Adrenal Cortex Carcinoma

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.

These molecular insights have direct clinical implications, enabling refined disease classification, improved prognostic stratification, and the identification of actionable therapeutic targets, including EGFR, MAPK, PKA, and glucocorticoid receptor-associated pathways. Collectively, the integration of multi-omics approaches is redefining the conceptual framework of Cushing's syndrome and paving the way toward precision medicine strategies in endocrine oncology.

A punctate LC3B expression accumulation, associated with less aggressive malignant features, namely absence of metastasis, appears to result from a blockade at the late stages of autophagy. Whereas active autophagy may be associated with a more aggressive cellular phenotype in ACC, particularly by promoting migration and invasion.

P2, N=798, Active, not recruiting, National Cancer Institute (NCI) | Trial primary completion date: May 2027 --> May 2026

Histopathological examination confirmed a differentiating NB. The postoperative course was uneventful.

Markers of pluripotency and self-renewal of embryonic stem cells are expressed until mid-pregnancy, contributing to the adult adrenal stem cell niche. They are absent postnatally but are expressed in a subset of ACT. Specifically, pS45P beta-catenin-mutated ACTs express more NANOG. Increased OCT4 expression in pACT is associated with worse prognosis, and inhibiting the Wnt/beta-catenin pathway in these cells impairs NANOG expression.

We present the first case of a TP53 mutation from non-carrier parents affecting both mother and child to date. We describe the pathogenic variant and the possible mechanism underlying the co-occurrence of the proband's LFS and her mother's gestational choriocarcinoma.

This is the second report of ACC associated PJS in a rare germline variant of STK11. Although rare, loss of STK11 function may lead to cancers outside expected sites in PJS cases.