Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/ijms22020756
Keywords
estrogen receptor; breast cancer; endocrine resistance; mutation; receptor folding
Funding
- MENRT scholarships from the French Minister of High Education, Research and Innovation
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Breast cancer is the most common cancer among women worldwide. While most ER-positive breast cancer cases initially respond to antiestrogen therapies, a high percentage develop resistance over time. Research on mutated forms of ER alpha has led to potential developments in new antiestrogen treatments.
Breast cancer (BC) is the most common cancer among women worldwide. More than 70% of BC cases express estrogen receptor alpha (ER alpha), a central transcription factor that stimulates the proliferation of breast cancer cells, usually in the presence of estrogen. While most cases of ER-positive BC initially respond to antiestrogen therapies, a high percentage of cases develop resistance to treatment over time. The recent discovery of mutated forms of ER alpha that result in constitutively active forms of the receptor in the metastatic-resistance stage of BC has provided a strong rationale for the development of new antiestrogens. These molecules targeting clinically relevant ER alpha mutants and a combination with other pharmacological inhibitors of specific pathways may constitute alternative treatments to improve clinical practice in the fight against metastatic-resistant ER-positive BC. In this review, we summarize the latest advances regarding the particular involvement of point mutations of ER alpha in endocrine resistance. We also discuss the involvement of synonymous ER alpha mutations with respect to co-translational folding of the receptor and ribosome biogenesis in breast carcinogenesis.
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