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Abstract
This article presents a general discussion about the participation of oxidative stress in relevant points related to breast cancer progression in vitro. All of the evidences presented here are based on published papers that used breast cancer cells with different phenotype characteristics in their research. We observed that oxidative stress could modulate by several manners the tumor progression and these effects are directly related to its concentration and time of cell exposure to these substances. Furthermore, oxidative stress produced and released by breast cancer cells is able to interfere in the metabolism of the adjacent normal cells in a manner that improve the survival of the neoplastic cells. In relation to breast cancer treatment, the role of oxidative stress is complex. At the same time that it can be responsible to the induction of cell death, oxidative stress can also modulate pathway that leads to increased expression of anti-apoptotic and resistance-related proteins. Therefore, the participation of oxidative stress in breast cancer is complex and very broad and its better understanding could be important to the development of more effective therapeutic strategies for the different forms clinically found of the disease.
Highlights
The oxidative stress is caused by an imbalance between pro-oxidant substances and intracellular antioxidant defense system promoting the establishment of an environment composed of highly unstable molecules that are able to react with significant cellular structures such as proteins, lipids and DNA
It was concluded that the importance of the involvement of the oxidative stress in breast cancer cells can be divided into three fundamental points: Oxidative stress and tumor progression; oxidative stress and tumor microenvironment influence and oxidative stress and treatment response
The studies using breast cancer cell lines with different phenotype characteristics showed that, in most cases, the increase in oxidative stress is related to cell death
Summary
The oxidative stress is caused by an imbalance between pro-oxidant substances and intracellular antioxidant defense system promoting the establishment of an environment composed of highly unstable molecules that are able to react with significant cellular structures such as proteins, lipids and DNA. By presenting high heterogeneity due to many phenotypes and different clinical and morphological presentations, the disease has a wide variation in clinical responses, which hinders the cancer treatment availability Within this context, the term targeted therapy has been used to describe new drugs that were planned based on the knowledge of the fundamental molecular pathology of the disease. Studies have shown that more than 30% of mammary carcinomas over express the HER 2 receptor and this increased expression is most frequent in cells that do not possess Estrogen Receptors (ER) than in those ones that do This cancer type has characteristics that are more aggressive and the target of its therapy consists of the administration of a monoclonal antibody specific for HER 2 or the administration of inhibitors of tyrosine kinases EGFR/HER2, thereby blocking the intracellular signaling
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