Evidence of cellular senescence during the development of estrogen-induced pituitary tumors.

SABATINO ME; PETITI JP; SOSA LDEL V; PÉREZ PA; GUTIÉRREZ S; LEIMGRUBER C; LATINI A; TORRES AI; DE PAUL AL

BIOSCIENTIFICA LTD

Lugar: Bristol; Año: 2015 vol. 3 p. 299 - 299

lthough pituitary adenomas represent 25% of intracranial tumors, they are usually benign, with the mechanisms by which these tumors usually avoid an invasive profile and metastatic growth development still remaining unclear. In this context, cellular senescence might constitute a plausible explanation for the benign nature of pituitary adenomas. In this study, we investigated the emergence of cellular senescence as a growth control mechanism during the progression of estrogen-induced pituitary tumors. The quantification of Ki67-immunopositive cells in the pituitaries of estrogenized male rats after 10, 20, 40, and 60 days revealed that the mitogenic potential rate was not sustained for the whole period analyzed and successively decreased after 10 days of estrogen exposure. In addition, the expression of cellular senescence features, such as the progressive rise in the enzymatic senescence-associated b-galactosidase (SA-b-gal) activity, IL6, IL1b, and TGFb expression, was observed thro