KRAS (KRAS proto-oncogene GTPase)

P1, N=160, Recruiting, SystImmune Inc. | N=120 --> 160

P1, N=210, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2033 --> Feb 2029 | Trial primary completion date: Jun 2031 --> Feb 2029

P1, N=34, Completed, M.D. Anderson Cancer Center | Active, not recruiting --> Completed | Trial completion date: Dec 2026 --> Mar 2026 | Trial primary completion date: Dec 2026 --> Mar 2026

P2, N=50, Recruiting, Emory University | Trial completion date: Sep 2028 --> Sep 2029 | Trial primary completion date: Mar 2028 --> Mar 2029

www.clinicaltrials.gov identifier is NCT06119581. EudraCT: 2023-503412-33-00.

As targeted therapies continue to expand across disease stages and treatment lines, CV toxicity is expected to play an increasingly important role in therapeutic decision-making. Integrating CV considerations into oncologic care is therefore essential to preserve treatment continuity, optimize long-term outcomes, and maximize the benefits of modern targeted therapies in NSCLC.

The Pan Lung Cancer PCR Panel was highly concordant with other assays. The panel can be performed in local laboratories with a rapid turnaround time and represents an attractive alternative to next-generation sequencing for patients with lung cancer.

Our study highlights the complementary diagnostic value of p53 and Smad4 IHC relative to molecular testing in PDAC, especially when tissue is limited, as commonly encountered in FNB specimens. The newly established Smad4 IHC classification system, which integrates an intermediate expression category into the conventional two-tier framework, demonstrates superior clinical utility and enhances predictive accuracy for SMAD4 genomic alterations.

In addition, 089 exhibited good tolerability in a nude mouse HCT-116 xenograft model, but it was less effective at a dose of 40 mg/kg compared with Apremilast at a dose of 30 mg/kg in 8-s day's assay. While 089 had lower in-vivo efficacy than apremilast, its novel 3-aminoisoquinoline scaffold and high tolerability make it a superior candidate for further optimization.

RBM10 mutation is frequent in Japanese patients with NSCLC with EGFR mutation, especially those with L858R or uncommon mutations, and was associated with late-onset and features of indolent tumor growth.

In this review, we highlight these recent advances and discuss how lipid-driven circuits intersect with major oncogenic pathways, including KRAS effectors and phosphoinositide 3-kinase-AKT. By integrating mechanistic insights with therapeutic perspectives, we outline new opportunities to exploit lipid-based vulnerabilities in pancreatic cancer.

By modifying the miR-3073a-3p/CAMKK2 axis, SCO improved MASLD, indicating its potential therapeutic utility in the management of metabolic liver disorders.