An exon 5 deletion variant of the estrogen receptor frequently coexpressed with wild-type estrogen receptor in human breast cancer
(1993) In Cancer Research 53(24). p.4-5882- Abstract
Recent evidence suggests that the expression of estrogen receptor (ER) variants in breast cancer may interfere with wild-type (wt) ER function and be related to tumor progression and resistance to hormone treatment. One of these variants, ER delta E5, lacking that part of the hormone-binding domain encoded by exon 5, has previously been identified in breast tumors with the unusual estrogen receptor negative (ER-) and progesterone receptor positive (PgR+) phenotype and found to possess constitutive and hormone-independent transcriptional activity. Using a ribonuclease protection assay, we analyzed 27 breast tumors and 4 breast cell lines for the presence of this variant. We found the ER delta E5 variant to be expressed, not only in all... (More)
Recent evidence suggests that the expression of estrogen receptor (ER) variants in breast cancer may interfere with wild-type (wt) ER function and be related to tumor progression and resistance to hormone treatment. One of these variants, ER delta E5, lacking that part of the hormone-binding domain encoded by exon 5, has previously been identified in breast tumors with the unusual estrogen receptor negative (ER-) and progesterone receptor positive (PgR+) phenotype and found to possess constitutive and hormone-independent transcriptional activity. Using a ribonuclease protection assay, we analyzed 27 breast tumors and 4 breast cell lines for the presence of this variant. We found the ER delta E5 variant to be expressed, not only in all of three ER-/PgR+ tumors but also in 19 of 20 ER+/PgR+ or ER+/PgR- tumors. Moreover, the variant was always coexpressed with and often in excess of wtER. ER delta E5 was also found in three breast cancer cell lines (MCF7, T47D, and ZR75-1), although to a lesser extent than wtER. A complete absence of both ER delta E5 and wtER was noted in four ER-/PgR- tumors and one normal breast cell line (HBL-100). Thus, our data suggest that the occurrence of ER delta E5 in breast cancer may represent a critical stage in tumor progression to autonomy.
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- author
- Zhang, Q X ; Borg, A LU and Fuqua, S A
- organization
- publishing date
- 1993-12-15
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Breast Neoplasms/metabolism, Exons, Female, Gene Deletion, Humans, Phenotype, Receptors, Estrogen/analysis, Receptors, Progesterone/analysis, Tumor Cells, Cultured
- in
- Cancer Research
- volume
- 53
- issue
- 24
- pages
- 4 - 5882
- publisher
- American Association for Cancer Research Inc.
- external identifiers
-
- scopus:0027138874
- pmid:8261397
- ISSN
- 0008-5472
- language
- English
- LU publication?
- yes
- id
- 9dfa169c-fb09-4c2e-b97e-dfa912cabece
- alternative location
- https://cancerres.aacrjournals.org/content/53/24/5882
- date added to LUP
- 2019-05-22 09:38:30
- date last changed
- 2024-01-01 06:35:39
@article{9dfa169c-fb09-4c2e-b97e-dfa912cabece, abstract = {{<p>Recent evidence suggests that the expression of estrogen receptor (ER) variants in breast cancer may interfere with wild-type (wt) ER function and be related to tumor progression and resistance to hormone treatment. One of these variants, ER delta E5, lacking that part of the hormone-binding domain encoded by exon 5, has previously been identified in breast tumors with the unusual estrogen receptor negative (ER-) and progesterone receptor positive (PgR+) phenotype and found to possess constitutive and hormone-independent transcriptional activity. Using a ribonuclease protection assay, we analyzed 27 breast tumors and 4 breast cell lines for the presence of this variant. We found the ER delta E5 variant to be expressed, not only in all of three ER-/PgR+ tumors but also in 19 of 20 ER+/PgR+ or ER+/PgR- tumors. Moreover, the variant was always coexpressed with and often in excess of wtER. ER delta E5 was also found in three breast cancer cell lines (MCF7, T47D, and ZR75-1), although to a lesser extent than wtER. A complete absence of both ER delta E5 and wtER was noted in four ER-/PgR- tumors and one normal breast cell line (HBL-100). Thus, our data suggest that the occurrence of ER delta E5 in breast cancer may represent a critical stage in tumor progression to autonomy.</p>}}, author = {{Zhang, Q X and Borg, A and Fuqua, S A}}, issn = {{0008-5472}}, keywords = {{Breast Neoplasms/metabolism; Exons; Female; Gene Deletion; Humans; Phenotype; Receptors, Estrogen/analysis; Receptors, Progesterone/analysis; Tumor Cells, Cultured}}, language = {{eng}}, month = {{12}}, number = {{24}}, pages = {{4--5882}}, publisher = {{American Association for Cancer Research Inc.}}, series = {{Cancer Research}}, title = {{An exon 5 deletion variant of the estrogen receptor frequently coexpressed with wild-type estrogen receptor in human breast cancer}}, url = {{https://cancerres.aacrjournals.org/content/53/24/5882}}, volume = {{53}}, year = {{1993}}, }