tamoxifen

P3, N=984, Active, not recruiting, Astellas Pharma Global Development, Inc. | Recruiting --> Active, not recruiting | N=540 --> 984 | Trial completion date: Jun 2027 --> Apr 2028

These findings establish a mechanistic link between hormonal signaling, p53 allelic status, and m6A-dependent post-transcriptional regulation. Although further in vivo validation is required, disruption of the ALKBH5-REG1A axis may contribute to heterogeneous endometrial responses to tamoxifen, thereby providing a conceptual framework for biomarker-oriented investigation.

Pak1 has been reported to be mechanistically contributing to drug resistance to tamoxifen and gemcitabine. The study analysis revealed that mutated Pak1 and more than one kinase were likely to be involved in drug resistance in patients associated with poor prognosis. The study concluded that the detection of altered kinases in resistant tumors is imperative, and a combination of kinase inhibitors could be useful for treatment rather than single agents to improve treatment outcomes.

P2, N=393, Active, not recruiting, Dana-Farber Cancer Institute | Recruiting --> Active, not recruiting | Trial primary completion date: Sep 2026 --> Mar 2026

P3, N=1100, Not yet recruiting, Karolinska Institutet

P3, N=230, Recruiting, Hoffmann-La Roche | Trial primary completion date: Sep 2026 --> Dec 2026

P2, N=140, Not yet recruiting, Dana-Farber Cancer Institute

Hot flashes were frequent, affecting 33% of patients, but showed no clear pharmacogenetic associations. This study demonstrates that pharmacogenetic variation is associated with interindividual differences in treatment-related side effects, underscoring the need to expand research in African populations to better inform precision endocrine therapy.

The pro-migratory effects of PFIs on MCF-7 cells were abolished by an ERα antagonist of 4-hydroxytamoxifen, indicating the substantial role of ERα signaling in cancer cell progression...Although PFI-induced RARα antagonism alone had no effects on the migration of MDA-RARα cells, it did recover that compromised by atRA. This study provides new evidence on the promotion effects of PFIs on breast cancer cells, and reveals the multi-nuclear receptor-regulated mechanisms for understanding intricate toxicological effects of emerging pollutants.

To investigate the mechanisms leading to valve loss, we combined the lymphatic-specific and tamoxifen-inducible Flt4CreERT2 with Kras-loxP-stop-loxP-G12D (Kras+/G12D) mice and Prox1GFP reporter mice to induce the restricted expression of KRAS-G12D and enable valve quantification in postnatal pups...We conclude that hyperactive KRAS signaling upregulates MMPs that become excessively activated by the upregulation of the PA pathway. MMPs then degrade the lymphatic valve ECM core, preventing valve formation.

Adjuvant treatment included combination chemotherapy, radiotherapy, and dual hormonal therapy with tamoxifen and an AR inhibitor. This case highlights the diagnostic and therapeutic challenges of hormone receptor-positive AC and underscores the importance of comprehensive immunohistochemical profiling for individualized management.