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36,55-57 While not all have been studied specifically in CLE, and some have had mixed results, their mechanisms target relevant inflammatory pathways

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EstrogenER interactions at estrogen response elements (EREs) enhance the transcription of oncogenic targets such as Cyclin D1, MYC, BCL-2, and VEGF, collectively reinforcing proliferative signaling, apoptosis resistance, and angiogenic potential

nonetheless, critical avenues for future investigation include the advancement of precise therapeutics, the mitigation of resistance, the comprehension of tumour heterogeneity, and the reduction of systemic toxicity [241]