Engineering a Prostate-Specific Membrane Antigen–Activated Tumor Endothelial Cell Prodrug for Cancer Therapy

Author:

Denmeade Samuel R.1,Mhaka Annastasiah M.1,Rosen D. Marc1,Brennen W. Nathaniel1,Dalrymple Susan1,Dach Ingrid2,Olesen Claus2,Gurel Bora1,DeMarzo Angelo M.1,Wilding George3,Carducci Michael A.1,Dionne Craig A.4,Møller Jesper V.25,Nissen Poul26,Christensen S. Brøgger7,Isaacs John T.1

Affiliation:

1. The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.

2. Centre for Membrane Pumps in Cells and Disease (PUMPKIN), Danish National Research Foundation, DK-8000 Aarhus, Denmark.

3. University of Wisconsin, Madison, WI 52792, USA.

4. GenSpera Inc., San Antonio, TX 78258, USA.

5. Institute of Physiology and Biophysics, Aarhus University, DK-8000 Aarhus, Denmark.

6. Department of Molecular Biology and Genetics, Aarhus University, DK-8000 Aarhus, Denmark.

7. Department of Medicinal Chemistry, University of Copenhagen, DK-2100 Copenhagen, Denmark.

Abstract

A prostate-specific membrane antigen–activated prodrug selectively kills cancer cells and is being tested in patients with advanced cancer.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

Reference60 articles.

1. The role of calcium, pH, and cell proliferation in the programmed (apoptotic) death of androgen-independent prostatic cancer cells induced by thapsigargin;Furuya Y.;Cancer Res.,1994

2. Expression of bcl-2 and the progression of human and rodent prostatic cancers;Furuya Y.;Clin. Cancer Res.,1996

3. A supramicromolar elevation of intracellular free calcium ([Ca2+]i) is consistently required to induce the execution phase of apoptosis

4. Inhibition of caspase activity does not prevent the signaling phase of apoptosis in prostate cancer cells

5. Mechanism and role of growth arrest in programmed (apoptotic) death of prostatic cancer cells induced by thapsigargin

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