CHGA (Chromogranin A)

Since cases of early-stage gallbladder NETs are rare, their clinical behavior and long-term prognosis remain poorly understood. This case underscores the need for continued case accumulation and careful postoperative follow-up to establish appropriate management strategies for this rare entity.

P2, N=45, Active, not recruiting, University of Michigan Rogel Cancer Center | Trial completion date: Dec 2025 --> Apr 2026

P1, N=28, Active, not recruiting, Novartis Pharmaceuticals | Recruiting --> Active, not recruiting

This case illustrates a particularly rare and aggressive presentation of ovarian YST in a postmenopausal patient. Early recognition, accurate pathological characterization, and individualized treatment are essential, although prognosis remains poor in this setting. Reporting such cases is crucial to improve understanding and management of these exceptional tumors.

Following enzalutamide (ENZ) treatment, GSTA1 expression is inhibited...TNFRSF13B induces c-Fos expression, forming a transcriptional complex with c-Jun, thereby regulating chromogranin A (CHGA) and promoting the neuroendocrine phenotype. Our study suggested that GSTA1 deficiency leads to elevated ROS levels and activation of TNFRSF13B and c-FOS, which subsequently transcriptionally regulate CHGA and ultimately drive neuroendocrine differentiation in PCa.

These results demonstrate that LCNEC-P represents a distinct subgroup of LCNEC that is characterized by a specific morphological, immunohistochemical, and genetic profile, closely resembling SCLC-P. This study provides insights into the biology of LCNEC-P and supports its classification as a unique entity within LCNEC.

P2, N=30, Recruiting, National Cancer Institute (NCI) | Trial completion date: Nov 2025 --> Nov 2026 | Trial primary completion date: Nov 2025 --> Nov 2026

INSM1 overexpression in SH-SY-5Y cells upregulated neuroendocrine and thyroid hormone-related genes (CHGA, CHGB, DDC, NCAM1, DIO3, TH), while suppressing genes involved in cell cycle (RRM, CDC25A), methionine metabolism (AHCY, MAT2A), transcriptional regulation (MYBL2, EZH2), and oncogenic signaling (ALK, LINC011667). These findings suggest that INSM1 promotes NB aggressiveness by sustaining a neuroendocrine progenitor-like phenotype through metabolic-epigenetic coupling.

Treatment with second-generation androgen receptor (AR) inhibitors, such as enzalutamide, can trigger lineage plasticity, promoting the transdifferentiation of PCa cells into an AR-independent, poorly differentiated neuroendocrine phenotype (NEPC)...Conclusions. These findings establish HOC as a multifaceted therapeutic entity capable of disrupting key NEPC oncogenic networks, highlighting its potential as a novel lead intervention for aggressive NEPC.

Definitive diagnosis relies on pathology and immunohistochemistry. Surgical resection remains the primary treatment, and the prognosis is generally favorable.

Multivariate COX regression analysis demonstrated that DLGAP1 was an independent prognostic factor for PAAD. Six hub genes might exert an influence on the initial lymphatic metastasis of PAAD through immune cell infiltration and ferroptosis.

Long-term surveillance is warranted in view of the potential for metastasis. This case underscores the importance of including rare neuroendocrine tumors in the differential diagnoses for atypical abdominal presentations.