CACNA1H (Calcium Voltage-Gated Channel Subunit Alpha1 H)

Ion channels and ecDNA are central to the disease progression and treatment resistance of PCa through regulation of EMT, CSC phenotype, and tumor microenvironment (TME) interactions. Targeting the drivers-through ion channel modulators, ferroptosis induction, and ecDNA-targeting interventions (BET/HDAC inhibitors, CRISPR-based methods) offers a promising way to overcome resistance. Integration of multi-omics, and combination treatments will be key to construct precision medicine strategies and improve clinical outcomes in advanced PCa.

We confirmed the predominance of known somatic drivers and identified a uniquely high frequency of ATP2B3 variants, refining their clinical phenotype. These findings underscore the influence of population-specific genetic backgrounds and expand the global understanding of PA genetics.

These findings do not currently support widespread germline testing in routine clinical management of adrenal incidentalomas. Nevertheless, the detection of potentially pathogenic variants may inform future studies exploring their possible role in adrenal tumorigenesis.

This is the first report showing in vitro antitumor activity, disruption of the mitotic spindle, activation of the Mitotic Roles of Polo-like kinase pathway in GB. This is also the first report showing feasibility and clinical activity in patients with brain tumor.

The influence of MLA on F1 Macro and Accuracy was not statistically significant. Altogether, the genetic biomarkers identified in this study hold potential for use in biosensors aimed at breast cancer diagnosis and treatment.

CACNA1H, KCNJ11, and S100B are potential diagnostic and prognostic biomarkers in TNBC. Their immune-related functions highlight their potential for guiding targeted immunotherapy strategies.

Lastly, peripheral glucocorticoid and mineralocorticoid pathway disorders due to germline mutations in HSD-11B2, codifying the enzyme 11β-dehydrogenase type 2, NR3C1 and NR3C2 genes codifying the nuclear receptor subfamily 3 group C members 1 and 2 may also be responsible. A systematic diagnostic approach based on published guidelines is still lacking, and diagnostic suspicions with referral for gene sequencing need to be identified. This review discusses the known causes of endocrine hypertension in children and adolescents, with an emphasis on prevalence, clinical presentation, genetic predisposition and therapeutic strategies.

In summary, we characterized the genomic landscape of MM in diverse Chinese populations, confirmed clonal evolution, and identified prognostic genes.

Mutation profiles and pathway enrichment were analyzed, providing insights into potential therapeutic targets. A PANoptosis-related prognostic model was successfully developed for triple-negative breast cancer, offering a novel approach for predicting patient prognosis and guiding treatment strategies.

The rescue experiment revealed that CACNA1H overexpression in drug-resistant OCCC cells reduced autophagy-induced DDP resistance via CaMKII/Akt signaling. Overall, CACNA1H increased intracellular Ca2+ concentration and activated CaMKII/Akt signaling pathway in OCCC, thereby repressing autophagy to maintain the sensitivity of OCCC cells to DDP.

Expression of rCacna1h in PC12 cells induced differential protein expression profiles determined by mass spectrometry as well as a shift in the membrane potential where maximum calcium currents were observed as determined by electrophysiology. The findings suggest the involvement of CACNA1H/CaV3.2 in pheochromocytoma development and establish a potential link between the aetiology of adrenomedullary and adrenocortical tumor development.

Patients in the low-risk group performed better on immunological and chemotherapeutic therapies and had lower TIDE scores. In conclusion, the DGRG model we developed has significant clinical application potential because it can accurately predict the prognosis of BC, TME, and pharmacological treatment responses.