“…Biochemical measurements of ER activity have long been known to be of value for predicting the outcome of endocrine therapy (NIH Consensus Meeting 1974, reported by McGuire et al, 1975) and also as a guide to prognosis (Walt et al, 1976;Knight et al, 1977). Since 1980, however, the use and acceptance of receptor assays in the management of breast cancer has had a chequered history for a variety of reasons, including: poor quality control of biochemical assays; poor control of specimen quality; changes in methodology; use of receptor measurements as a discontinuous variable (Altman, 1991;Simon and Altman, 1994) with an arbitrary 'cut-off' to decide receptor 'positivity/ negativity'; the advent of the relatively non-toxic endocrine agent, tamoxifen; initial reports that benefit from adjuvant therapy with tamoxifen was unrelated to receptor activity (Novaldex Adjuvant Trial Organisation, 1983), although subsequent reports have disagreed (Rose et al, 1985;Scottish Breast Trials Committee, 1987;De Placido et al, 1990;Early Breast Cancer Trialists, 1992); the need for an adequate tumour specimen (50-250 mg); the advent of the Breast Cancer Screening Program (Forrest, 1986), which yields many impalpable tumours too small for biochemical assay; the widely quoted view that '8-10%' 'receptornegative' tumours respond to endocrine therapy -likely to be untrue for the reasons discussed by, for example, Wittliffe, (1988), andRobertson, (1996); the misconception that tumour grade provides exactly the same information as oestrogen receptor measurements, but at a lesser cost.…”