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Anna Spada

Researcher at University of Milan

Publications -  326
Citations -  13577

Anna Spada is an academic researcher from University of Milan. The author has contributed to research in topics: Pituitary tumors & Acromegaly. The author has an hindex of 60, co-authored 322 publications receiving 12683 citations. Previous affiliations of Anna Spada include Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico.

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GTPase inhibiting mutations activate the α chain of G s and stimulate adenylyl cyclase in human pituitary tumours

TL;DR: A subset of growth hormone-secreting human pituitary tumours carries somatic mutations that inhibit GTPase activity of a G protein α chain, αs, which results in the activation of adenylyl cyclase, which bypasses the cells' normal requirement for trophic hormone.
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Altered Gs and adenylate cyclase activity in human GH-secreting pituitary adenomas.

TL;DR: A profoundly altered Gs protein is found in a group of human growth hormone-secreting pituitary adenomas, characterized by high secretory activity and intracellular cyclic AMP levels.
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Clinical Characteristics and Therapeutic Responses in Patients with Germ-Line AIP Mutations and Pituitary Adenomas: An International Collaborative Study

Adrian Daly, +63 more
TL;DR: Prisposition for aggressive disease in young patients, often in a familial setting, suggests that earlier diagnosis of AIPmut pituitary adenomas may have clinical utility.
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Dopamine inhibits adenylate cyclase in human prolactin-secreting pituitary adenomas

TL;DR: It is reported here that in homogenates of human PRL adenomas, in which dopaminergic agonists act as inhibitors of PRL secretion, basal adenylate cyclase is inhibited by DA and the DA receptors mediating this inhibition have the same pharmacological properties as those regulatingPRL secretion.
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Clinical, biochemical, and morphological correlates in patients bearing growth hormone-secreting pituitary tumors with or without constitutively active adenylyl cyclase

TL;DR: The results suggest that patients with constitutively active adenylyl cyclase have hyperactive tumors; the sensitivity of these tumors to inhibitory agents (somatostatin and dopamine), possibly counteracting the expression of activating mutations, might explain the low rate of tumor growth.