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Carcinogenesis Advance Access published online on December 29, 2005

Carcinogenesis, doi:10.1093/carcin/bgi323
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received September 12, 2005
Revised October 30, 2005
Accepted December 17, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Inhibition of CWR22R{nu}1 tumor growth and PSA secretion in athymic nude mice by green and black teas

Imtiaz A. Siddiqui 1, Najia Zaman 1, Moammir H. Aziz 1, Shannon R. Reagan-Shaw 1, Sami Sarfaraz 1, Vaqar M. Adhami 1, Nihal Ahmad 1, Sheikh Raisuddin 2, and Hasan Mukhtar 1 *

1 Department of Dermatology, University of Wisconsin-Madison, WI-53706
2 Department of Medical Elementology and Toxicology, Hamdard University, New Delhi, India

* To whom correspondence should be addressed.
Hasan Mukhtar, E-mail: hmukhtar{at}wisc.edu


   Abstract

Cancer of the prostate gland (CaP), the most common invasive malignancy and a major cause of cancer related deaths in male population in the USA, is an ideal candidate disease for chemoprevention because it is typically detected in elderly population with a relatively slower rate of growth and progression. Many dietary phytochemicals are showing promising chemopreventive effects, at-least in pre-clinical models of CaP. Our published data in cell culture and animal studies, supported by the work from other laboratories, as well as epidemiological observations and case control studies, suggest that polyphenols present in green tea possess CaP chemopreventive and possibly therapeutic effects. This present study was designed to compare CaP cancer chemopreventive effects of green tea polyphenols (GTP), water extract of black tea (BTE), and their major constituents epigallocatechin-3-gallate (EGCG) and theaflavins (TF), respectively, in athymic nude mice implanted with androgen sensitive human CaP CWR22R{nu}1 cells. Our data demonstrated that the treatment with all the tea ingredients resulted in i) significant inhibition in growth of implanted prostate tumors, ii) reduction in the level of serum prostate specific antigen, iii) induction of apoptosis accompanied with upregulation in Bax and decrease in Bcl-2 proteins, and iv) decrease in the levels of VEGF protein. Furthermore, we also found that GTP (0.01% or 0.05% w/v; given after establishment of CWR22R{nu}1 tumor), causes a significant regression of tumors suggesting therapeutic effects of GTP at human achievable concentrations.


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