Many investigations propose that menopausal status, reproductive factors and exogenous hormone use may differently or even quite inversely affect the risk of TNBCs and steroid receptor positive cancers. Controversies concerning the exact role of even the same risk factor in TNBC development justify that the biological mechanisms behind the initiation of both TNBCs and non-TNBCs are completely obscure. The grade of defect in metabolic and hormonal equilibrium seems to be directly associated with TNBC risk for women during their whole life. Inverse impact of menopausal status or parity on the development of ER+ and ER- breast cancers is quite impossible; these erroneous results derive from the misinterpretation of statistical evaluations. There are fairly complex associations between excessive and defective estrogen signaling (multiparity and nulliparity) and cancer development. The tumor suppressing effect of excessive and the deliberating effect of defective estrogen signaling have disproportional impact on ER+ and ER- breast cancers. Exogenous or parity associated excessive estrogen supply is highly defensive against all breast cancer subtypes, but ER- tumors; such as TNBCs are more resistant. The most important preventive strategy against breast cancers - included TNBCs - in women is the strict control and maintenance of hormonal equilibrium from early adolescence through a lifetime, particularly during the periods of great hormonal changes. Effective breast cancer therapy requires complete conversion. Worldwide administration of antiestrogens for breast cancer treatment yielded thorough disappointment. By contrast, publications on successful estrogen treatment of advanced breast cancer cases are increasing in number and their results are encouraging.
|Title of host publication||Recent Avenue to Cancer Prevention|
|Publisher||Nova Science Publishers, Inc.|
|Number of pages||30|
|ISBN (Print)||9781629487120, 9781629486703|
|Publication status||Published - Jan 1 2014|
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