Diverse pathomechanisms leading to the breakdown of cellular estrogen surveillance and breast cancer development: new therapeutic strategies.

摘要: Recognition of the two main pathologic mechanisms equally leading to breast cancer development may provide explanations for apparently controversial results obtained by sexual hormone measurements in cases. Either insulin resistance or estrogen receptor (ER) defect is initiator processes and both them lead development. Primary induces hyperandrogenism deficiency, but during these ongoing processes, ER also develops. Conversely, when onset hormonal metabolic disturbances, initial counteraction hyperestrogenism. Compensatory improve damaged reactivity ERs; however, their failure leads secondary resistance. The final stage pathways breakdown surveillance, Among premenopausal cases, preponderant alterations with hyperandrogenism, which reflected majority studies suggesting a causal role In postmenopausal tumor be initiated resistance, while typically coupled elevated levels within low range. This mild hyperestrogenism remnant reactive synthesis against refractory ERs that were successfully counteracted at younger age. When refractoriness reactively increased found young older they exhibit clinical symptoms deficiency. Studies justifying correlation between compile such conclusion, quantitative evaluation cases has great importance, since stronger higher promising dose therapy.