KRAS G12S

Experimentally, KRASQ61R mutation led to KRAS exon 3 skipping, which in turn could be rescued by expression of U2AF1I24T. Our findings provide evidence that splicing factor mutations can rescue splicing defects caused by oncogenic mutations in a dynamic process of cascading selection.

P1, N=20, Recruiting, Memorial Sloan Kettering Cancer Center

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

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

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

P1, N=665, Recruiting, TheRas, Inc., d/b/a BBOT (BridgeBio Oncology Therapeutics) | N=387 --> 665

CAC exhibits distinct mutational characteristics compared with sporadic CRC and different genetic abnormalities in each lesion may contribute to the dysplasia-carcinoma sequence.

When combined with cytotoxic agents, including paclitaxel, SN38, gemcitabine and cisplatin, MRTX1133 reduced the sensitivity to cell cycle-dependent chemotherapeutic agents, namely paclitaxel, SN38 and gemcitabine, while not affecting the activity of the non-cell cycle-dependent agent cisplatin. The present study therefore provided preclinical evidence for the potential utility of KRAS (G12D)-targeted therapy in OMC and highlights the importance of sequential rather than concurrent scheduling of MRTX1133 with cell cycle-dependent chemotherapy to optimize therapeutic efficacy.

P1, N=48, Not yet recruiting, Kumquat Biosciences Inc.

The uncommon KRAS mutation group had numerically inferior progression-free survival (PFS) and overall survival (OS); however, this difference did not reach statistical significance in our study (mean PFS: 15.14 months vs. 30.39 months, p = 0.074; mean OS: 24.50 months vs. 38.79 months, p = 0.157). These findings underscore the value of broad molecular profiling in establishing critical links between specific morphologic features, genetic alterations, and clinical behavior for tumors harboring these uncommon KRAS variants.

P1, N=750, Active, not recruiting, Eli Lilly and Company | Recruiting --> Active, not recruiting

BRAF V600E was detected in 3.7%.ConclusionsWe report a rise in EOCRC in Serbia, especially in ages 45-49, and recommend policy makers to lower the screening age to 45. We present the first detailed molecular profile of Serbian EOCRC and recommend that policy makers implement routine KRAS variant testing and ensure access to KRAS G12C-targeted therapies to improve personalized care.