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Marcella Motta

Researcher at University of Milan

Publications -  171
Citations -  5084

Marcella Motta is an academic researcher from University of Milan. The author has contributed to research in topics: Receptor & LNCaP. The author has an hindex of 42, co-authored 171 publications receiving 4931 citations. Previous affiliations of Marcella Motta include Sapienza University of Rome.

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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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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.
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Expression of a leptin receptor in immortalized gonadotropin-releasing hormone-secreting neurons.

TL;DR: The present results indicate that GT1-7 cells possess OB-Rs and that leptin may directly affect their function, and suggest that leptin might participate in the regulation of reproductive processes by acting at multiple levels, both centrally and peripherally.
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The Androgen Derivative 5α-Androstane-3β,17β-Diol Inhibits Prostate Cancer Cell Migration Through Activation of the Estrogen Receptor β Subtype

TL;DR: In this paper, the 5alpha-reduced testosterone derivative, dihydrotestosterone (the most potent natural androgen) inhibits cell migration with an androgen receptor-independent mechanism.