KRAS G12

P1, N=387, Recruiting, TheRas, Inc., d/b/a BBOT (BridgeBio Oncology Therapeutics) | N=287 --> 387

P2, N=68, Active, not recruiting, ETOP IBCSG Partners Foundation | Trial primary completion date: Dec 2025 --> Jul 2025

Initial evaluations of C29h alone or together with the standard-of-care chemotherapeutic drug gemcitabine were conducted on NQO1high human and mouse PDAC cell lines and patient-derived organoids...Importantly, C29h treatment induced tumor regression and increased the survival of PDAC-bearing mice and optimal C29h-induced tumor regression was dependent on CD8+ T lymphocytes whose tumoral recruitment was enhanced by drug treatment. This study supports the use of C29h alone or as part of a drug combination as an effective and promising strategy for selective eradication of NRF2high PDAC.

Taken together, we demonstrate that Rad18 has context-specific tumor-suppressive activity. Given the prevalence of 4NQO-like environmental exposures, RAD18 is highly likely to shape human cancer genomes and perhaps influence other aspects of the tumorigenic process.

Our study demonstrates that ELK1 is a potential therapeutic target for AML, due to its critical role in regulating neutrophils differentiation.

Together, this study demonstrated that KRASG12R is capable of driving tumorigenesis despite the reduced ERK/MAPK nuclear translocation and transcriptional output. Although human KRASG12D and KRASG12R-mutant tumors display unexpected similarities in PI3K activity, the differential ERK/MAPK signaling activity and the extrinsic consequences on the TME provide support for using KRASG12R mutation status as a prognostic biomarker for therapeutic strategies.

The study results identified ENPP1 as a contributor to pancreatitis-mediated pancreatic cancer and a potential therapeutic target for pancreatic carcinogenesis.

By integrating multi-omics data from clinical cohorts and validating findings in vivo, we show that combining KRAS inhibitors with CXCL9/10 restoration effectively overcomes this immune suppression and controls tumor growth. Our work delineates a targetable immune evasion mechanism and provides a cohesive prognostic and therapeutic framework for KRASG12/13-mutant CRC.

The frequencies of dMMR and Lynch syndrome in patients under 50 years old was comparable to our previous report in which testing was conducted as part of research. Our results suggest that in patients under 50 years old(, 1)the utility of BRAF testing as an adjunctive diagnostic tool for Lynch syndrome is limited, and (2)BRAFV600E or KRASG12C was not detected;however, a larger accumulation of cases is necessary.

Our work defines the LY6D+ gastric-like cell state as a key driver linking early pre-malignant heterogeneity to PDAC initiation and progression. LY6D represents a pan-stage therapeutic target and a candidate biomarker for early detection and therapeutic targeting.

P1/2, N=140, Recruiting, InxMed (Shanghai) Co., Ltd. | Trial completion date: Dec 2026 --> Dec 2028 | Trial primary completion date: Dec 2025 --> Dec 2027

P1, N=574, Recruiting, Revolution Medicines, Inc.