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An exon 5 deletion variant of the estrogen receptor frequently coexpressed with wild-type estrogen receptor in human breast cancer

Zhang, Q X ; Borg, A LU and Fuqua, S A (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
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organization
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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}},
}