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Mechanisms of hormone resistance in breast cancer
1Dept. of Medicine, University of Colorado Health Sciences Center, Denver 80262.
Abstract:
At least half of all advanced breast cancers are positive for estrogen receptor (ER) and progesterone receptor (PR), but many nevertheless fail to respond to endocrine therapy. Studies of breast cancer cell lines and breast tumor specimens are beginning to reveal molecular heterogeneity of the receptors in subpopulations of these cells, leading to altered receptor function and sometimes to hormone resistance. Here we will review the data on molecular and cellular heterogeneity involving ER and PR, and possible underlying mechanisms of resistance to tamoxifen and progestins.
Insights
Many advanced breast cancers with estrogen receptor (ER) and progesterone receptor (PR) positivity resist endocrine therapy. This review explores the molecular and cellular heterogeneity of ER and PR, contributing to hormone resistance mechanisms.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Estrogen receptor (ER) and progesterone receptor (PR) positivity is common in advanced breast cancer.
- A significant proportion of these ER/PR-positive cancers do not respond to endocrine therapy.
- This lack of response suggests underlying complexities beyond simple receptor status.
Purpose of the Study:
- To review current data on the molecular and cellular heterogeneity of ER and PR in breast cancer.
- To explore how this heterogeneity influences receptor function and endocrine therapy response.
- To discuss potential mechanisms driving resistance to tamoxifen and progestins.
Main Methods:
- Review of existing literature on breast cancer cell lines and tumor specimens.
- Analysis of studies investigating molecular and cellular heterogeneity of ER and PR.
- Examination of data linking receptor heterogeneity to hormone resistance.
Main Results:
- Evidence suggests molecular and cellular heterogeneity within ER and PR populations in breast cancer.
- This heterogeneity can lead to altered receptor function.
- Altered receptor function is implicated in the development of resistance to endocrine treatments.
Conclusions:
- Molecular heterogeneity of ER and PR is a key factor in endocrine therapy resistance.
- Understanding these heterogeneous mechanisms is crucial for developing more effective breast cancer treatments.
- Further research into tamoxifen and progestin resistance mechanisms is warranted.