KRAS wild-type

Mouse embryonic fibroblasts transformed with KRASG12C also contain more saturated lipids than KRASG12D MEFs. Thus, activities of KRAS mutants depends on lipid acyl chain remodeling in an allele-specific manner.

The NTZ-AG regimen demonstrated meaningful anti-tumor activity and an acceptable safety profile as first-line therapy for unselected advanced pancreatic cancer patients, providing a rational basis for larger randomized controlled trials. This trial was registered at the Chinese Clinical Trial Register (ChiCTR) under the registration number ChiCTR2300072843 having URL https://www.chictr.org.cn/showprojEN.html?proj=198791.

Although recent advances have led to covalent inhibitors such as Sotorasib and Adagrasib for the KRAS G12C mutation, effective therapies for other common variants, particularly KRAS G12D, which is highly prevalent in aggressive pancreatic cancers, remain limited...To further validate the predictive capability of the models, two compounds identified as high-confidence candidates, Cobimetinib and Etrasimod, were selected for experimental evaluation...While additional biochemical and pathway-level studies are required to confirm direct target engagement, these results support the model's utility in prioritizing candidate compounds with allele-specific activity profiles. Overall, this study provides a data-driven framework for identifying potential KRAS-targeted therapies and highlights the value of integrating machine learning predictions with experimental validation.

The minimally invasive anatomical approach allowed precise vascular control and achievement of oncologically adequate margins in a technically demanding central segment. Larger clinical series are needed to define optimal management strategies and long-term oncologic outcomes in this setting.

P1, N=18, Recruiting, Joint Biosciences Ltd.

P2/3, N=574, Recruiting, SUNHO（China）BioPharmaceutical CO., Ltd. | N=90 --> 574 | Trial completion date: Jul 2028 --> Jul 2029 | Trial primary completion date: Jul 2026 --> Jul 2028

P1, N=47, Terminated, BeOne Medicines | N=514 --> 47 | Trial completion date: Dec 2026 --> Apr 2026 | Recruiting --> Terminated | Trial primary completion date: Dec 2026 --> Apr 2026; The Sponsor has made the decision to terminate this study due to the lack of promising efficacy, internal prioritization, and highly competitive landscape.

Poor survival outcomes were observed across all 1 L treatment options. Patients with KRAS-mutated NSCLC and low PD-L1 expression had especially poor outcomes, highlighting the need for more effective treatment options.

This review summarizes current evidence on the crosstalk between KRAS signaling and Furin-like enzymes, emphasizing their cooperative roles in tumour progression and immune escape. Targeting protein maturation by these enzymes may therefore represent a therapeutic approach for KRAS-mutant colorectal cancer, offering new opportunities for personalized treatment.

Nonetheless, K. rosea emerges as a candidate taxon differentially enriched in PDAC, with potential stage- and KRAS-associated patterns. These findings highlight the need for orthogonal validation (qPCR, FISH, culture) and larger prospective cohorts to differentiate true biological associations from residual contamination or stochastic noise in low-biomass settings.

High Cdc42 expression may serve as an adverse prognostic marker in CRC. Cdc42 shows moderate concordance between primary tumors and matched metastases without a consistent directional shift.

Oncologists should consider broad next-generation sequencing, including fusion detection, for patients with KRAS-wildtype PDAC. When an ALK fusion is identified, ALK inhibitor therapy can yield durable disease control.