKI treatment in patients with EGFR-mutant NSCLC who experience disease progression could be a predictive marker for ABCP rather than Chemo efficacy.

Patients were treated in first-line (1L) with osimertinib or other TKIs (non-osimertinib). This study demonstrates that real-world treatment patterns and outcomes of TKIs are comparable with those found in both clinical trials and other real-world studies. RWE studies can support clinicians in investigating the best treatment strategy and decision makers to drive new health policies.

The pan-AKT inhibitor, Capivasertib (AZD5363), suppressed some but not all tested PIK3CA -mutated cell lines and one PIK3CA -wt cell line (SiHa). Further research on targeted therapies will improve the prognosis of patients with cervical cancer. Identified 3 molecular subtypes of CC based on PIK3CA and YAP1 amplification status Cervical cell lines with PIK3CA mutation are suppressed by targeted inhibitors PI3K inhibitors Alpelisib/Inavolisib selectively block PIK3CA-mutant cells PIK3CA mutation is associated with higher expression of the checkpoint CD274/PD-L1 PI3K inhibitors cooperate with donor-derived T cells to kill cervical cells.

Therapeutic targeting of BRAFV600E has led to the approval of dabrafenib plus trametinib for solid tumours [excluding colorectal cancer (CRC)] refractory to standard therapies...In CRC, intrinsic epidermal growth factor receptor (EGFR) activation circumvents BRAF inhibition, necessitating the concurrent use of EGFR inhibitors, whose treatment strategy led to the approval of encorafenib plus cetuximab for BRAF V600E CRC...While noteworthy results have been achieved with BRAFV600E inhibition, further research is needed to optimize BRAF-targeted therapies and address resistance mechanisms. Continued research and innovation are crucial to improving patient outcomes and addressing the complexities of BRAF mutations in human cancers.

The nanoparticle was developed by transfection of four plasmids (Gag-Cas9, Gag, sgRNA, VSV-G Azi) into 293T cells to form a type of bionanoparticle and modifying it with a targeted polymer material (DBCO-PEG-FA), and it showed a cancer-targeted property, faster cancer cellular uptake, higher gene editing efficiency with lower off-target effects, and therapy efficacy in mice, indicating a translational prospect. In conclusion, the study provides a recombinant bionanoparticle in vitro expressing a Cas9 gene editing system and offers a potential strategy for gene therapy of EGFR mutant lung cancer.

P3, N=390, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Oct 2026 --> Feb 2027 | Trial primary completion date: Oct 2026 --> Dec 2025

P2, N=16, Not yet recruiting, Jonsson Comprehensive Cancer Center | Trial completion date: Dec 2029 --> Jun 2030 | Initiation date: Jan 2026 --> Jun 2027 | Trial primary completion date: Dec 2028 --> Jun 2029