Oestrogen receptor mutants and variants in breast cancer

Dowsett, Mitchell; Daffada, Angela A.I.; Chan, Christina M.W.; Johnston, Stephen

doi:10.1016/s0959-8049(97)00100-7

Cited by 41 publications

(14 citation statements)

References 43 publications

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“…inhibitors of epidermal growth factor receptor tyrosine kinase) and prognostic markers (e.g. oestrogen receptor levels in breast cancer) (Levitzki et al, 1995;Dowsett et al, 1997). Using classical metaphase cytogenetic techniques, many chromosomal aberrations have been identified in human cancer cell lines and primary culture of haematological malignancies.…”

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confidence: 99%

Comparative genomic hybridization and chromosomal instability in solid tumours

et al. 1999

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Comparative genomic hybridization analysis detects frequent, often high-level overrepresentation of DNA sequences at 3q, 5p, 7p and 8q in human non-small-cell lung carcinomas. Cancer Res 57: 2116-2120 Björkqvist A-M, Tammilehto L, Anttila S, Mattson K and Knuutila S (1997) Recurrent DNA copy number changes in 1q, 4q, 6q, 9p, 13q, 14q and 22q detected by comparative genomic hybridization in malignant mesothelioma.

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confidence: 99%

Comparative genomic hybridization and chromosomal instability in solid tumours

et al. 1999

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“…Of these H222 that has its epitope in the hormone-binding domain, has been widely used for detecting ER-a in breast tumors. Specimens that are categorized as ER-negative actually may express mutant ER lacking relevant epitopes and consequently some functional domains of the wild-type (wt) ER [18][19][20][21][22]. For example loss of exon 4 results in an in-frame deletion in ER without a nuclear localization signal and part of the hormone-binding domain.…”

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confidence: 99%

Observations on the presence of E domain variants of estrogen receptor‐α in the breast tumors

Kumar

Srivastava

2006

Journal of Surgical Oncology

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“…Regarding ER␣, multiple variants have been described in human breast cancer biopsies, cell lines, and pituitary tumors (7)(8)(9)(10). Regarding ER␣, multiple variants have been described in human breast cancer biopsies, cell lines, and pituitary tumors (7)(8)(9)(10).…”

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Novel Intronic Promoter in the Rat ERα Gene Responsible for the Transient Transcription of a Variant Receptor

et al. 2001

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To analyze the molecular origin of an ER variant, the truncated ER product-1, transiently expressed at the proestrus in lactotrope cells, we generated a 2.5-kb sequence of a genomic region upstream and downstream the specific sequence truncated ER product-1. Genomic Southern blot analysis showed that truncated ER product-1 is spliced from a noncoding leader exon localized within the intron 4 of the ER alpha gene. Analysis of the promoter sequence revealed the presence of a major transcriptional start site, a canonical TATA box and putative cis regulatory elements for pituitary specific expression as well as an E-responsive element. In transient transfection, the truncated ER product-1 promoter was transcriptionally the most active in the lactotrope cell lines (MMQ). Analysis of truncated ER product-1 functionality showed that: 1) the protein inhibited ER alpha binding to the E-responsive element in electromobility shift assays, 2) inhibited the E2 binding to ER alpha in binding assays, 3) the truncated ER product-1/ER alpha complex antagonized the transcriptional activity elicited by E2, 4) nuclear localization of green fluorescent protein-ER alpha was altered in Chinese hamster ovary cell lines stably expressing truncated ER product-1. Collectively, these data demonstrated that the protein exerts full dominant negative activity against ER alpha. Moreover, truncated ER product-1/ER alpha complex also repressed the activity of all promoters tested to date, suggesting a general inhibitory effect toward transcription. In conclusion, the data suggest that truncated ER product-1 could regulate estrogen signaling via a specific promoter in lactotrope cells.

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Oestrogen receptor mutants and variants in breast cancer

Cited by 41 publications

References 43 publications

Comparative genomic hybridization and chromosomal instability in solid tumours

Comparative genomic hybridization and chromosomal instability in solid tumours

Observations on the presence of E domain variants of estrogen receptor‐α in the breast tumors

Novel Intronic Promoter in the Rat ERα Gene Responsible for the Transient Transcription of a Variant Receptor

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