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Anna C. Ferrari

Researcher at New York University

Publications -  32
Citations -  5933

Anna C. Ferrari is an academic researcher from New York University. The author has contributed to research in topics: Prostate cancer & LNCaP. The author has an hindex of 16, co-authored 32 publications receiving 5385 citations. Previous affiliations of Anna C. Ferrari include Icahn School of Medicine at Mount Sinai.

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Journal ArticleDOI

Sipuleucel-T immunotherapy for castration-resistant prostate cancer.

Philip W. Kantoff, +12 more
- 23 Jul 2010 - 
TL;DR: The use of sipuleucel-T prolonged overall survival among men with metastatic castration-resistant prostate cancer and immune responses to the immunizing antigen were observed in patients who received sipuleUcel- T.
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Dual action on promoter demethylation and chromatin by an isothiocyanate restored GSTP1 silenced in prostate cancer

L. G. Wang, +5 more
- 01 Jan 2007 - 
TL;DR: The PEITC‐mediated cross‐talk between the DNA and chromatin in demethylating and reactivating GSTP1 genes, which is critically inactivated in prostate carcinogenesis, underlines a primary mechanism of cancer chemoprevention.
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A phase II study of YM155, a novel small-molecule suppressor of survivin, in castration-resistant taxane-pretreated prostate cancer

Anthony W. Tolcher, +7 more
- 01 Apr 2012 - 
TL;DR: YM155 has modest activity in taxane-pretreated CRPC with 25% of patients having prolonged stable disease (≥18 weeks) and the regimen appears to be well tolerated.
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mTOR Signaling Pathway and mTOR Inhibitors in Cancer Therapy

Alejandro Gomez-Pinillos, +1 more
- 01 Jun 2012 - 
TL;DR: In this paper, dual PI3K/mTOR kinase inhibitors have been developed with the idea of overcoming resistance to the mTOR inhibition through preventing the activation of PI 3K/Akt as a result of release negative feedback loops.
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LEF1 in Androgen-Independent Prostate Cancer: Regulation of Androgen Receptor Expression, Prostate Cancer Growth, and Invasion

Yirong Li, +12 more
- 15 Apr 2009 - 
TL;DR: It is shown that LEF1 overexpression in LNCaP cells resulted in increased AR expression and consequently enhanced growth and invasion ability, whereas LEF 1 knockdown in L NCaP-AI cells decreased ARexpression and, subsequently, growth and invade capacity.