tamoxifen

P3, N=1156, Suspended, Alliance for Clinical Trials in Oncology | Recruiting --> Suspended

We report an extremely rare case of MCNS relapse triggered by ST combination therapy.A 55-year-old woman with a history of breast cancer treated with tamoxifen developed nephrotic syndrome and was diagnosed with MCNS by renal biopsy...Discontinuation of ST, atorvastatin, and esomeprazole while continuing prednisolone 40 mg/day led to a second remission. Drug-induced lymphocyte stimulation tests for all agents were negative, possibly due to concurrent corticosteroid therapy.Metabolites of sulfamethoxazole have been shown to activate CD4+ T cells and induce multiple cytokines including interleukin-13, interferon-γ, interleukin-22, and granzyme B. Such immune activation could explain the simultaneous occurrence of cutaneous manifestations (drug eruption) and renal relapse (MCNS).Relapse of drug-induced MCNS may occur through either direct podocyte injury or immune-mediated allergic mechanisms. Given the concurrent drug eruption, the latter mechanism appears most consistent with this case.When introducing new medications under immunosuppressive conditions, clinicians should consider the possibility of drug-induced relapse if proteinuria reappears.

Drug sensitivity analysis showed that the DSN1 high expression group was resistant to drugs such as Epirubicin, Cyclophosphamide, Ribociclib, and Palbociclib, but relatively sensitive to tamoxifen and lapatinib. DSN1 contributes to breast cancer progression by modulating cell cycle pathways, making it a potential diagnostic and therapeutic target with clinical applicability.

P3, N=1670, Recruiting, NRG Oncology | Trial primary completion date: Jan 2026 --> Apr 2026

Our findings suggest efficacy of PI3K inhibition + tamoxifen beyond second-line treatment and after prior targeted therapies, including CDK4/6 inhibition in metastatic HR+/HER2- breast cancer although the magnitude of benefit did not outweigh the tolerability of this combination. Exploratory biomarker analysis indicates that tumor fraction determined in ctDNA differentiates patients based on prognosis and may help to optimize patient selection for targeted treatment strategies.

We successfully established a spontaneous GAC model and its corresponding cell line in C57BL/6J mice, enabling a comprehensive investigation of tumor progression, metastasis, therapeutic response, and resistance mechanisms in vivo. This model represents a valuable platform for advancing precision medicine in gastric cancer.

P=N/A, N=500, Not yet recruiting, Ente Ospedaliero Ospedali Galliera | Initiation date: Oct 2025 --> Jun 2026

Among the most studied SERMs are Tamoxifen and Raloxifene. The pharmacological profile of SERMs therefore reflects a delicate equilibrium between receptor-mediated vascular protection and thrombotic liability. Indeed, their raison d'être increasingly extends beyond oncology into cardiovascular endocrine pharmacology, where they serve as prototypes for designing next-generation agents with optimized receptor selectivity and safer vascular outcomes.

Drug sensitivity analyses suggested that high-risk GBM may respond better to paclitaxel and tamoxifen. Random Forest modeling and in vitro experiments identified GJB2 as an oncogenic driver that promotes GBM cell proliferation and migration. Our findings provide a clinically applicable EMT-based prognostic framework that links transcriptional plasticity to patient outcomes in GBM and identify GJB2 as a promising therapeutic target.

Our results may establish evidence supporting the omission of adjuvant chemotherapy in premenopausal women with low genomic risk scores and limited nodal involvement (p-N1), potentially reducing treatment-related morbidity while preserving comparable oncologic outcomes.

P3, N=8000, Active, not recruiting, Eli Lilly and Company | Recruiting --> Active, not recruiting

In vitro functional assays demonstrated that either DHCR7 knockdown or treatment with the targeted inhibitor tamoxifen significantly suppressed AML cell proliferation...Mechanistic investigations further revealed that DHCR7 exerts pro-leukaemic effects through activation of the IL-6/JAK2/STAT3 signalling axis. Collectively, this study establishes the novel function of DHCR7 in AML pathogenesis and provides robust evidence supporting its potential as a therapeutic target for AML.