OBJECTIVES

Inflammatory mammary carcinoma (IMC) is the most aggressive spontaneous type of mammary cancer both in women and in dogs. It is considered the most malignant type of mammary carcinoma with a fulminant clinical course and extremely poor survival rate. The occurrence of IMC is generally in the luteal phase, previous treatments with progestagens are usually associated with a worse clinical course and increased histological malignancy, and there is histological evidence of a relative high proportion of lipid-secreting tumors. These findings seem to indicate that probably different endocrine mechanisms seem to be involved in canine IMC and that IMC could be a source of steroids. The aim of the present study was to characterize the serum steroid hormone profile of IMC and to compare with mammary dysplasias, benign mammary tumors and other malignant mammary tumors non-IMC.

MATERIALS

Animals. 30 female dogs (aged 7-14 years) with mammary dysplasias or tumors were clinically examined at the Veterinary Teaching Hospital of Madrid (VTHM). Serum samples were obtained from the saphenus vein. 10 female dogs without a history of endocrine or neoplastic disorder were used as controls.

Dehydroepiandrosterone, Androstenedione, Testosterone, Progesterone, Estrone Sulphate and 17-ß-estradiol Enzyme immunoassay (EIA). DHEA, A4, T4, P4, E1SO4 and 17-ß-E2 serum levels were assayed by competitive EIA previously validated for this specie. Serum samples were extracted with 2 ml of diethyl ether. All hormone concentrations were expressed in ng/ml.

The BMDP (Biomedical Data Program, Statistical Software Inc., Los Angeles, CA, USA) was used for statistical analysis. Differences between individual means were analyzed by Pair wise t-test and Bonferroni post-test to determine whether values were statistically different. All values were expressed as mean ± SE. In all statistical comparisons, p< 0.05 was accepted as denoting significant differences.

RESULTS

Inflammatory Carcinoma concentrations displayed the following serum steroid profile: progesterone (P4): 0.27± 0.03 ng/ml, 17â-estradiol (E2): 177.56 ± 8.46 pg/ml, androstenedione (A4): 3.89 ± 0.69 ng/ml, dehydroepiandrosterone (DHEA): 11.82 ± 1.26 ng/ml, and estrone sulphate (E1SO4): 6.24 ± 0.40 ng/ml. Hormone profiles were significantly higher (p<0.001) in IMC compared with the hormone steroid profile determined for malignant non-IMC tumors, benign tumors, mammary dysplasias and normal mammary gland. Levels of all the steroids analyzed were elevated two or three times in IMC respect to other malignant tumors non-IMC. Concentrations of both DHEA and E1SO4 were especially elevated in IMC respect to other groups.

CONCLUSION

Our results suggest the hypothesis that an autocrine mechanism could be especially involved in the pathogenesis of canine inflammatory carcinoma. Future studies about the production and metabolism of steroid hormones of inflammatory mammary carcinoma could be useful to the development of new therapies directed to the block of determined steroidogenic enzymes.