What is it about?

Antiestrogen compounds were developed against breast cancer based on the erroneous concept that increased estrogen signaling is a promoter of DNA-damage and tumor growth. However, estrogen signal is the chief regulator of genomic machinery and its blockade is a serious medical mistake.

Featured Image

Why is it important?

Whatever type of available endocrine therapies may be used, including estrogen, antiestrogen treatment or oophorectomy, an extreme upregulation of estrogen signaling may lead to successful prevention and treatment for breast cancer. De novo or acquired "antiestrogen resistance" of tumors may be attributed to the defective or later exhausted genetic capacity of patients for the extreme upregulation of estrogen receptor expression and aromatase synthesis.

Perspectives

Upregulation of estrogen signaling displays a unique dichotomy, ensuring the survival and safe proliferative activity of privileged healthy cells, whilst inducing apoptotic death of malignant tumor cells. Estrogens provide the physiologic surveillance of genome stability and estrogen withdrawal from either healthy or ill patients is a major medical mistake.

professor Zsuzsanna Suba
National Institute of Oncology Budapest

Read the Original

This page is a summary of: The pitfall of the transient, inconsistent anticancer capacity of antiestrogens and the mechanism of apparent antiestrogen resistance, Drug Design Development and Therapy, August 2015, Dove Medical Press, DOI: 10.2147/dddt.s89536.
You can read the full text:

Read
Open access logo

Contributors

The following have contributed to this page