6 Loss of Hormonal Responsiveness in Cancer

Hamm, John; Allegra, Joseph C.

doi:10.1159/000415344

Cited by 4 publications

(7 citation statements)

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“…The conflicting results,in human breast cancer may derive from the inclusion of patients on tamoxifen (Taylor et al, 1982), which causes a marked apparent reduction in ER concentration (this study and Hull et al, 1983) or from the difficulties in comparing different tumour deposits (Taylor et al, 1982;Hamm & Allegra, 1988).…”

Section: Discussionmentioning

confidence: 83%

“…Previous studies in patients with breast cancer (Taylor et al, 1982;Hamm & Allegra, 1988;Toma et al, 1986) and in experimental animals (Vignon & Rochefort, 1976;Hawkins et al, 1977b;Cho-Chung et al, 1978) have shown a decrease in receptor concentration after endocrine manipulation or, as in the present study, no consistant change (Hull et al, 1983;Mobbs et al, 1987). The conflicting results,in human breast cancer may derive from the inclusion of patients on tamoxifen (Taylor et al, 1982), which causes a marked apparent reduction in ER concentration (this study and Hull et al, 1983) or from the difficulties in comparing different tumour deposits (Taylor et al, 1982;Hamm & Allegra, 1988).…”

Section: Discussionmentioning

confidence: 99%

“…Studies of the effect of therapy on the oestrogen receptor (ER) concentration of breast cancer have previously relied upon examination of different tumour deposits (Taylor et al, 1982;Hamm & Allegra, 1988). Since these deposits may differ in biological characteristics, including the concentration of ER (Hoehn et al, 1979;Hawkins et al, 1981), this may lead to erroneous conclusions.…”

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confidence: 99%

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Does the oestrogen receptor concentration of a breast cancer change during systemic therapy?

Hawkins¹,

Tesdale²,

Anderson³

et al. 1990

Br J Cancer

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Summary The effect of systemic therapy on tumour oestrogen receptor (ER) concentration has been studied in 88 patients with large, operable, primary tumours (total 89) of the breast. In 26 patients, tumour was not available for study on one occasion (usually post-treatment). Forty-five patients were treated initially by endocrine therapy but, of these, 13 who had failed to respond went on to receive chemotherapy also. Seventeen patients with low concentrations of ER (<20 fmol mg-' protein) were treated directly by chemotherapy. Patients underwent an incisional biopsy for confirmation of diagnosis and determination of pre-treatment ER by radioligand binding assay, followed by systemic therapy for 3 months (or 6 months for both endocrine and cytotoxic therapies). Following 3 months of systemic therapy (6 months when patients received both endocrine and cytotoxic therapies), patients proceeded on to mastectomy and axillary lymphnode clearance. When residual tumour was present within the mastectomy specimen, a portion was selected for ER assay by the pathologist.In both pre-and post-treatment specimens, a section was cut from the face of the tissue portion used for receptor analysis, fixed in formol-saline and stained with haematoxylin and eosin to permit histopathological confirmation of the presence of tumour. Twenty-six patients in whom either the pre-or post-treatment specimen contained <10% tumour, as assessed by the pathologist, have been excluded from the Correspondence: R.A. Hawkins.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Does the oestrogen receptor concentration of a breast cancer change during systemic therapy?

Hawkins¹,

Tesdale²,

Anderson³

et al. 1990

Br J Cancer

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“…It can be observed that when the cell culture attains confluence (7 days, not shown), 20% SA, 15% MA, and 5% LA cells are ER-deprived. In the MCF-7 cell line, ER has been shown to be principally expressed during the G1 phase of the cell cycle (4,12). Thus, in the case of a homogeneous population, ERnegative cells should be S or G2/M cells of large nuclear size.…”

Section: Discussionmentioning

confidence: 99%

“…Likewise, the expression of ER by tumoral breast tissue is believed to indicate the hormonal sensitivity of cancer cells (19,23). Although ER is used for the selection of patients with advanced disease who might benefit from hormonal therapy, a large number of breast tumors (40-50%) fail to respond to endocrine therapy, in spite of the presence of functional ER (3,12). Breast cancer is not a single disease.…”

Section: Key Terms: Breast Cancer Cell; Phenotypic Alterations; Imagementioning

confidence: 99%

Distribution of estrogen receptor heterogeneity in growing MCF‐7 cells measured by quantitative microscopy

et al. 1997

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The existence of interactive subpopulations is a biological feature that can modulate the proliferation of tumor cells. The hormone-responsive breast cancer cell line MCF-7 has been described as heterogeneous in terms of density. In this study we describe a quantitative image analysis methodology that we developed for the in situ detection of different subpopulations in MCF-7 cell cultures. Using this technology, we demonstrate the heterogeneity of the MCF-7 cell line in terms of both nuclear size and estrogen-receptor content. Analysis of the organization (topography) of the different subpopulations in culture reveals a nonrandom distribution of cells. When studying the development of these cell subpopulations as a function of time of culture, we observe modifications of their topography associated with an increase of estrogen-receptor-expressing cells. Moreover, the use of cluster analysis allows study of the local organization of these subpopulations. These changes appear to be independent of cell proliferation.

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Morphological Evidence for a Subpopulation Selection Effect by Estrogen and Antiestrogen Treatments in the Heterogeneous MCF-7 Cell Line

Berard¹,

Berthois²,

Martin³

et al. 2000

Analytical Cellular Pathology

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Recently, we developed a method to quantitatively study tumour cell heterogeneity in terms of both nuclear size and estrogen receptor (ER) content by image cytometry. The method, previously used to analyse the proliferation of the breast cancer cell line MCF‐7, was applied here to analyse the growth of this cell line under estradiol (E2), hydroxytamoxifen (OH‐TAM), and both E2 and OH‐TAM treatments. The method extracts characteristic parameters of single nuclei and features that measure the global and local organisation of the cells in their growing phase. Modifications of the heterogeneity of the cell line are emphasised through phenotypic changes and modifications of the spatial organisation of the cells. The hormone (E2) generates a very fast growth of cells with small nuclei that became ER negative in the long term. The antihormone (OH‐TAM) produces a gradual selection of ER negative or poorly positive cells with large nuclei. These modifications are reversed when E2 and OH‐TAM are simultaneously used. Moreover, estradiol induces a permissive context of proliferation, whereas hydroxytamoxifen acts only on some subpopulations. The combination of cell count, cytomorphology, and cell organisation revealed the magnitude of the potential of structuration of hormones or antihormones on in vitro growing cells.

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6 Loss of Hormonal Responsiveness in Cancer

Cited by 4 publications

References 0 publications

Does the oestrogen receptor concentration of a breast cancer change during systemic therapy?

Does the oestrogen receptor concentration of a breast cancer change during systemic therapy?

Distribution of estrogen receptor heterogeneity in growing MCF‐7 cells measured by quantitative microscopy

Morphological Evidence for a Subpopulation Selection Effect by Estrogen and Antiestrogen Treatments in the Heterogeneous MCF-7 Cell Line

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