Análisis de la expresión del pepsinógeno C en metástasis ganglionares de carcinoma de mama / Analysis of pepsinogen C expression in lymph node metastases of breast cancer

En este estudio analizamos en los tumores primarios y en ganglios axilares metastásicos de 30 mujeres con cáncer de mama, mediante análisis inmunohistoquímico, la expresión tumoral del pepsinógeno C, una proteína normalmente expresada por la mucosa gástrica. De los tumores mamarios primarios, 16 (53,3 por ciento) mostraron una tinción inmunohistoquímica positiva para el pepsinógeno C, mientras que 17 (56,6 por ciento) lo hicieron en sus ganglios linfáticos tumorales. Además existió una relación significativamente positiva entre la expresión tumoral de pepsinógeno C en los tumores primarios y los ganglios metastásicos (p < 0,002). Sin embargo, sólo la expresión tumoral de esa proteína en los tumores primarios alcanzó significación estadística (p < 0,05) como factor pronóstico de evolución favorable para predecir la supervivencia de las pacientes. (AU)

Androgens, adrenal androgen precursors, and their metabolism in untreated primary tumors and lymph node metastases of human prostatic cancer.

Activities of several steroid metabolizing enzymes (steroid sulfate-sulfatase, 17 beta-hydroxysteroid dehydrogenase, 5 alpha-reductase, and 3 alpha beta-hydroxysteroid dehydrogenase) as well as total tissue content and subcellular distribution (nuclear-extranuclear) of several androgen precursors, active androgens, and androgen deactivation products (DHEA sulfate, DHEA, 5-androstenediol, 4-androstenedione, testosterone, DHT, and 3 alpha-androstanediol) were quantified in primary tumors and lymph node metastases of human prostatic cancer obtained from patients without previous endocrine manipulation. Primary tumors were compared to benign parts of the same prostates, and the metastases were compared to their primary tumors. All enzymes and steroids found in benign prostatic tissues could also be detected in the malignant tissues. Even the capacity to accumulate active androgens in the nuclei was found to be unchanged in nearly all of the samples. Lower activities of hormone-dependent enzymes were observed in the cancers, suggesting a less efficient utilization of hormonal stimuli. Most striking changes found in the malignant tissues were a subtotal loss of 5 alpha-reductase activity and a metabolic shift to testosterone, which was more pronounced in samples from metastatic disease as compared to samples from non-metastatic disease. In conclusion, primary tumors and metastases of prostatic cancers not treated by endocrine manipulations retain their androgen receptor system and possess the same capacity to metabolize adrenal androgen precursors along the pathway to DHT as benign prostatic tissue. Consequently, they should be able to use at least androstenedione for production of active androgens directly in the target tissue.

Ectopic creatine kinase MB production in metastatic cancer.

This case concerns the presence of high serum levels of creatine kinase MB isoenzyme in a patient with metastatic cancer. This patient did not have a myocardial infarction, so the source of the CK-MB was investigated. Because of the observation of macro-creatine kinase in patients with cancer, it was necessary to rule out the presence of this form of the enzyme. Extensive laboratory analysis demonstrated that the isoenzyme was true CK-MB, not an atypical or macro CK. Results of the study showed that ectopic production of the isoenzyme was the apparent source of the high serum activity. Homogenization of the cancer tissue demonstrated the presence of a high percentage of CK-MB activity. The implications of CK-MB production in cancer are discussed, including the use of various technics to rule out interfering activities when situations such as this occur.