KRAS wild-type

Concomitant treatment with, N-acetylcysteine reversed cell death response induced by investigated compounds (75.7 ± 15.1 % and 33.1 ± 9.9 % in average for MCF7 and A549 cells, respectively), suggesting that the generation of reactive oxidative species (ROS) was the key trigger of the cell death...Additionally, ultrastructural analysis confirmed significant mitochondrial damage in both cell lines. Investigated compounds potently disrupt mitochondrial function and can serve as a valuable asset for testing capacity of new antioxidant agents.

These findings demonstrate that AuNP-mediated co-delivery of siRNA and saRNA effectively modulates the KRAS-p53 signaling axis and enhances therapeutic potential in KRASmutant, TP53-wild-type cancers. Further studies, including in vivo investigations, are warranted to evaluate the translational feasibility and clinical relevance of this combinatorial approach.

P2, N=59, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027

Moreover, IGFBP-3 deletion in tumor cells and small molecule inhibition of TGF-βR1/2 attenuated myotube wasting. Collectively, these results suggest that PDAC derived IGFBP-3 promotes SMW via non-canonical binding of TGF-βRs, warranting formal investigation of IGFBP-3 as a potential therapeutic target for PDAC-related SMW through a novel pathway.

PBRM1 maintains chromatin accessibility for hepatocyte differentiation-related genes. Its loss promotes differentiation toward cholangiocytes during injury or tumorigenesis, driving iCCA development.

To investigate this, we synthesized statin-dye conjugates by attaching a fluorescent dye (Cy5.5) to two statins: simvastatin and pravastatin, aiming to assess whether selective uptake indeed occurs. Notably, in the PCC and CAF co-culture model, the pravastatin-Cy5.5 conjugate selectively killed KRASMUT PCCs without affecting the KRASWT CAFs. These findings highlight the unique synergistic potential of statin-Cy5.5-distinct from either component alone-as targeted delivery vehicles for KRASMUT cancer therapy.

Management involved permanent discontinuation of cetuximab, high-dose intravenous methylprednisolone (1.5 mg∙kg-1∙day-1), cyclosporine (3 mg∙kg-1∙day-1), supportive wound care in a burn unit, and topical ocular/oral care...Therapy was successfully transitioned to bevacizumab plus FOLFOX after dermatologic recovery, with no rash recurrence during follow-up. This case highlights the importance of early recognition, multidisciplinary management, and protocol-driven intervention for severe cetuximab-induced skin toxicity to ensure patient safety and treatment continuity.

P2, N=16, Active, not recruiting, Gruppo Oncologico del Nord-Ovest | Recruiting --> Active, not recruiting

This study is the first to investigate the interplay between KRAS mutations and PD-L1 expression in a real-world stage IV lung AC cohort treated with ICIs. Our findings indicate that the p.G12D mutation is associated with an extremely severe disease upon ICI monotherapy. These preliminary results need further validation in larger, prospective cohorts.

P1, N=47, Completed, Boehringer Ingelheim | Active, not recruiting --> Completed

Integration of molecular sub-group as a stratification parameter might be considered for randomized trials in advanced/metastatic endometrial carcinoma after carboplatin-based chemotherapy. Deeper characterization of mismatch repair-proficient tumors might enhance prognostication.