JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit)

Our study demonstrates that chronic stress induces a robust, cross-paradigm PFC signature characterized by downregulation of glia/myelin and vascular pathways and suppression of immediate-early gene activity, highlighting cellular processes linking chronic stress exposure, PFC dysfunction, and psychiatric disorders.

These findings highlight the regulatory role of RBPs in ICI-induced colitis and identify cell-type-specific alterations that may drive disease progression. Importantly, we pinpoint immune checkpoint-related RBPs as potential therapeutic targets, offering new strategies to manage this clinically significant irAE.

PBMC expression showed high diagnostic accuracy (AUROC > 0.92 for SPHK1, WNT10A, JUNB). In conclusion, combining PBMC gene expression profiling with in-silico analyses highlights JUNB, WNT10A, SPHK1, EDN1, and KLF4 as promising non-invasive biomarker panel for HCC risk in DAA-SVR patients, reflecting their integration into epigenetic and oncogenic networks and supporting their potential for risk stratification and therapeutic targeting.

Finally, we show that NeuMap enables inference of the pathophysiological state of the host by profiling blood neutrophils. Our study delineates the global architecture of the neutrophil compartment and establishes a framework for exploration and exploitation of neutrophil biology.

The relative expression of PRKCQ and its associated signaling components suggests their critical role in breast cancer progression. These molecules, especially PRKCQ, may serve as potential biomarkers for early detection and prognosis, as well as targets for therapeutic intervention following further validation.

Finally, integrative analyzes demonstrated strong correlations between promoter accessibility, transcription factor occupancy, and gene expression, and uncovered cooperation between epigenetic and genetic drivers. Together, these findings reveal context-dependent functional hierarchies among HMEs and underscore the necessity of multi-layered analyses to resolve the complexity of epigenetic regulation in cancer.

Our study identifies how oncogenic KRAS/ERK signaling suppresses GATA6 to cause dedifferentiation in pancreatic cancer. Combining KRAS/ERK inhibitors with standard-of-care chemotherapies could be a promising therapeutic strategy for treating pancreatic cancers.

Facultative stem cells balance between their resting mode and regenerative mode. In the lung, alveolar type 2 (AT2) cells produce surfactants at baseline and, upon injury, activate to self-renew and differentiate into alveolar type 1 (AT1) cells. Such activation, observed in acute lung injury, fibrosis, and tumorigenesis, proceeds through a high-KRT8 transitional phase. Using multiomic profiling and mouse genetics, we identify activator protein-1 (AP-1) transcription factors as central regulators of a CLDN4⁺ transitional substate, promoting AT2 cell dispersion, fibroblast signaling, and region-specific AT1 differentiation. AP-1 activation is conserved during oncogenic transformation in both mouse and human lungs. These findings refine our understanding of AT2 cell fate transition and chromatin dynamics, and reinforce a molecular connection between alveolar repair and tumorigenesis.

In these studies, mice that had experienced chronic stress showed a decreased amount of mRNA related to a variety of non-neuronal support cells (glia) and blood vessels, and general neural activity. The mouse chronic stress signature overlapped with gene-activity patterns reported in human psychiatric conditions, suggesting a biological bridge between chronic stress and the onset of psychopathology.

This study elucidates cellular heterogeneity, the epigenetic regulatory landscape, and the key genes driving ccRCC progression. The integration of multi-omics data offers novel insights into precise diagnostic strategies and therapeutic interventions, highlighting the pivotal role of genes such as YBX3.

S1P1 contributes to the immunosuppressive phenotype of microglia. Inhibiting the S1P/S1P1 axis impairs viability and crosstalk between melanoma cells and tumor-activated microglia, offering a potential therapeutic strategy for melanoma brain metastases.

We therefore measured global chromatin accessibility across iPSC-derived cardiomyocytes derived from four healthy individuals that we treated with topoisomerase II (TOP2) inhibiting ACs, Doxorubicin, Epirubicin, and Daunorubicin, and the anthracenedione, Mitoxantrone as well as the TOP2-independent monoclonal antibody Trastuzumab, for three and 24 hours. Our results demonstrate large-scale changes in chromatin accessibility in cardiomyocytes treated with ACs, which correspond to several regions harboring AF and HF risk loci. The identified drug-responsive chromatin regions can be used to annotate variants in cancer patient populations to contribute to risk estimation for CVD.