KRAS G12

Our findings emphasize that when imaging or cytology suggests multiorigin components, clinicians should pursue thorough intraoperative exploration, multisite biopsies, and prophylactic appendectomy. Ultimately, the management of such patients requires highly individualized surgical and chemotherapeutic strategies that account for the divergent biological behaviors and therapeutic sensitivities of both HGSOC and well-differentiated appendiceal mucinous adenocarcinoma to optimize oncological outcomes.

P1/2, N=67, Recruiting, D3 Bio (Wuxi) Co., Ltd | Active, not recruiting --> Recruiting | Trial completion date: Apr 2028 --> Aug 2028 | Trial primary completion date: Apr 2028 --> Aug 2028

The procedure includes tissue perfusion, controlled enzymatic digestion, gentle mechanical dissociation, red blood cell lysis, filtration, and viability assessment, and achieves >85% viable cells prior to scRNA-seq. Finally, the tdTomato+ tumor cells are efficiently isolated by FACS and can be detected as distinct clusters by scRNA-seq using this protocol.

Overall survival analysis showed no consistent prognostic disadvantage for CO, except in EGFR-KRAS co-mutant NSCLC. These findings further refine the ME landscape of BRAF, KRAS, and EGFR variants, offering a variant-level reference to support mutation-informed precision oncology.

P1, N=76, Not yet recruiting, Beijing Youcare Kechuang Pharmaceutical Technology Co., Ltd.

P3, N=356, Recruiting, Astellas Pharma Global Development, Inc. | Not yet recruiting --> Recruiting

[18F]KRAS490 showed specific, blockable tumor uptake and favorable pharmacokinetics, making it a promising tracer for noninvasive imaging of KRAS-G12C mutant tumors. Its ability to penetrate the CNS supports potential application in imaging both peripheral and brain lesions.

Genetic depletion of Fbln3 led to reduced tumor progression and increased Cd8 + T cell infiltration in mice. Together these findings identify a previously unknown signaling axis driving immunosuppressive phenotypes in PDAC, uncovering multiple potential nodes to relieve the immunosuppressive pressures within the PDAC TME.

P1/2, N=265, Recruiting, Blueprint Medicines Corporation

These metabolic shifts were accompanied by increased AMPK phosphorylation and reduced AKT phosphorylation, two key mediators of the response to KRAS G12C inhibition. Our data reveal GSTZ1‑associated metabolic and signaling alterations that contribute to drug resistance and identify GSTZ1 as a potential complementary target to sensitize KRAS mutant NSCLC to KRAS‑directed treatments.

When reformatted as chimeric antigen receptors or bispecific T-cell engagers, these antibodies mediated selective cytotoxicity against target-positive cells. Together, these findings establish a practical design-to-function pipeline for TCR-like antibody discovery and demonstrate the feasibility of therapeutically targeting KRAS G12D-driven malignancies.

Comprehensive genomic profiling is essential for patients with PAAD and carries both prognostic and predictive value. MTAP loss KRAS-mutant PAAD represents a subgroup of immune-excluded PAADs with a poor prognosis.