EGR1 (Early Growth Response 1)

These data indicate that Caspase14 promotes survival, proliferation, and metabolic reprogramming in resistant MCF7 cells via the EGR1/HIF-1α pathway. Our findings reveal a mechanistic link between Caspase14 and endocrine therapy resistance and nominate Caspase14 as a therapeutic target to overcome tamoxifen resistance, with potential translational relevance.

The EGR1-ZNF768-SLC7A11 axis constitutes a critical adaptive shield limiting lenvatinib efficacy in HCC. ZNF768 serves as a predictive biomarker and a high-value therapeutic target. Disrupting this axis offers a rational strategy to overcome therapeutic resistance and maximize the clinical potential of lenvatinib.

Collectively, our findings demonstrate that CEP72 functions as a key negative regulator of inflammation-driven hepatic fibrosis. CEP72 deficiency accelerates the progression of liver fibrosis through the EGR1-TNF-α signaling pathway. This study identifies a previously unrecognized protective role of CEP72 in hepatic fibrosis and highlights its potential as a novel therapeutic target for the treatment of S. japonicum-induced and other types of inflammation-associated liver fibrosis.

Interleukin-6 receptor inhibitors (e.g., tocilizumab) show robust efficacy in GCA but with notable non-responders; the JAK inhibitor upadacitinib demonstrated efficacy in a Phase III study, whereas IL-17 blockade (secukinumab) yielded inconsistent results...Mavrilimumab (GM-CSF receptor blockade) is promising in GCA. Recent studies have increasingly focused on short-term glucocorticoid therapy in combination with biologic agents. Advances in biomarker research, including investigation of the IL-6 receptor and IL-17A gene polymorphisms, may enable more targeted therapeutic strategies.

Immune differentiation analysis showed patients with NRF2High tumors enriched with CD68 have lower survival (p = 0.038) than those with CD68Low tumors, whereas NRF2Low tumors enriched with immune-activated markers such as CD3E and CD80 exhibit a better prognosis. This study is the first that shows classification of HGSOC based on NRF2 levels, highlights new biomarkers, and suggests IHC-labeling and genomic evaluation of NRF2 and immune markers for better prognosis.

AML samples exhibited deregulated TOE1 expression versus normal hematopoietic stem/progenitor cells (HSPCs), and TOE1 depletion suppressed the proliferation of myeloid leukemia cell lines, and primary human HSPCs, partly through a p21-activated-kinase 2 (PAK2) mediated mechanism. In summary, these data reveal TOE1 as a novel regulator of hematopoietic cell proliferation via the modulation of important growth-regulating pathways.

This multimodal mechanism positions GA as a promising therapeutic candidate for NSCLC.

Ultimately, a novel conceptual framework that redefines METTL3 not merely as a static oncogene, but as a dynamic, context‑dependent regulatory hub, is proposed. Under therapeutic stress, METTL3 amplifies cellular phenotypic plasticity, systematically orchestrating tumor adaptation and treatment resistance.

Understanding EGR1's cell type-specific functions at the various levels will be helpful in understanding the normal development and in finding therapeutic targets in reproduction, cancer, and immune-related diseases. In this review, we briefly summarize the genetic anatomy with the molecular and developmental roles of EGR1.

This study demonstrates evidence for EBV particle exposure to influence microglial immune phenotypes by suppressing IFN production, providing a putative mechanism for EBV virion expression in the CNS to suppress anti-tumoral immunity against EBV+ cancers. These results are particularly relevant to the etiology of EBV+ primary CNS cancers in immunocompromised people, where microglial play a heightened role in protecting the CNS in the absence of adaptive immunity.

After eight years and treatment with lenalidomide with excellent clinical response, she developed progressive cytopenias and transformation to acute myeloid leukemia, myelodysplasia-related (AML-MR)...The patient was treated with combination azacitidine and venetoclax and an investigational immunotherapy within a clinical trial...Our findings expand the spectrum of dmin-associated oncogenic amplifications in myeloid neoplasms and highlight FLI1 and ETS1 as recurrent targets of 11q24-derived ecDNA amplification. Recognition of such rare events underscores the importance of integrative cytogenomic profiling for uncovering novel mechanisms of leukemic transformation and potential therapeutic targets.

We defined a novel ISG signature in iCCA and identified EGR1 as a critical driver of senescent tumor cells in iCCA.These findings offer new insights into senescent tumor cells and the immunosuppressive microenvironment.