DNA Damage Responses in Tumors Are Not Proliferative Stimuli, but Rather They Are DNA Repair Actions Requiring Supportive Medical Care
Abstract
:Simple Summary
Abstract
1. Introduction
2. Endocrine Disruptor Synthetic Estrogens Increase the Risk for Certain Cancers and Cardiovascular Complications
2.1. Controversial Correlations between Menopausal Hormone Therapy (MHT) and Women’s Health
2.2. Oral Contraceptives Are Endocrine Disruptors Inducing either Increased or Decreased Cancer Risk in Different Organs
3. In BRCA Gene Mutation Carriers, the Defect of Liganded ER Activation Is the Initiator of DNA Damage and Cancer Development
Both Healthy Cells and Tumor Cells with BRCA Mutation Show Compensatory Molecular Changes, Improving Genomic Stability
4. Estrogens Are the Principal Regulators of Genomic Machinery in Mammalian Cells
5. Estrogens Are Master Regulators of Metabolism and Energy Homeostasis via Orchestrating Adipose Tissue Functions
Secretory Activities of Visceral Adipose Tissue in Healthy Lean and Obese Cases
6. The Tumor Cell Itself Is the Frontline of Anticancer Combat
7. Peritumoral Microenvironment: The Second Line of the Antitumor Battle
8. Molecular Changes in Tumors Responsive and Non-Responsive to Endocrine Therapy
8.1. Successful Fight of Anti-estrogen Responsive Tumors against the Endocrine Disruptor Treatment
8.2. Unsuccessful Fight of Tumors Non Responsive to Endocrine Disruptor Treatment
9. Estrogen Induced Apoptosis Is Promising in Both the Prevention and Therapy of Cancer
10. Conclusions
Funding
Conflicts of Interest
References
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Subtype of Breast Cancer | Receptor Status | Signs of DNA Damage | Sigs of DNA Repair | Proliferative Activity Endocrine | Response to Therapy |
---|---|---|---|---|---|
Luminal A type | ER overexpression | no | ER overexpression | low | good in 50% |
(50–60%) | PR positive | ||||
Luminal B type | ER positive | PR negative | ER positive | increased | moderate/inverse |
(10%) | PR pos/neg | PR positive | |||
HER2 pos/neg | HER2 positive | ||||
HER2 enriched | ER negative | ER negative | HER2 rich | high | no |
(20%) | PR negative | PR negative | |||
HER2 rich | |||||
Triple negative | ER negative | ER negative | no | high | no |
(10%) | PR negative | PR negative | |||
HER2 negative | HER2 negative |
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Suba, Z. DNA Damage Responses in Tumors Are Not Proliferative Stimuli, but Rather They Are DNA Repair Actions Requiring Supportive Medical Care. Cancers 2024, 16, 1573. https://doi.org/10.3390/cancers16081573
Suba Z. DNA Damage Responses in Tumors Are Not Proliferative Stimuli, but Rather They Are DNA Repair Actions Requiring Supportive Medical Care. Cancers. 2024; 16(8):1573. https://doi.org/10.3390/cancers16081573
Chicago/Turabian StyleSuba, Zsuzsanna. 2024. "DNA Damage Responses in Tumors Are Not Proliferative Stimuli, but Rather They Are DNA Repair Actions Requiring Supportive Medical Care" Cancers 16, no. 8: 1573. https://doi.org/10.3390/cancers16081573