AKT2 (V-akt murine thymoma viral oncogene homolog 2)

Phytochemicals derived from Pithecellobium dulce, particularly oleanolic acid and rutin, emerge as promising selective modulators of AKT1 and AKT2, respectively. These findings provide a mechanistic and structural foundation for the development of isoform-guided AKT-targeted therapies and support further experimental validation toward precision oncology applications.

This study suggests that CRO may reduce ferritinophagy-induced colonic oxidative damage in rats via modulating AKT/mTORC1/ULK1. Ferritinophagy as an attractive therapeutic target in different experimental and clinical conditions deserves further investigation.

Furthermore, we identify a PTEN-dependent crosstalk between NOTCH and TGFβ pathways that governs liver tumor development. Together, this work provides mechanistic insight into lineage plasticity in liver cancer with implications for pathway-directed therapy.

Results support causal effects on HCC for TMCC3, METTL1, SNRPF, KRT19, MED4, RFNG, IL26, NRXN1, MSH2, CLCA2, AKT2, CRYZL1, RDH16, CSF3, CPA4, EPHA2, and COPS7B. Experimental validation and mechanistic study are warranted to confirm findings.

The patient eventually developed resistance to both first-line gefitinib and later almonertinib...He received ivonescimab monotherapy, achieving disease control for nearly 5 months before transitioning to ivonescimab plus pemetrexed with continued benefit and a manageable safety profile. This case illustrates the potential benefit of ivonescimab in patients with EGFR-mutant LUAD and baseline MPE who develop complex, non-canonical resistance to EGFR-TKIs. These findings support further clinical evaluation of ivonescimab in this poor-prognosis subgroup and highlight the importance of repeated molecular profiling in guiding treatment strategy.

P2, N=33, Suspended, National Cancer Institute (NCI) | Recruiting --> Suspended

This study analyzed 321 tumor samples from 244 Chinese patients with genitourinary cancers using targeted NGS. Distinct mutational landscapes and PD-L1-associated genes were identified across bladder, renal, and prostate cancers. Comparative analysis with Western cohorts revealed population-specific genomic heterogeneity, supporting region-tailored precision oncology.

The tumor volume growth, tumor weight, and Ki67 expression in tumor tissues were sharply repressed by GTN, along with increased MDA, restrained SOD activity, downregulated GPX4 and SLC7A11, diminished total m6A methylation level and AKT2 N6-methyladenosine, and reduced METTL3 level in tumor tissues. Collectively, our findings demonstrate that GTN restrains CRC progression by inducing ferroptosis through the inhibition of the novel METTL3/AKT2/HIF1α/SLC7A11 axis, highlighting its potential as a promising therapeutic agent for CRC.

Among ML models, XGBoost demonstrated the highest performance (accuracy 98%, sensitivity 98%, specificity 97%, F1-score 0.99, AUC 0.86), outperforming other algorithms. These findings indicate that age-related transcriptomic changes impact survival in Luminal A breast cancer and that an ML-based integrative approach combining clinical and molecular variables provides superior prognostic accuracy, supporting its potential for clinical application.

Our study highlights the novel role and regulatory mechanisms of CCL7+ TAMs in ICIs immunotherapy resistance, suggesting that CCL7 may serve as a potential combined therapeutic target for ICIs immunotherapy.

The FOXK1/AKT2 signaling axis contributes to cisplatin resistance in ESCC. Triptonide reverses resistance by inhibiting this axis, offering a promising strategy to enhance cisplatin efficacy in ESCC therapy.

Molecular docking revealed that R274H, in kinase domain, disrupts key hydrogen bonds with THR292 and GLU279, leading to more flexible binding pocket and significantly reduced binding affinity for Capivasertib and Ipatasertib. These findings suggest that these mutations may contribute to inhibitor resistance by weakening inhibitor interactions and destabilizing the protein-inhibitor complex. This study underscores the importance of genetic screening in optimizing cancer treatment and highlights the need for mutation-specific therapeutic strategies targeting AKT2.