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Patrizia Limonta

Researcher at University of Milan

Publications -  128
Citations -  4452

Patrizia Limonta is an academic researcher from University of Milan. The author has contributed to research in topics: Receptor & Prostate cancer. The author has an hindex of 36, co-authored 120 publications receiving 3813 citations. Previous affiliations of Patrizia Limonta include Population Council.

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miR-205 Exerts Tumor-Suppressive Functions in Human Prostate through Down-regulation of Protein Kinase Cε

TL;DR: Overall, it is shown for the first time that miR-205 exerts a tumor-suppressive effect in human prostate by counteracting epithelial-to-mesenchymal transition and reducing cell migration/invasion, at least in part through the down-regulation of protein kinase Cepsilon.
Journal Article

Antiproliferative Effects of Luteinizing Hormone-releasing Hormone (LHRH) Agonists on Human Androgen-independent Prostate Cancer Cell Line DU 145: Evidence for an Autocrine-inhibitory LHRH Loop

TL;DR: The data seem to indicate that an autocrine/paracrine L HRH (or LHRH-like) loop is present in androgen-independent prostate cancer cells, and may participate in the regulation of tumor cell growth.
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Antiproliferative effects of luteinizing hormone-releasing hormone agonists on the human prostatic cancer cell line LNCaP

TL;DR: The results clearly suggest that the antiproliferative effect of LHRH agonists on LNCaP cells may be mediated by specific receptors.
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GnRH and GnRH receptors in the pathophysiology of the human female reproductive system

TL;DR: Increasing knowledge about the regulation of GnRH pulsatile release, as well as the therapeutic use of its analogues, offers interesting new perspectives in the diagnosis, treatment and outcome of female reproductive disorders, including tumoral and iatrogenic diseases.
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The biology of gonadotropin hormone-releasing hormone: role in the control of tumor growth and progression in humans.

TL;DR: Observations point to GnRH-I as an autocrine negative regulatory factor on tumor growth progression and metastatization, and the molecular mechanisms underlying the peculiar antitumor activity of Gn RH-I are clarified.