Evidence indicates that prolactin plays a crucial role in the normal function and development of the prostate, but abnormal high levels of the hormone are associated with hyperplasia and cancer of the gland. Aims: The present study was designed to describe the progressive specific histological abnormalities in the prostate of rats with chronic hyperprolactinemia. Material and Methods: Prolactin was administered during 4; 12 or 24 weeks, and the resulting prostatic alterations were compared with control rats, and also with those treated with testosterone, or the combination of prolactin + testosterone. Results: Rats treated with prolactin, testosterone or prolactin + testosterone expressed precancerous histological abnormalities in the dorsolateral and ventral portions of the prostate as early as in 4 weeks of treatment, but in all cases the malignancy increased after 12 or 24 weeks of treatment. Conclusion: Our study confirms that chronic hyperprolactinemia is a cause of prostate precancerous pathologies.
Breast cancer (BC) is the first malignant neoplasm in women, with a high death rate despite early diagnoses and treatment advances. Significant differences exist between the most common BC and triple-negative breast cancer (TNBC). TNBC presents molecular differences such as lacking expression of the estrogen receptor (ER), progesterone receptor (PR), and HER2 proteins, making this cancer have a poor clinical prognostic and lack clear strategies for its treatment. However, growing evidence points to metabolic dysregulation as another differential process between stages and types of BC. Therefore, the study of this crucial hallmark could identify new therapeutic targets to treat this aggressive form of BC. These differences induce an in vitro exploration of the metabolic behavior of the MCF7 cells (nTNBC) and MDA-MB-231 (TNBC) cells under lipidomic based LC–MS. The results show more significant differences in lipid regulation (phosphatidylethanolamine) that could be associated with the aggressiveness and difficulties of the treatment of TNBC.
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