A multicentre study into the reliability of steroid receptor immunocytochemical assay quantification

McClelland, Richard Andrew; Wilson, Davidb .; Leake, Robin; Finlay, Pauline; Nicholson, R. I.

doi:10.1016/0277-5379(91)90171-9

Cited by 57 publications

(34 citation statements)

References 10 publications

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“…The results of staining for ER and EGFR following the D-ICA are similar to those achieved in the two single assays of proven prognostic significance (McClelland et al, 1986;Lewis et al, 1990) with only small variations in the proportion of tumour cells being detected as positive. Such relatively minor variations may result from observer errors, which are inherent in immunocytochemical procedures (McClelland et al, 1991), or may be due to tumour heterogeneity, which is well documented (Walker et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Dual immunocytochemical analysis of oestrogen and epidermal growth factor receptors in human breast cancer

Sharma

Horgan²,

Douglas-Jones³

et al. 1994

Br J Cancer

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Section: Discussionmentioning

confidence: 99%

Dual immunocytochemical analysis of oestrogen and epidermal growth factor receptors in human breast cancer

Sharma

Horgan²,

Douglas-Jones³

et al. 1994

Br J Cancer

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“…These areas were then viewed at Â40 for more detailed tumour cell immunostaining assessment. After checking assay internal positive and negative controls for acceptable positive staining and minimal non-specific binding, cell percentages of low, moderate or high staining intensity were recorded for at least two fields ($2000 cells)/coverslip (with three cover-slips/treatment) so that an H-score (see equation below) or field staining index for each marker could be assigned as described previously (McClelland et al 1991) . Representative photomicroscopy was performed using an Olympus Camedia C-200 digital camera and Olympus DP software.…”

Section: Immunostaining Analysismentioning

confidence: 99%

Insulin-like growth factor-I receptor signalling and acquired resistance to gefitinib (ZD1839; Iressa) in human breast and prostate cancer cells

Jones

Goddard²,

Gee³

et al. 2004

Endocr Relat Cancer

277

189

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De novo and acquired resistance to the anti-tumour drug gefitinib (ZD1839; Iressa), a specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) has been reported. We have determined whether signalling through the IGF-I receptor (IGF-1R) pathway plays a role in the gefitinib-acquired resistance phenotype. Continuous exposure of EGFR-positive MCF-7-derived tamoxifen resistant breast cancer cells (TAM-R) to 1 mM gefitinib resulted in a sustained growth inhibition (90%) for 4 months before the surviving cells resumed proliferation. A stable gefitinibresistant subline (TAM/TKI-R) was established after a further 2 months and this showed no detectable basal phosphorylated EGFR activity. Compared with the parental TAM-R cells, the TAM/ TKI-R cells demonstrated (a) elevated levels of activated IGF-1R, AKT and protein kinase C (PKC)d, (b) an increased sensitivity to growth inhibition by the IGF-1R TKI AG1024 and (c) an increased migratory capacity that was reduced by AG1024 treatment. Similarly, the EGFR-positive androgen-independent human prostate cancer cell line DU145 was also continuously challenged with 1 mM gefitinib and, although substantial growth inhibition (60%) was seen initially, a gefitinibresistant variant (DU145/TKI-R) developed after 3 months. Like their breast cancer counterparts, the DU145/TKI-R cells showed increases in the levels of components of the IGF-1R signalling pathway and an elevated sensitivity to growth inhibition by AG1024 compared with the parent DU145 cell line. Additionally, DU145/TKI-R cell migration was also decreased by this inhibitor. We have therefore concluded that in breast and prostate cancer cells acquired resistance to gefitinib is associated with increased signalling via the IGF-1R pathway, which also plays a role in the invasive capacity of the gefitinib-resistant phenotype.

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“…Assessment of specific immunocytochemical staining of tumour cells was performed on at least ten fields per section and the H-score calculated as previously described (McClelland et al, 1991). Previous studies show that a cut-off for ERICA positivity of > 0.02 has significance as a predictor of the endocrine responsiveness of recurrent breast cancer, and this value is used here (Nicholson et al, 1991 Oestrogen-regulated genes in breast cancer 1655 within these small subgroups are reported as two-sided P-values. Comparative analysis of levels of mRNA and protein expression were assessed by calculation of the non-parametric Spearman rank correlation coefficient.…”

Section: Immunocytochemistrymentioning

confidence: 99%

“…However, the predictive capability of ER status alone is not absolute (Nicholson et al, 1991). While few ERnegative patients respond to such therapies, perhaps half of ERpositive patients will also gain no clinically defined benefit.…”

mentioning

confidence: 99%

Oestrogen-regulated genes in breast cancer: association of pLIV1 with response to endocrine therapy

McClelland

Manning²,

Gee³

et al. 1998

Br J Cancer

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Summary Northern hybridization analyses of the oestrogen-inducible mRNAs pLIV1 and pS2 were compared with oestrogen receptor (ER) immunocytochemistry assessments in 40 untreated primary or early recurrent breast tumours. Significant associations were observed between pLIVl/ER (P < 0.03), pS2/ER (P < 0.001) and pLIV1/pS2 (P < 0.04) status. After disease recurrence, patients were treated with assessable courses of endocrine therapies. Positive pLIV1, pS2 and ER statuses in primary disease were consequently found to be predictive of endocrine responsiveness in the secondary lesions (P < 0.03, P < 0.02, P < 0.005 respectively). However, despite these associations, a number of pLIV1i-and/or pS2-positive tumours failed to respond to therapy.Keywords: oestrogen-regulated genes; breast cancer; oestrogen receptor The selection of breast cancer patients for endocrine therapy is most frequently made on the basis of tumour oestrogen-receptor (ER) protein content. However, the predictive capability of ER status alone is not absolute (Nicholson et al, 1991). While few ERnegative patients respond to such therapies, perhaps half of ERpositive patients will also gain no clinically defined benefit. It has been postulated that coassessment of ER and oestrogeninducible genes or protein products, as markers of functioning ER-mediated cellular growth mechanisms, might give better predictive results. As such, the additional measurements of tumour PR and pS2 protein content have been shown to partly improve selectivity (Horwitz and McGuire, 1977;Foekens et al, 1990).Our study evaluates the significance of expression of the oestrogen-inducible pLIVl (Manning et al, 1988) 13 as grade 2 and 22 as grade 3. Twenty-seven tumours were described as infiltrating ductal (no special type), five mixed/tubular, two mixed ductal/lobular and the remainder as single cases of lobular, medullary, atypical medullary, mixed ductal/mucinous and ductal carcinoma in situ.

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A multicentre study into the reliability of steroid receptor immunocytochemical assay quantification

Cited by 57 publications

References 10 publications

Dual immunocytochemical analysis of oestrogen and epidermal growth factor receptors in human breast cancer

Dual immunocytochemical analysis of oestrogen and epidermal growth factor receptors in human breast cancer

Insulin-like growth factor-I receptor signalling and acquired resistance to gefitinib (ZD1839; Iressa) in human breast and prostate cancer cells

Oestrogen-regulated genes in breast cancer: association of pLIV1 with response to endocrine therapy

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