Adenomyoepithelial adenosis of the breast is a form of adenosis not previously described. It is similar in several ways to microglandular adenosis, but one significant difference is the presence of myoepithelial cells. The present case originated as adenomyoepithelial adenosis in a 46-year-old woman. In the course of 18 years it proliferated and changed into a low-grade malignant adenomyoepithelioma. Electron microscopy confirmed the presence of myoepithelial cells in the adenosis, and immuno-histochemical study demonstrated cells containing actin (representing myoepithelial cells) in the adenosis as well as in the adenomyoepithelioma.

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In an attempt to create uniform nationwide guidelines for the management of all stages of endometrial carcinoma, and to limit the use of adjuvant radiation therapy in stage I disease to high‐risk patients only, a protocol was developed by the Danish Endometrial Cancer group (DEMCA). From September 1986 through August 1988, 1214 women in Denmark with newly diagnosed carcinoma of the endometrium have been treated according to this protocol. This figure represents all endometrial carcinomas diagnosed in Denmark during this 2‐year period. The primary treatment was total abdominal hysterectomy and bilateral salpingo‐oophorectomy and no preoperative radiation therapy was delivered. In 1039 cases no macroscopic residual tumor and/or microscopic tumor tissue in the resection margins was found following surgery. Based on surgery and histopathology, these patients were classified as: P‐stage I low‐risk (grade 1 & 2 and 50% myometrial invasion), P‐stage I high‐risk (grade 1 & 2 and> 50% myometrial invasion, and grade 3), P‐stage II and P‐stage III (Group 1). Distribution was as follows: P‐I low‐risk 641 patients, P‐I high‐risk 235, P‐II 105 and P‐III (Group 1) 58 patients. No postoperative radiation therapy was given to P‐I low‐risk cases. P‐I high‐risk, P‐II, and P‐III (Group 1) cases received external radiation therapy. Recurrence rate at 68–92 months follow‐up was 45/641 (7%) in P‐I low‐risk, 36/235 (15%) in P‐I high‐risk, 30/105 (29%) in P‐II, and 27/58 (47%) in P‐III (Group 1) cases. Fifteen of 17 vaginal recurrences in P‐I low‐risk cases were salvaged (mean observation time 61 months).

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Hereditary haemochromatosis is an autosomal recessive disease that is genetically expressed by excessive accumulation of iron in the tissues, resulting in cirrhosis, diabetes mellitus, cardiomyopathy and hypogonadism. As the disease may be diagnosed before the appearance of symptoms, and prevented by repeated phlebotomies, there are strong implications for adoption of a screening procedure. Determinations of transferrin saturation (TS) and serum ferritin concentration (SF) were used to screen 4302 blood donors, who were selected for follow-up studies if they fulfilled any of the following three criteria: (i) TS greater than or equal to 0.7; (ii) TS greater than or equal to 0.5 together with SF greater than or equal to 150 micrograms l-1; (iii) SF greater than or equal to 300 micrograms l-1. A total of 58 subjects who fulfilled at least one of these criteria were reinvestigated, after which 18 individuals still fulfilled at least one criterion. Fifteen subjects having SF greater than or equal to 300 micrograms l-1 were offered liver biopsy and thirteen of these accepted. In one individual, no stainable iron was detected, and two subjects did not fulfil the previously established diagnostic criteria for the diagnosis of hereditary haemochromatosis. Ten subjects who had a high TS and liver iron grade 2-4 according to Bassett were classified accordingly as homozygotes. On the basis of these results, the prevalence of haemochromatosis in Denmark was estimated to be 0.0037-0.0046.

Three cases of invasive mammary carcinoma with stromal osteoclast-like giant cells are reported. All the specimens were grossly of reddish-brown colour. On microscopical examination two were invasive ductal carcinomas and the third was of mixed ductal and mucoid type. In the stroma all specimens showed numerous osteoclast-like giant cells, vascular proliferation, and accumulation of haemosiderin pigment. Supplementary immunohistochemical and electron microscopical investigations indicated that the giant cells originated from mononuclear stromal cells with only slight histiocytic properties. The giant cell formation was probably induced by the infiltrating carcinomatous tissue which is also believed to induce new blood vessel formation. However, there is no evidence of a direct relationship between these features.

Neonatal hemochromatosis (NH), an uncommon and generally fatal disorder of infancy, is defined by hepatic disease of antenatal onset, generally manifest at birth, and by stainable iron in a tissue distribution like that seen in heritable adult-onset hemochromatosis (HH). It is not known if parents and sibs of infants with NH are at risk of iron storage disease in later life. We provide 30-year follow-up for iron overload of a family in which 6 of 9 children died in utero or early in the neonatal period. Four of the 6 came to autopsy, where severe liver disease was found; in 3 of the 4, autopsy material could be reviewed. These 3 children had NH. Studies 30 years later did not identify HH or other iron storage disease in the parents or surviving sibs. These findings suggest that first-degree relatives of persons with NH are not necessarily at increased risk of iron storage disease in later life.