NOTCH3 (Notch Receptor 3)

Across in vivo models, pathway inhibition reduced tumor growth, decreased CD206-positive tumor-associated macrophages, and attenuated sciatic nerve invasion. Together, these findings identify a targetable JAG2-NOTCH3-STAT3-CCL2 signaling programmed through which CRC cells reprogramed macrophages to establish a neurotropic microenvironment permissive for PNI, suggesting potential therapeutic strategies to limit neural dissemination in CRC.

P=N/A, N=500, Recruiting, Jeju National University Hospital

Six genes (CD36, CLU, FLNA, NOTCH3, TAGLN, TIMP1) were identified as key regulators during ECs phenotypic transition.ConclusionsThis study demonstrates the key roles of disulfidptosis and anoikis, and establishes a novel CCDI model with prognostic value in colon cancer. Additionally, it insights into ECs phenotypic transition and their regulatory genes, provides new therapy targets for colon cancer.

Clinically, NOTCH3 mutation or low expression independently predicted improved survival in immunotherapy-treated CRC and pan-cancer cohorts. NOTCH3 is a pivotal regulator of immune evasion in CRC via the RBPJ-PVR axis.

Gastrin-high tumors exhibit CD8+ T cell infiltration alongside PD-1/PD-L1 upregulation, suggesting potential responsiveness to immune checkpoint blockade. These findings define a molecular taxonomy of pNETs and nominate tumor-intrinsic and microenvironmental programs as actionable targets.

P3, N=578, Not yet recruiting, The First Affiliated Hospital of Zhengzhou University

The information in this review provides a practical framework for clinicians and researchers to improve risk assessments, to employ biomarkers, and to develop therapies that go beyond vasodilation to address upstream drivers of pulmonary arterial remodeling. This framework may also serve as a model for other difficult-to-treat diseases in which incomplete genetic explanations and limited attention to environmental exposures have slowed progress in prevention, early detection, and personalized treatment.

These findings suggest that dysregulated gene expression may contribute to the activation of stromal cells and macrophages within the spleen, facilitating malignant transformation. Overall, these findings deliver novel transcriptomic insights into canine splenic tumorigenesis that may improve diagnostic precision, inform prognostic assessment, and support the development of targeted therapeutic strategies in veterinary oncology.

Collectively, our findings identify the functional Pin1/Notch3 axis as an escape strategy from chemotherapy-induced cell death, thus suggesting a novel predictive role of the Pin1/Notch3 axis in the platinum response, which could be useful for implementing frontline treatments for HGSOC patients before recurrence.

Moreover, nanoroughness mediates a cross-talk between cancer cells and astrocytes through induced senescence. These findings implicate a role for stochastic biophysical cues in driving a potential malignant transformation of astrocytes.

It specifically identifies distinct subpopulations characterized by differential Notch3 activity, which is enriched in a synthetic subset and absent in a contractile subset, further supporting our in vivo findings. Our results establish Notch3 as a key regulator of pericyte phenotypic plasticity in CRC and suggest that targeting this pathway could represent a promising strategy for improving therapeutic outcomes through vascular normalization.