The likelihood of this type of response occurring by chance is extremely low. It is hoped that this report will encourage oncologists, scientists, and clinicians to further investigate the use of SPRMs in a larger cohort of patients with stage IV lung cancer, and potentially in those with less advanced disease.

PGCCs contributed to alisertib insensitivity in TNBCs that may be targeted by mifepristone.

P=N/A, N=108, Not yet recruiting, Affiliated Hospital of Nantong University; Affiliated Hospital of Nantong University

The expression levels of GR and FOXO1 or p-FOXO1 were strongly correlated in bladder cancer. Specific GR/FOXO1 and GR/p-FOXO1 expression profiles served as independent predictors of disease recurrence or progression.

In brief, our study demonstrates that stress-corticosterone axis induces exhaustion of tumor-infiltrating CD8+ T cells, contributing to accelerated progression of non-small cell lung cancer.

Monitoring of estradiol(E2) levels before the management is recommended. Risk assessment and preventive strategies, such as intermittent treatment, transvaginal ultrasound and levonorgestrel intrauterine system (LNG-IUS), should be considered.

P4, N=1900, Not yet recruiting, Ibis Reproductive Health

P3, N=1186, Recruiting, Leiden University Medical Center | Not yet recruiting --> Recruiting

P2, N=400, Recruiting, Chelsea and Westminster NHS Foundation Trust | Trial primary completion date: Oct 2025 --> Dec 2026

Fifty 8-week-old healthy male Wistar rats were divided into five groups (n=10 each) as follows: control, CS, CS+Mifepristone (CS+Mif), CS+Metyrapone (CS+Met), and Corticosterone (Cort). In this study, we investigated the molecular mechanism underlying the CS-related NAFLD. GC mediates the development of oxidative stress and inflammation in the liver, and inhibition of the GC signalling may be a new therapeutic strategy.

These findings suggest that DPT exerts its anticancer effects by disrupting the GR/TSC22D3 axis in NSCLC cells, highlighting its potential as a therapeutic agent for GR-associated cancers.

The NNK-induced increase in COX-2 expression and PGE2 production was inhibited by glucocorticoids, and this effect was antagonized by the GR antagonist, RU38486...The ROS scavenger N-acetylcysteine inhibited the NNK-induced increase in COX-2 mRNA levels and promoter activity. Furthermore, dexamethasone significantly inhibited NNK-induced cell invasion. Conclusively, the data collectively indicate that NNK-induced ROS activates the COX-2/PGE2 pathway and cell invasion in lung cancer cells. These findings elucidate the pathophysiological connection between NNK, GR, inflammatory responses, and cell metastasis.