AHR (Aryl hydrocarbon receptor)

Deep learning-derived CTBC metrics, especially VAT/SAT ratio, enhance prognostic stratification beyond TNM staging in locally advanced gastric cancer. This ratio captures a systemic and tumor-level immunometabolic phenotype marked by mitochondrial dysfunction and immune suppression. Our findings highlight VAT/SAT as a noninvasive, clinically actionable biomarker to guide personalized therapy and risk-adapted algorithm in gastric cancer management.

The expression levels of ARNTL2 and miR-204-5p in NSCLC are closely associated with patient age, tumor differentiation, and lymph node metastasis, and they have high predictive value for NSCLC-related mortality.

Using a luciferase reporter assay, we demonstrated that active series analogs exhibit AhR antagonism while inactive compounds do not. Since deletion of AhR has severe peripheral effects, chronic inhibition of AhR is not an attractive therapeutic approach for Alzheimer's disease; nevertheless, these results position AhR as a modulator of ApoE secretion and a biological pathway worth exploring.

These findings establish miR-124-3p as a key suppressor of STAD progression via AHR-mediated autophagy, underscoring its promise as both a diagnostic biomarker and a therapeutic candidate.

Pre-treatment of blasts with an AHR inhibitor (AHRi) prior to NK cell killing assay downregulated key checkpoint molecules, including HLA-E, and key IFN-g signaling transcription factors (STAT1, IRF1) and led to enhanced NK cell killing among multiple FAB subsets in AML. The data support targeting the AHR pathway as a dual tumor intrinsic and immune targeting therapeutic strategy for AML, particularly in combination with NK cellular therapy.

Moreover, our data also establish that under low cell density conditions SLC1A5, SLC3A2, and AHR expression are under β-catenin and c-MYC control. As β-catenin promotes c-MYC gene induction, the current data allow us to propose that once cell-cell interaction is lost, the release of β-catenin from its interaction with cadherin triggers AHR activation and nuclear internalization.

Peripheral blood mononuclear cells (PBMCs) from patients with PDAC and healthy donors were isolated and treated ex vivo with two AHR agonists (Carbidopa and Tapinarof) and one antagonist (BAY 2416964). Baseline AHR expression critically shapes the immune response to pharmacological modulation in PBMCs from PDAC patients. These findings suggest that AHR profiling may serve as a clinically relevant biomarker for stratifying patients and guiding personalized immunotherapy approaches for PDAC.

Immunohistochemical analysis revealed that decreased PI3K, m-TOR, β-catenin, and AhR expression, along with enhanced PTEN expression, correlated with the induction of apoptotic events. Thus, dihydromyricetin ruthenium-p-cymene complex has been proven as a strong chemotherapeutic drug by modifying PI3K/β-catenin/AhR signalling cascade inside lung cancer microenvironment, thereby causing apoptotic cell death.

Tumor cell intrinsic AhR inhibits MHC-I expression in PDAC cells by epigenetic regulation mediated by PRMT5, resulting in reduced immunogenicity of pancreatic tumor cells. The discovery of the AhR-PRMT5-H4R3me2s-MHC-I axis provides critical mechanistic insights into how tumor-intrinsic epigenetic regulation of antigen presentation promotes the progression of PDAC.

Importantly, the combination of anti-PD1 and compound 7k enhanced antitumor immunity by augmenting cytotoxic T lymphocyte (CTL)-mediated activity. Collectively, a new pyrazolopyrimidine derivative, 7k, shows promise as a potential therapeutic agent for treating colorectal cancer.

Thus, our data indicate that AhR activation in APC might be required for UV-B-mediated immunosuppression during MOG-induced EAE. Hence, activation of AHR in tissue-resident APC, potentially by low-dose UV-B irradiation, might be beneficial as an adjuvant treatment in inflammatory or degenerative diseases of the central nervous system.

Our finding show that benzene could contribute to hematopoietic effects developed in highly exposed children. These results highlight the necessity of implementing environmental policies aim at reducing benzene exposure in children.