ABSTRACT
In the last decade, a group of Ca2+ channels called Piezo were discovered, demonstrating a decisive role in the cellular response to mechanical stimuli and being essential in the biological behavior of cells regarding the extracellular compartment. Several investigations have suggested a potential role in carcinogenesis, with a tumor suppressor role in some cases but increased expression in several high-grade neoplasms. Regarding Piezo2 expression in mammary gland neoplasms, a protective role for Piezo2 was initially suggested, but a subsequent study demonstrated a relationship between Piezo2 expression and the highly aggressive triple-negative phenotype of breast carcinoma. A cohort of 125 patients with clinical follow-up was chosen to study Piezo2 expression and clarify its clinical implications using the same immunohistochemical evaluation performed for other breast carcinoma parameters. Fisher's exact test was chosen to identify potential relationships between the different variables. A significant association was found with the Ki67 proliferation index, but not with mitoses. The tendency of most proliferative tumors was to have an increased score for Piezo2. A similar association was found between Piezo2 expression and perineural invasion.
ABSTRACT
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Subject(s)
Humans , Female , Middle Aged , Dyspnea/etiology , Adenocarcinoma, Bronchiolo-Alveolar/diagnosis , Lung Neoplasms/diagnosis , Radiography, ThoracicABSTRACT
Bartter syndrome can manifest in three different forms and is rarely concomitant with glomerular nephropathies. However, this association is more frequently observed in children. We report the case of a 50-year-old woman with Gitelman syndrome for the past 30 years who also had a nephrotic syndrome of recent appearance. Her renal biopsy revealed hyperplasia of the juxtaglomerular apparatus and mesangial deposits of C1q, with no clinical or serological evidence of systemic erythematous lupus. We have not found any reports of instances of association of Gitelman syndrome and nephrotic syndrome arising from C1q nephropathy in adult patients. Our case suggests the possible existence of an association between hypokalaemic tubular nephropathies and glomerular nephropathies that may cause nephrotic syndrome.
