Adrenal Cortex Carcinoma

ENPP3 is a novel target for CAR T-cell therapy in ACC. ENPP3 CAR T cells, when combined with CD206 modulation to overcome immune suppression within the TME, have therapeutic efficacy in ACC by mediating robust tumor growth suppression. This combinatorial strategy, which includes CAR T cells alongside therapies that recalibrate immunosuppressive CD206+ TAMs, may be a novel approach for improved immunotherapy of solid cancers beyond ACC.

Steroidogenesis assays employing the adrenocortical carcinoma cell line H295R demonstrated that TPPU and several other urea-type sEH inhibitors induce dose-dependent suppression of multiple steroid hormones without cytotoxicity, whereas the amide-based GSK2256294A had no effect on steroid production or cell survival...Collectively, these findings reveal that urea-based sEH inhibitors suppress adrenal steroidogenesis via scaffold-dependent, off-target mechanisms independent of sEH. In addition, it suggests that sEH is not involved directly in steroid metabolism.

High-risk patients showed increased sensitivity to chemotherapeutic agents including Gallibiscoquinazole, Cisplatin, Axitinib, and Zoledronate. The anoikis-based risk model may serve as a useful prognostic tool for ACC. ARGs may contribute to ACC progression and are associated with immune microenvironment features, providing a potential basis for further mechanistic and translational studies.

Hyperandrogenemia stands on a dual source (potential CEL-driven insulin resistance for the ovary and OACC-originating for the adrenal glands). Also, this is the first case to receive OSP in OACC, noting that a tailored multidisciplinary management is mandatory.

This case supports the existence of a shared pathogenic mechanism linking PPGLs and GCTBs, likely mediated by postzygotic H3F3A mutations. Recognition of this association is crucial for early diagnosis, genetic counseling, and management of similar cases.

Given the presence of distant metastases, the patient was commenced on neoadjuvant chemotherapy and mitotane. Genetic testing for TP53 to evaluate Li-Fraumeni syndrome was declined. Despite initial response to the treatment, the disease remained refractory, and the patient succumbed after seven months of therapy.

Despite the complex organogenesis and limb-like morphology, the absence of a vertebral column or ossified long bones supported a diagnosis of mature cystic teratoma with fetiform features (FT) over FIF. This report highlights the diagnostic ambiguity within the "gray zone" of these lesions and emphasizes the role of axial skeletal organization and serum AFP levels as complementary tools for classification and oncologic surveillance.

According to the pharmacogenomic analysis from GDSC2 dataset, tumor cells that express higher DNA2 are more sensitive to Tozasertib, and Daporinad. DNA2 is at the core of several interrelated modules, including flap processing, telomerase extension, and cell-cycle progression, according to the enrichment study. These findings have suggested DNA2 as a therapeutic vulnerability in cancer, a context-dependent biomarker with implications for treatment response, prognosis, and immunity.

In conclusion, this study provides a comprehensive pan-cancer characterization of CHRNA7, offering novel insights into its potential role as a prognostic biomarker and immunotherapeutic target. These findings could facilitate the development of personalized cancer treatment strategies customized according to the expression level and functional status of CHRNA7.

Immunohistochemistry demonstrated diffuse Melan-A positivity and chromogranin A negativity, with synaptophysin immunoreactivity in corresponding tumor regions on serial sections, supporting adrenocortical origin with partial neuroendocrine differentiation. Postoperatively, urinary catecholamine metabolite concentrations normalized, and serial blood pressure monitoring at approximately monthly re-evaluations documented no recurrence of systemic hypertension without antihypertensive therapy over an 11-month postoperative follow-up period, supporting the adrenal cortical tumor as the source of the preoperative biochemical and hemodynamic abnormalities.

We go on to review the biology and clinical phenotypes of TP53 hypomorphic variants that have detailed reports of their effects on p53 tumor suppressive functions. Using this framework, we propose possible modifications to the standard LFS screening protocol for individuals with hypomorphic TP53 variants that should be studied in prospective clinical trials.

Pathway analysis in patients with high MKI67 expression revealed an enrichment of genes associated with cell cycle regulation and p53 signaling, suggesting a potential link between high proliferative activity and these molecular pathways. In conclusion, this study provides valuable insights into the clinical and pathological profiles of ACC in the Chinese population, facilitating better diagnostic approaches.