Colorectal Adenocarcinoma

P3, N=560, Recruiting, Akeso | Not yet recruiting --> Recruiting

P2, N=50, Recruiting, Sun Yat-sen University

P2, N=37, Recruiting, Memorial Sloan Kettering Cancer Center | Trial primary completion date: Jun 2026 --> Jul 2027

P=N/A, N=20, Recruiting, Yale University | Not yet recruiting --> Recruiting

This approach offers a robust framework for addressing tissue-specific challenges in predicting driver mutations. All code, trained models, and processed data are available at https://github.com/Zubair11122/ResMLP-GL to promote transparent and reproducible precision oncology research.

Mutual interaction between B cells and memory-like Tfh cells was promising immune response for the treatment of MSS COAD. MSD promoted the formation of TAA to intensify Tfh cell/B cell collaboration in a CCL20 dependent-manner.

P3, N=834, Recruiting, Canadian Cancer Trials Group | Not yet recruiting --> Recruiting

P=N/A, N=71, Active, not recruiting, Istituto Oncologico Veneto IRCCS | Recruiting --> Active, not recruiting | N=200 --> 71 | Trial primary completion date: Jan 2026 --> Sep 2025

SIGNIFICANCE: Extended O-glycans from the Tn antigen GalNAcα1-Ser/Thr/Tyr (CD175) have many biological functions but roles are poorly understood. Here we show that targeted deletion of Cosmc (C1GalT1C1) in murine intestinal epithelial cells leads to CD175 expression and a loss of extended O-glycans, dysregulation of multiple pathways, and spontaneous colorectal tumors.

Cancer cells were treated for 48 h with ABQ-48, cisplatin, or vehicle, and cytotoxicity was assessed by determining IC50 by fluorescence analysis...Annexin V assays confirmed apoptotic induction, while caspase activation demonstrated engagement of both intrinsic and extrinsic pathways. ABQ-48 demonstrates potent anticancer activity through activation of multiple programmed cell death mechanisms, supporting further investigation as promising therapeutic candidate.

The hub genes act as molecular bridges connecting the observed genomic and epigenetic variations, particularly driving chromatin-related regulation and MAPK signaling pathways. In particular, PSMC1, SNW1, H3C2, H1-2, and H2BC14 genes offer promising molecular targets for future therapeutic approaches in SACs.

In vitro and in vivo experiments demonstrated that RPS6KA1 inhibits malignant progression of colon cancer and modulates fatty acid metabolism. Integrated multi-dimensional bioinformatic and experimental analyses reveal that RPS6KA1 remodels fatty acid metabolism and suppresses malignant progression, indicating its value as a prognostic biomarker in CRC and providing new insights for therapeutic strategies.