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Oestrogen receptor-α (ERα) is an important prognostic marker in breast cancer and endocrine therapies are designed to inhibit or prevent ERα activity. In vitrostudies have indicated that phosphorylation of ERα, in particular on serine 118 (S118), can result in activation in a ligand-independent manner, thereby potentially contributing to resistance to endocrine agents, such as tamoxifen and aromatase inhibitors. Here we report the immunohistochemistry (IHC) of S118 phosphorylation in 301 primary breast tumour biopsies. Surprisingly, this analysis shows that S118 phosphorylation is higher in more differentiated tumours, suggesting that phosphorylation at this site is associated with a good prognosis in patients not previously treated with endocrine agents. However, we also report that S118 phosphorylation was elevated in tumour biopsies taken from patients who had relapsed following tamoxifen treatment, when compared to pre-treatment biopsies. Taken together, these data are consistent with the view that S118 phosphorylation is a feature of normal ERα function and that increases in levels of phosphorylation at this site may play a key role in the emergence of endocrine resistance in breast cancer.

Blood flow patterns have been studied in 28 patients with soft tissue sarcoma (29 tumours) using 99mTc-labelled hexamethyl propyleneamineoxime with planar views of the tumour-bearing region. Tumour:back-ground ratios ranged from 1·13 to 6·60 (mean 2·74) and maximum:minimum tumour ratios (between peripheries and centres of tumours) ranged from 1·34 to 32·0 (mean 4·70). In eight of 29 tumours (seven of which were involving the trunk) the tumour could not be identified. This study demonstrates that the blood supply to soft tissue sarcomas is generally greater than that to adjacent normal tissues and that tumour centres are relatively underperfused compared with the tumour periphery. In this heterogeneous series there was no clear-cut relationship between blood flow and histological grade or type.

Fine-needle aspiration cytology (FNAC) of the breast was performed in 491 patients over a 3-year period. Some 365 examinations (74·3 per cent) were performed by palpation and the remaining 126 (25·7 per cent) by stereotaxis. Ninety-six patients were excluded because of inadequate follow-up. Using a standard method of reporting the results 247 smears were classified as Cl and C2, but based on clinical and radiological criteria excision biopsy was recommended and performed in 122 patients with these lesions. Twenty-two per cent of C2 lesions were found to be malignant after histological examination. Forty-two patients with C3 or C4 cytology were advised to have excision biopsy and 41 had surgery. In all but one case the lesion was found to be malignant histologically. Definitive surgery was performed on 106 patients with C5 cytology and the diagnosis of malignancy was confirmed histologically in 105 of them. FNAC is a useful diagnostic tool in breast screening but in view of the number of false-negative results, cytology alone is unreliable and, therefore, full triple assessment is recommended.

Although recent epidemiologic studies suggest that silicone augmentation of the breast is not associated with an increased risk of mammary carcinoma, cases of breast carcinoma arising in augmented breasts are being increasingly encountered as a large number of patients who had augmentation are getting older. A case of a 51-year-old woman with a 20-year history of breast augmentation who developed an invasive cribriform carcinoma associated with extensive microcalcification is presented. The patient had submammary silicone implants 20 years ago that were replaced, because of local complications, in subpectoral positions 10 years later. Dispersive X-ray microanalysis failed to demonstrate silicone in sections of the tumor and adjacent breast tissue. Appropriately fixed tumor tissue was available for electron microscopic examination. The tumor cells were rich in mitochondria, and their luminal surfaces were endowed with abundant microvilli, but the cell surfaces that came closest to the calcified microspheriols were devoid of microvilli and had cellular buddings between the microspheriols. It is suggested that the tumor cells might have been actively involved in the process of microcalcification.