ER (Estrogen receptor)

P3, N=541, Active, not recruiting, DualityBio Inc. | Recruiting --> Active, not recruiting

P2, N=68, Active, not recruiting, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins | Trial completion date: Feb 2026 --> Feb 2027

P=N/A, N=350, Suspended, City of Hope Medical Center | Initiation date: Jan 2026 --> May 2026

The patient therefore underwent adjuvant carboplatin/paclitaxel chemotherapy followed by vaginal brachytherapy and has remained recurrence-free for five years. This case demonstrates molecular classification of an unusual histological type of EC exhibiting an extremely short-term risk of early distant metastasis and its implication on aggressive adjuvant therapeutical approach. It, furthermore, exemplifies the pronounced heterogeneity of the NSMP subgroup.

P3, N=5018, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Oct 2032 --> Jan 2027

P=N/A, N=200, Completed, University College Cork | Active, not recruiting --> Completed | Trial completion date: Dec 2025 --> Mar 2026

P=N/A, N=30, Recruiting, University College Cork | Trial completion date: Feb 2027 --> Nov 2027

P2, N=95, Recruiting, Andrea DeCensi | N=70 --> 95

While its known α1A-AR antagonism may contribute to its effects, silodosin could also act as an ER ligand, modulating estrogen-driven pathways essential in breast cancer development. This study provides the first experimental and computational evidence supporting the repurposing of silodosin as a potential multi-targeted therapeutic agent for breast cancer, opening promising new opportunities for patients with limited treatment options and encouraging further preclinical and clinical studies.

For stage Ⅲ and above mismatch repair-deficient (MMRd) endometrial cancer, postoperative paclitaxel plus carboplatin chemotherapy combined with ICIs and maintenance therapy are recommended. Many issues remain to be resolved, such as whether MMRd endometrial cancer caused by MLH-1 methylation or mutations in MMR-encoding genes has consistent responses to ICIs, and how to predict treatment efficacy. The reduced cost and rapid popularization of high-throughput technologies, as well as the continuous expansion and improvement of evidence from prospective cohorts, will provide high-quality evidence for further refinement of molecular characteristics and risk stratification of endometrial cancer, and guide the implementation of precision treatment for this disease.

The study suggests that DOTP may exhibit carcinogenic potential by interfering with cell proliferation, gene transcription regulation, the tumor microenvironment, and related carcinogenic signaling pathways (primarily the PI3K-Akt-mTOR pathway). This study reveals the molecular mechanisms of DOTP in the occurrence and development of common tumors, providing a new theoretical framework for studying the carcinogenic mechanisms of environmental pollutants and laying the foundation for targeted prevention.