IRF7 (Interferon Regulatory Factor 7)

Combining CTX with the next generation MERTK-selective inhibitor UNC2371 (MRX-2843) drives complete remissions in both models, but durable long-term responses occurred selectively in the basal-like subtype model. Suppressive myeloid programing limits effective adaptive immune engagement in TNBC usually resulting in ICB treatment resistance and tumor recurrence. This study identifies a therapeutically actionable myeloid interferon checkpoint in which MERTK inhibition stabilizes CXCL9⁺ monocyte-macrophage programming to promote CD4⁺ T cell dependent immune memory and durable tumor control in basal-like TNBC.

In vivo, co‑treatment enhanced IFN‑β induction, increased CD8⁺ T‑cell infiltration and reduced tumor burden relative to monotherapies, whereas efficacy was not observed in athymic nude mice, supporting T‑cell dependence. Together, these data provide preclinical evidence that a rational oncolytic virus and STING combination can amplify antitumor immunity without overtly compromising viral persistence.

We propose that lidocaine can be repurposed as an immunomodulator for treating immune-mediated inflammatory diseases. However, future research should define optimal dosing strategies, validate its mechanisms of action in clinical trials, and explore its novel clinical applications as a complementary immunotherapy.

Collectively, our work unveiled a novel strategy whereby LMWF, as a TLR7 agonist, synergizes with ICB therapy to overcome ICB resistance. These findings provide critical insights for overcoming the bottleneck of ICB refractoriness in cancer immunotherapy.

Recognizing the risk for first-degree relatives may potentially increase awareness of early symptoms among family members of HL patients, leading to earlier diagnosis and better outcomes. Conversely, understanding that the hereditary risk, though higher than in the general population, remains relatively low may provide reassurance for affected families.

IRF7 is a novel prognostic biomarker in KIRC, influencing tumor immunity and therapy response. Its integration into clinical nomograms could guide precision immunotherapy strategies.

Our study suggests that NOS1 expression in melanoma characterizes IFN-I signal disorders in response to innate immune stimulation through IRF7 s-nitrosylation. Targeting NOS1 signaling might be beneficial for overcoming immune therapeutically resistance, particularly in immune-cold melanoma phenotype.

Interferon regulatory factor 7 (IRF7), a central transcription factor in interferon signaling, contributes to gemcitabine (GEM) resistance in pancreatic ductal adenocarcinoma (PDAC). Temozolomide (TMZ) suppressed IRF7 transcriptional activity and, when combined with GEM, synergistically reduced tumor progression. These findings define IRF7 as a key regulator of chemotherapy response in PDAC and highlight the therapeutic potential of targeting the IRF7-CCL5 axis using TMZ to enhance GEM efficacy.

Furthermore, non-viral microorganisms such as Helicobacter pylori CagA and aflatoxin A also participate in carcinogenesis by regulating the UPS/SUMO system. In summary, targeted modulation of the UPS/SUMO system constitutes a core oncogenic strategy for carcinogenic microorganisms (particularly viruses), providing molecular targets for precision cancer therapy.

Collectively, our findings unveiled that YTHDF3-mediated upregulation of STAT3 suppresses the type I ISG expression, thus promoting HPV carcinogenesis and establishing an ITME. Taken together, our results suggest that targeting the YTHDF3/STAT3/IRF7 axis could be a promising therapeutic strategy against HPV-associated malignancies.

The results of analysis viral genes mRNA expression suggested potential role of viral genes during BKV pathogenesis. The results of this limited study showed that at the mRNA level, certain genes of the immune system can be altered and that BKV reactivation has the potential to affect these genes.

Hypoxia-induced ADAR1 deficiency upregulates NOCT expression to induce PAEC interferon signaling activation, PAEC apoptosis, and PH. This study provides impetus to target the ADAR1-NOCT axis for more effective diagnostics and therapeutics for PH.