Variant human breast tumor estrogen receptor with constitutive transcriptional activity
Since progesterone receptor (PgR) is normally induced by estrogen, breast cancers lacking estrogen receptor (ER) would also be expected to lack PgR. However, a small percentage of breast cancers are ER- yet PgR+. These tumors might possess an ER which is defective in estrogen binding but is still functional in stimulating estrogen-responsive genes such as PgR. We have now detected such a variant, lacking exon 5 of the hormone-binding domain, using complementary DNA amplified by the polymerase chain reaction. This variant was the predominate ER RNA expressed in three ER-/PgR+ tumors. Furthermore, the variant ER constitutively activates transcription of a normally estrogen-dependent gene construct in yeast cells. The variant ER could explain the expression of PgR in certain tumors and have therapeutic implications.
Duke Scholars
Published In
ISSN
Publication Date
Volume
Issue
Start / End Page
Related Subject Headings
- Oncology & Carcinogenesis
- 1112 Oncology and Carcinogenesis
Citation
Published In
ISSN
Publication Date
Volume
Issue
Start / End Page
Related Subject Headings
- Oncology & Carcinogenesis
- 1112 Oncology and Carcinogenesis