What is it about?
A paradigm shift is suggested on estrogen's role in the breast cancer treatment. In tumors, estrogen signal rectifies genomic stability and at the same time activates the immune competent cells. Overexpression of estrogen receptors in breast cancer suggests asking for estrogen in the estrogen deficient milieu. Loss of estrogen receptors in breast cancer show the serious defect of estrogen signaling. In breast cancer, the overexpression of HER2 receptors shows the effort for unliganded activation of estrogen receptors helping genomic stability and apoptosis. Therapeutic estrogen treatment or activation of ER expression in breast cancer cases achieves excellent tumor regression.
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Why is it important?
There is no total chaos in the genome of breast cancer cells, but rather, the mixture of errors and compensatory activations may be observed inthe genomic processes. The differences between post- or pre-menopausal breast cancer treatment, the use of ER-targeted drugs, the ER resistance, the estrogen deficiency and the genome instability are discussed. Estrogen is an ideal medicament for breast cancer as activates the function of all healthy cells, while facilitates the self directed death of tumor cells.
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This page is a summary of: Estrogen Regulated Genes Compel Apoptosis in Breast Cancer Cells, Whilst Stimulate Antitumor Activity in Peritumoral Immune Cells in a Janus-Faced Manner, July 2024, MDPI AG,
DOI: 10.20944/preprints202407.1905.v1.
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