Ricerc@Sapienza

Stress is a risk factor for impaired general, mental, and reproductive health. The role of physiological and supraphysiological estradiol concentrations in stress perception and stress processing is less well understood.

Wound healing is a physiological process that involves several successive and often overlapping phases that lead to the restoration of the integrity of the skin after an injury, accident or surgery: haemostasis and inflammation, proliferation and remodeling. The interruption or slowing down of these processes can cause abnormal or impaired wound healing. There are now numerous data and clinical studies that highlight the roles of estrogens on normal cutaneous homeostasis and wound healing.

Background:Differences in genetics and receptor expression (phenotypes) of invasive ductal breast cancer (IDC) impact on prognosis and treatment response. Immunohistochemistry (IHC), the most used technique for IDC phenotyping, has some limitations including its invasiveness.

Background: Hormone replacement therapy (HRT) has been tested in women with BRCA1 and BRCA2 mutations who underwent risk-reducing salpingo-oophorectomy (RRSO), but its effect on breast cancer (BC) risk has never been appraised using meta-analysis comparison. We performed the first meta-analysis aimed to clarify whether HRT after RRSO could negatively impact on BC risk in women carriers of BRCA1 and BRCA2 mutations. Methods and material: Pubmed and Scopus databases were searched to retrieve articles written in the English language.

Wound healing is a physiological process that involves several successive and often overlapping phases that lead to the restoration of the integrity of the skin after an injury, accident or surgery: haemostasis and inflammation, proliferation and remodeling. The interruption or slowing down of these processes can cause abnormal or impaired wound healing. There are now numerous data and clinical studies that highlight the role of estrogens on normal cutaneous homeostasis and wound healing.

Estrogen and hypoxia promote an aggressive phenotype in prostate cancer (PCa), driving transcription of progression-associated genes. Here, we molecularly dissect the contribution of long non-coding RNA H19 to PCa metastatic potential under combined stimuli, a topic largely uncovered. The effects of estrogen and hypoxia on H19 and cell adhesion molecules' expression were investigated in PCa cells and PCa-derived organotypic slice cultures (OSCs) by qPCR and Western blot. The molecular mechanism was addressed by chromatin immunoprecipitations, overexpression, and silencing assays.