Oestrogen receptors in benign epithelial lesions and intraduct carcinomas of the breast: an immunohistological study

Giri, Dilip; Dundas, S. A. C.; Nottingham, J.; Underwood, James

doi:10.1111/j.1365-2559.1989.tb01623.x

Cited by 67 publications

(27 citation statements)

References 13 publications

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“…Our finding of a relatively lower frequency of ER expression in comedo and large cell DCIS as compared to small cell DCIS is consistent with three earlier studies (Barnes & Masood, 1990;Bur et al, 1992;Giri et al, 1989). Barnes and Masood (1990) (Ronay et al, 1990).…”

Section: Resultssupporting

confidence: 93%

“…Results of ER status in DCIS in the literature have often been described as a part of much larger series of symptomatic invasive breast tumours. Previous studies have indicated that positive ER status in DCIS is associated with certain morphological subtypes of in situ mammary carcinoma (Barnes & Masood, 1990;Bur et al, 1992;Giri et al, 1989).…”

mentioning

confidence: 98%

“…Previous studies of ER (oestrogen receptor) expression in pure DCIS have been limited (Barnes & Masood, 1990;Bur et al, 1992;Giri et al, 1989;Malafa et al, 1990;Ronay et al, 1990) and of smaller size. Results of ER status in DCIS in the literature have often been described as a part of much larger series of symptomatic invasive breast tumours.…”

mentioning

confidence: 99%

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Oestrogen receptor expression in ductal carcinoma in situ of the breast: relationship to flow cytometric analysis of DNA and expression of the c-erbB-2 oncoprotein

Poller

Snead²,

Roberts³

et al. 1993

Br J Cancer

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Section: Resultssupporting

confidence: 93%

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confidence: 98%

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Oestrogen receptor expression in ductal carcinoma in situ of the breast: relationship to flow cytometric analysis of DNA and expression of the c-erbB-2 oncoprotein

Poller

Snead²,

Roberts³

et al. 1993

Br J Cancer

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“…However, unlike the latter (Bartkova et al, 1990), we found pS2 to be present in both the comedo and non-comedo types. Interestingly, the frequency of ER staining of paraffin embedded DCIS cases has been reported (Giri et al, 1989) to be much greater in cribriform, papillary and solid types (>50%) as compared with comedo (<20%). This discordance between pS2 and ER staining, also reflected by our own ER results, suggests that pS2 expression may not be obligatorily linked to that of ER as originally envisaged (Rio et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical localisation of pS2 protein in ductal carcinoma in situ and benign lesions of the breast

Luqmani

Campbell²,

Soomro³

et al. 1993

Br J Cancer

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Summary The expression of pS2 was examined histochemically in paraffin sections taken from biopsy material from patients diagnosed with ductal carcincoma in situ (DCIS). Often intense immunoreactivity, to an anti-pS2 monoclonal antibody, was observed in comedo, solid, cribriform and micropapillary types of DCIS, with significant positivity found in 63-67% of cases. In 15 samples analysed, we found a good correlation between pS2 expression and presence of progesterone receptor positive cells, but not with estrogen receptor. There was only a limited degree of correspondence between the cells staining with these anti-sera. Some pS2 positive cells were also seen in normal acini in areas adjacent to cancer but much less frequently in sections of normal breast from reduction mammoplasty. Most normal areas were negative, as were cysts. In benign proliferative conditions (seen in sections with and without DCIS) such as adenosis, sclerosing adenosis, mild and florid ductal epithelial hyperplasia, significant pS2 positivity was seen in about 50% of cases.These results suggest that there is a progressive increase in pS2 from normal to benign to cancer cells and that this gene is expressed in both the invasive and pre-invasive forms of breast cancer.The pS2 gene, which was originally isolated by virtue of its estrogen-inducibility (Masiakowski et al., 1982), has been shown to be predominantly associated with estrogen receptor (ER) positive breast cancers (Rio et al., 1987;Skilton et al., 1989;Henry et al., 1989). Limited pS2 immunostaining has also been reported in normal breast and in parts of the ileum (Piggott et al., 1991;Luqmani et al., 1992), as well as more extensive expression in the stomach, but is otherwise absent from the vast majority of normal tissues. It is however, widely expressed in other epithelial cancers Luqmani et al., 1989;Rio et al., 1988; Luqmani et al., 1991;Wysocki et al., 1990) as well as in inflammatory conditions of the gastro-intestinal tract Seitz et al., 1992). pS2 has significant sequence homology with the (pancreatic) spasmolytic polypeptide (hSP) Wright et al., 1990) with which it is co-expressed in gastric mucosa (Theisinger et al., 1991) and is also secreted into the gastric fluid (Rio et al., 1988).In a small study we have recently (Shousha et al., manuscript submitted) found pS2 to have no prognostic significance in patients with colo-rectal cancer, but high pS2 levels were predictive of both longer survival (Foekens et al., 1990) and favourable response of breast cancer patients to endocrine therapy (Henry et al., 1989;Skilton et al., 1989) and, in this regard, may be superior to ER (Schwartz et al., 1991). Little is known of the expression of pS2 in early breast cancer. We therefore carried out an immunohistochemical study using archival material obtained from patients who had been diagnosed with ductal carcinoma in situ (DCIS), a neoplastic condition in which the malignant cells are confined within the basement membranes of the mammary ducts. This is believed to constitute a fore...

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“…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.…”

mentioning

confidence: 99%

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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Oestrogen receptors in benign epithelial lesions and intraduct carcinomas of the breast: an immunohistological study

Cited by 67 publications

References 13 publications

Oestrogen receptor expression in ductal carcinoma in situ of the breast: relationship to flow cytometric analysis of DNA and expression of the c-erbB-2 oncoprotein

Oestrogen receptor expression in ductal carcinoma in situ of the breast: relationship to flow cytometric analysis of DNA and expression of the c-erbB-2 oncoprotein

Immunohistochemical localisation of pS2 protein in ductal carcinoma in situ and benign lesions of the breast

Oestrogen receptor: a stable phenotype in breast cancer

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