MAP3K1 (Mitogen-Activated Protein Kinase Kinase Kinase 1)

GIRPG independently predicts glioma outcomes, reflects glucose metabolism-immunity crosstalk in the TME, and provides a prognostic tool and potential therapeutic targets for glioma precision treatment.

Ectopic differentiated cells are also found within the incorrect organs after map3k1 RNAi, and ultimately, teratomas form. These findings implicate map3k1 signaling in controlling the positional regulation of progenitor behavior - restricting progenitor differentiation to targeted locations in response to external cues in the local tissue environment.

Using real-world CGP of tumour tissue and ctDNA, we identified key molecular features associated with endocrine resistance in patients with low RS who later developed metastases. PIK3CA mutation and other ER group-related mutations contributed to the low RS. Tissue CGP provides baseline for interpreting ctDNA, and ctDNA monitoring PIK3CA, TP53, ESR1 and other pathogenic or driver mutations in the early course of low RS cases may represent an excellent non-invasive option for identifying targets and early intervention to prevent disease progression, though a large validation study is needed.

Although driver mutations in sporadic medullary thyroid carcinoma (sMTC) mostly come from targeted NGS data in tumours from patients with localised disease, NGS findings can also be used for therapeutic purposes in advanced-stage sMTC cases with progressive local-regional or distant metastatic disease. We believe that additional studies should be conducted with a larger number of patients so that the findings can be included in the treatment guidelines to be prepared.

This international study identifies recurrent IM driver genes, IM-specific mutational signatures, and alterations in IM-associated immune landscapes and microbiomes. Our results highlight a role for nonepithelial somatic alterations (CH) in IM progression to gastric cancer, offering new translational opportunities for early cancer detection and interception.

Furthermore, indirubin treatment was linked to the inhibition of the MEKK1/SEK1/JNK/AP-1 signaling pathway, which may also contribute to its anti-tumor effects. These findings suggest that the anti-tumor activity of indirubin is associated with the regulation of the PI3K/AKT and MAPK pathways, the enhancement of autophagy, and the promotion of apoptosis, providing a theoretical basis for its therapeutic potential in cervical cancer treatment.

Our study delineates the distinct genomic mutational landscapes between TNBC and non-TNBC cohorts, and reveals somatic interactions, driver genes, mutational signatures and pathway enrichment. These findings highlight the distinct molecular features of TNBC, which may contribute to its aggressive clinical behavior.

This integrated transcriptomic and miRNA profiling study reveals subtype-specific dysregulation of MAPK-associated genes and their miRNA regulators in BC, with TNBC exhibiting the most profound alterations. These findings provide insight into potential targets for personalized therapeutic strategies.

Translocations occurred in 11 (61.1%) PCL patients; IGH::CCND1 and IGH::MYC were more frequent in PCL compared to MM (22% vs. 14%, p = NS, and 11% vs. 1%, p < 0.05). Druggable aberrations in BRAF, CCND1, PIK3R1, and RAS may be targeted in biomarker-driven therapeutic clinical trials.

Our findings establish MAP3K1 and MAP2K4 as key tumor suppressors in BRCA that operate via the JNK2-p53-FOSL1 axis. Their inactivation provides an alternative mechanism for p53 pathway disruption, adhering to the "minimal necessary alteration" principle in cancer signaling. This study highlights the dual regulatory mechanisms controlling FRA1 expression and offers insights into breast cancer heterogeneity, with potential implications for targeted therapy and patient stratification.

This finding suggests that BRCA1-associated USC may be sensitive to poly ADP-ribose polymerase inhibitors, and also raises the question of whether risk-reducing hysterectomy should be considered for patients with BRCA1 mutation. USC with a BRCA1 mutation may have molecular characteristics distinct from those of sporadic USC, and further accumulation and analysis of such cases are needed to evaluate the clinical implications.

Functional studies revealed that inhibition of the mutated oncogene ROS1 using crizotinib induces death in infected leukocytes, confirming its role in transformation...Our findings provide new insights into how T. annulata reprograms host cells through genomic instability and mutations, identifying ROS1 and TP53 as critical targets for therapeutic intervention. This work advances understanding of parasite-induced oncogenic transformation and offers pathways for future research.