What is it about?
In women, estrogen predominance seems to be protective against DNA damage and development of tumors as compared with men. Failure of high dose synthetic estrogen and antiestrogen treatment of breast cancer revealed that endocrine disruption is not an effective means to defeat breast cancer. Clarifying the role of estrogen signal in genomic stability and human health seemes to be a great progress in cancer therapy. Cancers gain genomic plasticity under natural estrogen treatment promoting their own DNA repair, apoptotic death and survival of patients
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Why is it important?
Antiestrogens block the liganded actvation, while synthetic estrogens block the unliganded activation of ERs. Endogenous estrogens induce balanced ER activation via both pathways, which is the key to genomic stability. Recognition of the molecular mechanisms of estrogen receptor deregulation via synthetic estrogen and antiestrogen treatment, helped to reveal the omnipotent curing capacity of endogenous estrogens via balanced liganded and unliganded activation of estrgen receptors. Synthetic estrogens and antiestrogens are endocrine disruptors causing genomic damage, while endogenous estrogens have DNA repairing capacities motivating activation in healthy cells and apoptosis in tumor cells.
Perspectives
Recognition of the principal gene regulative and gene editing capacities of endogenous estrogens may thoroughly repurpose the genomic and proteomic therapy of cancer and all human diseases. In the emergency states of genomic damage, liganded ER activation is capable of beneficial mutagenesis even in tumor cells facilitating their apoptotic death. In tumors, estrogen regulated genes drive apoptotic death, while activate immune competent cells in the peritumoral region.
professor Zsuzsanna Suba
National Institute of Oncology Budapest
Read the Original
This page is a summary of: Rosetta Stone for Cancer Cure: Comparison of the Anticancer Capacity of Endogenous Estrogens, Synthetic Estrogens and Antiestrogens, Oncology Reviews, April 2023, Frontiers,
DOI: 10.3389/or.2023.10708.
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