KRAS (KRAS proto-oncogene GTPase)

P2, N=70, Recruiting, Innate Pharma | Trial completion date: Sep 2026 --> Jun 2027 | Trial primary completion date: Jun 2025 --> Jun 2027

P=N/A, N=305, Active, not recruiting, Shanghai Chest Hospital | Recruiting --> Active, not recruiting | Trial completion date: Mar 2026 --> Dec 2027 | Trial primary completion date: Mar 2025 --> Dec 2026

ICIs included standard programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) antibodies, chemotherapy was platinum-based doublet therapy, and anti-angiogenic therapy was limited to bevacizumab (BEV)...ICIs + CHE is the preferred first-line treatment regimen for patients with locally advanced/metastatic KRAS-mutant non-squamous NSCLC, and the addition of anti-angiogenic agents does not improve therapeutic efficacy. Clinical treatment regimens should be selected individually based on patient characteristics and PD-L1 expression level did not serve as a survival stratification factor for immunotherapy-based treatment regimens.

Tumor tissue and serial plasma samples were collected from 15 patients with aUC treated with dose-dense methotrexate, vinblastine, doxorubicin, and cisplatin (ddMVAC). While the NOIR-SS-based assay proved sensitive and informative, limitations include the cost and time required for sequencing, potential temporal discordance between tissue and plasma sampling, and the absence of correction for clonal hematopoiesis of indeterminate potential. Overall, ctDNA profiling using this targeted panel and NOIR-SS suggested the feasibility of sensitive, non-invasive molecular monitoring in aUC, and may have future clinical applicability if validated prospectively in larger cohorts.

This multi-omics framework identified ACP2 as a lysosomal regulator of glioma aggressiveness and immune remodeling. ACP2 functions as a robust biomarker of malignancy and may represent a candidate target for therapeutic exploration in glioma.

We show that while many of the new compounds exhibited a dramatic increase in binding affinity to KRAS, in many cases, that did not translate into improved potency in inhibiting cell growth. Considering the high binding affinities (up to single-digit nanomolar) and low micromolar inhibitory activities across multiple KRAS mutant cancer cells, we propose that these new derivatives will serve as useful investigational agents for KRAS studies or as starting points for further derivatization and structure-activity relationship studies.

We present a 57-year-old man with KRAS G13D-mutant, liver-dominant metastatic rectal adenocarcinoma and recurrent fluoropyrimidine-associated coronary vasospasm precluding 5-fluorouracil and capecitabine. After multimodal first-line therapy and regorafenib, trifluridine/tipiracil (TAS-102) plus bevacizumab was initiated and integrated with liver-directed treatments for oligoprogressive disease. This combined strategy achieved approximately 16.6 months of disease control, substantially exceeding the median progression-free survival reported in the SUNLIGHT trial, with manageable hematological toxicity and preserved performance status. This case highlights the value of TAS-102 plus bevacizumab combined with focal liver-directed therapy as a feasible long-term strategy for selected patients with oligoprogressive mCRC when fluoropyrimidines cannot be used.

P1, N=999999, Not yet recruiting, Theras Inc.

P2, N=86, Recruiting, Abbisko Therapeutics Co, Ltd | Not yet recruiting --> Recruiting

P2, N=39, Recruiting, University of Chicago | Not yet recruiting --> Recruiting

P1, N=140, Not yet recruiting, Clasp Therapeutics, Inc.

P1, N=24, Recruiting, Ruijin Hospital