Prognostic value of estrogen receptors in primary breast cancer

Hähnel, R.; Drrernat,; Woodings, Terry; Vivian, Analú

doi:10.1002/1097-0142(197908)44:2<671::aid-cncr2820440238>3.0.co;2-v

Cited by 249 publications

(66 citation statements)

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“…Response to therapy has been reported to correlate significantly with both oestrogen receptor (ER) status (Blamey et al, 1980;Jensen, 1981;Stewart et al, 1982;Williams et al, 1986) and progesterone receptor (PgR) status (Stewart et al, 1982;McGuire, 1978;Johnson et al, 1983). Survival from commencing endocrine therapy has also been reported to correlate significantly with ER status (Hahnel et al, 1979;Stewart et al, 1981;Kinne et al, 1981;Paterson et al, 1982;Howat et al, 1985;Williams et al, 1987) and PgR status (Howat et al, 1985;Howell et al, 1984) of the primary tumour.…”

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confidence: 99%

Comparison of two oestrogen receptor assays in the prediction of the clinical course of patients with advanced breast cancer

Robertson

Bates²,

Pearson³

et al. 1992

Br J Cancer

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Summary We have examined two new oestrogen receptor (ER) assays -an enzyme immunoassay (EIA) and an immunocytochemical assay (ICA) in a large series of primary breast tumours to compare their potential as predictors of (1) response to endocrine therapy and (2) survival in patients developing advanced breast cancer.Response to endocrine therapy was categorised at 6 months (UICC criteria). ERICA appears the better predictor of response to endocrine therapy than ER-EIA. Combining ICA and EIA results did not improve the prediction of response.With both assays patients with ER positive tumours survived longer from the time of diagnosis of advanced disease than those with ER negative tumours. The predictive power of these assay for progression of disease appears slightly better for the ER-ICA.

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confidence: 99%

Comparison of two oestrogen receptor assays in the prediction of the clinical course of patients with advanced breast cancer

Robertson

Bates²,

Pearson³

et al. 1992

Br J Cancer

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“…14 -16 In addition, lymph node metastasis, considered to be the most important prognostic factor in breast cancer, does not alter these findings. 17,18 However, the ER expression is gradually lost during tumor progression, leading to a more undifferentiated state. 19 The majority of ER ϩ tumors are diploid, well differentiated, more common in postmenopausal women and less aggressive than ER Ϫ breast tumors.…”

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Gene expression profiles in breast tumors regarding the presence or absence of estrogen and progesterone receptors

Nagai

Rós

Neto

et al. 2004

Intl Journal of Cancer

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Estrogen acts via its receptor (ER) to stimulate cell growth and differentiation in the mammary gland. ER and progesterone receptor (PR), which is regulated by estrogen via ER, have been used as prognostic markers in clinical management of breast cancer patients. Patients with ER ؊ breast tumors have a poorer prognosis than patients with ER ؉ tumors. The aim of the present study was the identification of tumor-associated genes differentially expressed in breast tumors regarding the presence or absence of ER and PR hybridized with cDNA microarrays containing 4,500 tumorderived expressed sequence tags generated using the ORESTES technique. Samples of human primary breast carcinomas from 38 patients were analyzed. The experiments were performed in triplicates and data from each element were acquired by phosphoimage scanning. Data acquisition was performed using the ArrayVision software. After normalization statistical analysis was applied. In a preliminary analysis, 98 differentially expressed transcripts were identified, 46 were found to be more expressed in ER ؉ /PR ؉ and 52 were found to be more expressed in ER ؊ /PR ؊ breast tumors. Estrogens exert important roles in the development, differentiation and maintenance of several target tissues and are also associated with the development and growth of hormone-dependent tumors such as breast cancer. 1 Most estrogen actions are thought to be mediated through its nuclear estrogen receptors, ER␣ and ER␤, which are members of the nuclear receptors superfamily that are ligand-induced transcription factors. 2 The mechanism by which estrogen receptor (ER) mediates the transactivation of gene expression is complex. 3 Besides the classical ligand-dependent mechanism of ER action in which the hormone-receptor complex regulates gene transcription through its interaction with ERE consensus DNA sequences, the ERs can also regulate gene transcription interacting with other promoter elements such as AP1, 4 SP1 5 and CREs. 6 Thus, estrogen receptors ER␣ and ER␤ can transduce different hormonal signals depending on the ligand and the nature of the hormone-responsive element (HRE). 2 The transactivation elicited by those receptors complexed with E2 may result in opposite signal transduction leading to opposite biologic response in the presence of AP1 and/or CRE sites. 7,8 In addition, several E2-responsive genes are regulated by DNA-independent or -dependent interactions of the ER␣ and SP1 proteins. 9 Alternatively, the signal transduction by growth factors and their tyrosine kinase receptors, such as EGFR, IGFR, erbB-2 and other molecules like cAMP and dopamine, may lead to a ligand-independent ER activation, resulting from the phosphorylation of serine and tyrosine amino acid residues in the AF1 and AF2 domains in the estrogen receptor molecule. 10

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“…Intralaboratory variation in a number of studies using LBA is reported to range from 15% to 34% (Hawkins et al, 1975(Hawkins et al, , 1987bTaylor et al, 1982; Davis et al, 1984;Bojar, 1986;Anderson et al, 1989 Nicholson et al, 1986) and 3.7% to 16.7% (Bojar, 1986;Jordan et al, 1986;Leclerq et al, 1986;Nicholson et al, 1986) respectively. The interlaboratory CV for EIA was reported to range between 10% and 19% (Bojar, 1986;Leclerq et al, 1986).ER and the natural history of breast cancer Many studies have reported no correlation between ER status and axillary lymph node status (Maynard et al, 1978;Hahnel et al, 1979;Mason et al, 1983;Williams et al, 1987;Hawkins et al, 1987a). Nevertheless, it has been assumed that ER-negative cells have more metastatic potential.…”

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confidence: 99%

“…ER and the natural history of breast cancer Many studies have reported no correlation between ER status and axillary lymph node status (Maynard et al, 1978;Hahnel et al, 1979;Mason et al, 1983;Williams et al, 1987;Hawkins et al, 1987a). Nevertheless, it has been assumed that ER-negative cells have more metastatic potential.…”

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confidence: 99%

“…ER and the natural history of breast cancer Many studies have reported no correlation between ER status and axillary lymph node status (Maynard et al, 1978;Hahnel et al, 1979;Mason et al, 1983;Williams et al, 1987;Hawkins et al, 1987a (DCIS) have reported positivity in between 32% and 80% of tumours depending on the cut-off level chosen for positivity (Giri et al, 1989;Malafa et al, 1990;Bur et al, 1992;Pallis et al, 1992;Soomro et al, 1992;Poller et al, 1993;Wilbur and Barrows, 1993; Murphy et al, submitted). The positivity rates for DCIS are similar to reported rates for invasive breast cancer, which argues against phenotypic drift as tumours progress biologically from preinvasive to invasive carcinoma.…”

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Oestrogen receptor: a stable phenotype in breast cancer

Robertson

1996

Br J Cancer

127

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Summary Oestrogen receptor (ER) expression in breast cancer is regarded as a phenotype that may change during the natural history of the disease or during endocrine therapy. It has been suggested that in up to 70% of tumours that show acquired resistance the mechanism may be changed in ER status from positive to negative. This paper proposes an alternative hypothesis that ER expression is a stable phenotype in breast cancer. The paper reviews the literature on ER expression during the natural history of breast cancer in patients and also presents data on the effect of endocrine therapy on ER expression. If the alternative hypothesis is true it has important implications for treatment from chemoprevention to acquired endocrine resistance in advanced disease. Equally, if the hypothesis is true, attempts to develop laboratory models of endocrine resistance where ER-positive tumours become ER negative need to be re-evaluated.Keywords: breast cancer; oestrogen receptor; stable phenotypeThe oestrogen receptor (ER) is a 65 kDa oestrogen-binding protein expressed by 46-77% of breast cancers (Walt et al., 1976;Knight et al., 1977; Maynard et al., 1978;Brooks et al., 1980;Osborne et al., 1980; Croton et al., 1981;Howell et al., 1984;Hawkins et al.,1987a;Williams et al., 1987;Clarke and McGuire, 1988). It is a generally held view that ER expression is not a permanent phenotype in breast cancer cells Moolgavakar et al., 1980; Encarnacion et al., 1993; Morrow and Jordon, 1993;Nomura et al., 1985;Jordan, 1994;Paik et al., 1994). One reason for this view is the belief that patients with ER-positive primary breast tumours often develop ER-negative metastases in regional lymph nodes or distant sites. This has been interpreted to show that ER negativity correlates with more aggressive tumour biology and loss of cellular control. A second reason is the strong correlation between ER and therapeutic response to primary endocrine therapy (Samaan et al., 1981;Howell et al., 1984;Williams et al., 1987), which formed the basis for early hypotheses of endocrine sensitivity and resistance. Up to 60% of ER-positive tumours respond to hormone therapy (e.g. Tamoxifen), while for ER-negative tumours the figure is around 10% Samaan et al., 1981;Williams et al., 1987). Therapeutic response to endocrine therapy is not permanent and eventually all such tumours progress. As ER negativity is strongly associated with primary resistance to endocrine therapy it is generally accepted that when responding tumours subsequently progress that in the majority of tumours this is due to loss of ER expression by the tumour Moolgavakar et al., 1980;Nomura et al., 1985; Encarnacion et al., 1993;Morrow and Jordan, 1993;Jordan, 1994;Paik et al., 1994). This paper proposes the alternative hypothesis that ER is a stable phenotype in breast cancer cells.The discovery of monoclonal antibodies (Kohler and Milstein, 1975) subsequently led to specific antibodies being raised to ER (Green and Jensen, 1982 . The ER-ICA allowed assessment of tumour tissue sections (King ...

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Prognostic value of estrogen receptors in primary breast cancer

Cited by 249 publications

References 2 publications

Comparison of two oestrogen receptor assays in the prediction of the clinical course of patients with advanced breast cancer

Comparison of two oestrogen receptor assays in the prediction of the clinical course of patients with advanced breast cancer

Gene expression profiles in breast tumors regarding the presence or absence of estrogen and progesterone receptors

Oestrogen receptor: a stable phenotype in breast cancer

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