Mammary carcinoma arising in ectopic breast tissue is an uncommon occurrence. Most reported cases have involved ductal carcinoma, but other types, such as medullary, papillary, and lobular carcinomas, have been described. For pathologists, the diagnosis of mammary carcinoma arising in ectopic breast tissue can be difficult, especially in the axilla, where carcinoma of adnexal origin must be excluded. We describe a 46-year-old woman who developed invasive (juvenile) secretory carcinoma in ectopic right axillary breast tissue and micrometastatic carcinoma in an ipsilateral axillary lymph node. The carcinoma arose in a right axillary mass that had been present for 8 years, from which she had secreted fluid during prior breast-feeding. To our knowledge, this is the first report of secretory carcinoma arising in axillary breast tissue to be documented in the current literature.
To determine whether the increased activity of cathepsin D observed during starvation-induced cardiac atrophy results from activation of preexisting enzyme or synthesis of new enzyme, a solid phase double-antibody radioimmunoassay was developed for measurement of immunoreactive cathepsin D in extracts of rabbit myocardium. Cathepsin D activity was significantly increased in the hearts of animals starved for 3, 7, and 14 days (82.6 +/- 0.8, 87.2 +/- 3.8, and 95.3 +/- 3.5 U/g wet wt, respectively) compared to controls (65.5 +/- 1.4 U/g wet wt; P less than 0.001). Immunoreactive cathepsin D was increased to a greater extent (168 +/- 7, 179 +/- 16, 200 +/- 17, and 104 +/- 5 micrograms/g wet wt for 3-, 7-, and 14-day starvation and controls, respectively; P less than 0.001) than that expected on the basis of the observed increase in enzyme activity. Sephadex G100 gel filtration of cardiac lysosomal extracts from starved and control animals revealed no evidence of high or low molecular weight forms of cathepsin D. The results suggest the observed increase in cathepsin D activity during starvation-induced cardiac atrophy is accompanied by an increased synthesis and/or decreased degradation of cathepsin D protein, rather than activation of preexisting enzyme. The lower activity levels observed during starvation possibly result from alterations in the concentrations of endogenous inhibitors or activators of cathepsin D.
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