Polycystic ovary syndrome (PCOS) is currently the leading cause of menstrual complications in women. It is characterized by clinical and/or biochemical hyperandrogenism, ovulation abnormalities and the presence of enlarged and/or polycystic ovaries in ultrasound images (12 or more small bubbles located circumferentially and/or ovarian volume > 10 mL). It is often comorbid with hyperinsulinemia, dyslipidemia, overweight or obesity, and is a risk factor for the development of diabetes and cardiovascular diseases (CVDs). The treatment of patients with PCOS depends on the prevailing symptoms. The aim of this paper is to present the etiopathogenesis, clinical and biochemical implications, and non-pharmacological and pharmacological treatment options -those approved by worldwide scientific organizations as well as new therapies whose initial results are encouraging enough to prompt researchers to explore them further.

P53 is a transcription factor very often mutated in malignancies. It functions towards the regulation of important cellular activities, such as cell cycle, senescence and apoptosis. Since inflammation and cancer are strongly associated through common pathways, P53 can suppress inflammation in a plethora of human tissues. Growth Hormone - Releasing Hormone is a hypothalamic peptide with a great capacity to affect the complex networks of cellular regulation via GHRH - specific receptors. GHRH antagonistic and agonistic analogs have been developed for clinical applications, including treatment of benign prostatic hyperplasia, breast, prostate and lung cancers, diabetes and neurodegenerative diseases. The epicenter of the current manuscript is the protective role of P53 against inflammation and cancer and emphasizes the p53 – mediated beneficial effects of GHRH antagonists in various human diseases.

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OBJECTIVE To assess the mechanism by which the luteinizing hormone‐releasing hormone (LHRH) antagonist cetrorelix exerts its effects in men with benign prostatic hyperplasia (BPH), as it produces a long‐lasting improvement in lower urinary tract symptoms that is only partly accounted for by the transient reduction in testosterone levels, and the beneficial results could be due to direct inhibitory effects of cetrorelix on the prostate exerted through prostatic LHRH receptors. MATERIALS AND METHODS Using the BPH‐1 cell line we evaluated the effects of cetrorelix in vitro on the proliferation and the expression of receptors for LHRH, epidermal growth factor (EGF), α1A‐adrenergic receptor, STAT‐3 transcription factor and the response to growth factors insulin‐like growth factor (IGF)‐1 and ‐II and fibroblast growth factor (FGF)‐2. RESULTS There was expression of LHRH receptors in the human BPH‐1 cell line. Cetrorelix had inhibitory effects on the proliferation rate of BPH‐1 cells, also reflected by the decrease in the expression of the proliferating cell nuclear antigen (PCNA). Cetrorelix inhibited the stimulatory effect of the growth factors IGF‐I and ‐II and FGF‐2 on the proliferation of this line. Cetrorelix also downregulated the expression of the receptors for LHRH and EGF, as well as of α1A‐adrenergic receptors, and inhibited the activation of the STAT3 transcription factor. CONCLUSIONS The results show that in vitro cetrorelix can directly inhibit the proliferation rate of the human BPH‐1 cell line by counteracting growth factors like IGF‐I and ‐II and FGF‐2, and downregulating the LHRH receptor and α‐adrenergic receptors, as well as transcription factors.