Like all NSMG's posts, this is a lie too. Interestingly, the quercetin
in ProstaQ PREVENTS cancer in lab rats. A recent sampling of 120
published papers on the subject:

 
Induction of rat hepatic and intestinal UDP-glucuronosyltransferases
by naturally occurring dietary anticarcinogens.

Van Der Logt EM, Roelofs HM, Nagengast FM, Peters WH.

Department of Gastroenterology, University Medical Centre St Radboud,
Nijmegen, The Netherlands.

Gastrointestinal tumours are among the most common malignancies in
Western society, the majority of which is associated with dietary and
lifestyle factors. Many dietary or lifestyle factors have been
identified which may have toxic or carcinogenic properties. However,
also several dietary compounds able to reduce gastrointestinal cancer
rates both in humans and animals have been characterised. Though the
exact mechanism leading to the anticarcinogenic action of these
compounds is not fully known, it has been demonstrated that this
chemopreventive capacity may be due to elevation of the glutathione
S-transferase detoxification enzymes. Now we investigated the effect
of several anticarcinogens on the gastrointestinal
UDP-glucuronosyltransferase (UGT) enzymes. Diets of male Wistar rats
were supplemented with ellagic acid, ferulic acid, Brussels sprouts,
quercetin, alpha-angelicalactone, tannic acid, coumarin, fumaric acid,
curcumin and flavone separately, and combinations of
alpha-angelicalactone and flavone. Hepatic and intestinal (proximal-,
mid-, distal small intestine and colon) UGT enzyme activities were
quantified by using 4-nitrophenol and 4-methylumbelliferone as
substrates. All anticarcinogens tested increased UGT enzyme activity
with both substrates, at least at one of the five different sites
investigated. alpha-Angelicalactone, coumarin and curcumin showed
enhanced UGT enzyme activities at all five sites. Both small and large
intestinal UGT enzyme activities were increased by quercetin,
alpha-angelicalactone, coumarin, curcumin and flavone. Except for
tannic acid, all agents induced hepatic UGT enzyme activity.
Furthermore, dietary administration of alpha-angelicalactone and
flavone, given individually or in combination, enhanced the UGT
detoxification system in the liver and to a lesser extent in
intestine. In conclusion, induction of gastrointestinal UGT enzyme
activities after consumption of dietary anticarcinogens, may
contribute to a better detoxification of potentially carcinogenic
compounds and subsequently to the prevention of gastrointestinal
cancer.

PMID: 12869420 [PubMed - as supplied by publisher]

2: Nutr Cancer. 2002;43(2):193-201.
 
Suppression of intestinal crypt cell proliferation and aberrant crypt
foci by dietary quercetin in rats.

Gee JM, Hara H, Johnson IT.

Institute of Food Research Norwich Laboratory, Norwich Research Park,
Colney, Norwich, Norfolk NR4 7UA, UK. jenny.gee@bbsrc.ac.uk

Quercetin inhibits proliferation of human gastric and colonic cancer
cells in vitro by suppressing mitosis and increasing apoptosis.
Quercetin might therefore act as an anticarcinogen in the alimentary
tract, but previous findings have been inconsistent. We fed rats
quercetin at dietary concentrations of 1, 5, 20, and 50 g/kg. At < or
= 20 g/kg, we observed a statistically significant reduction in the
frequency of crypt cell mitosis in proximal, mid, and distal small
intestine and in distal colon, amounting to approximately 40% of
control at 1 g/kg. There was no effect on apoptosis. Quercetin
metabolites, but not quercetin aglycone, were detected in plasma of
rats fed quercetin at 20 and 50 g/kg. In a second experiment, rats
were fed quercetin at 1 g/kg after treatment with
1,2-dimethylhydrazine to induce aberrant crypt foci. In
dimethylhydrazine-treated and control rats, crypt cell mitosis was
suppressed at 48 h and 42 days after injection, and there was a
statistically significant reduction in the number of aberrant crypts
and larger aberrant crypt foci (> 4 crypts/focus) in the distal colon
of treated animals. These findings demonstrate that quercetin can
inhibit intestinal crypt cell proliferation in vivo, but the effect
diminishes as the level of dietary exposure increases. At low
concentrations, dietary quercetin inhibits induction of aberrant
crypts by a mechanism that does not involve increased crypt cell
apoptosis.

PMID: 12599752 [PubMed - indexed for MEDLINE]

3: Carcinogenesis. 2002 Sep;23(9):1447-54.
 
Altered expression of c-myc, p16 and p27 in rat colon tumors and its
reversal by short-term treatment with chemopreventive agents.

Tao L, Kramer PM, Wang W, Yang S, Lubet RA, Steele VE, Pereira MA.

Department of Pathology, HEB, Rm 202, Medical College of Ohio, 3055
Arlington Ave., Toledo, OH 43614-5806, USA. ltao@mco.edu

Modulation of gene expression in tumors has the potential of being a
surrogate end-point biomarker for chemoprevention. Thus, we determined
the modulation by chemopreventive agents of the protein and mRNA
expression of genes in rat colon tumors. Male F344 rats were
administered three weekly injections of 15 mg/kg azoxymethane.
Forty-seven weeks later, they received aspirin (600), calcium chloride
(50 000), 2-(carboxyphenyl) retinamide (2-CPR, 315),
alpha-difluoromethylornithine (DFMO, 3000), piroxicam (200), quercetin
(33 600), 9-cis retinoic acid (9-cis RA, 30), rutin (3000), or
sulindac (280) in their diet at the indicated mg/kg concentration for
7 days and were then killed. In colon tumors relative to the mucosa,
the protein and mRNA levels of c-myc were increased, while the levels
of p16 and p27 were decreased. Calcium chloride, DFMO, piroxicam and
sulindac administered for 7 days decreased the mitotic index and
reduced the protein and mRNA levels of c-myc in colon tumors. Calcium
chloride, DFMO and piroxicam increased the protein and mRNA levels of
p16 and along with sulindac increased the protein level of p27, but
not its mRNA. The other agents failed to modulate both the mitotic
index and the expression of the genes. The ability of the
chemopreventive agents to prevent colon tumors was determined. Male
F344 rats were administered three weekly injections of 15 mg/kg
azoxymethane and 8 weeks later they were administered aspirin, 2-CPR,
DFMO, piroxicam, 9-cis RA and rutin in their diet. The rats were
killed 26 weeks after they started to receive the chemopreventive
agents. The multiplicity of colon tumors was reduced by DFMO and
piroxicam, increased by rutin and not affected by the other agents.
Hence, agents that prevented colon cancer decreased the mitotic index
and altered the expression of c-myc, p16 and p27 suggesting that
modulation in the expression of these genes are potential biomarkers
for chemopreventive activity.

PMID: 12189186 [PubMed - indexed for MEDLINE]

4: Free Radic Res. 2001 Dec;35(6):779-88.


Anticarcinogenic antioxidants as inhibitors against intracellular
oxidative stress.

Feng Q, Kumagai T, Torii Y, Nakamura Y, Osawa T, Uchida K.

Laboratory of Food and Biodynamics, Graduate School of Bioagricultural
Sciences, Nagoya University, Japan.

Oxidative stress has been implicated in the pathogenesis of numerous
diseases, including cancer. In the present study, the protective
effect of natural antioxidants, such as quercetin and tea polyphenols,
on intracellular oxidative stress was studied. Here we report a novel
function of quercetin and tea polyphenols, as potential inhibitors of
4-hydroxy-2-nonenal (HNE)-induced intracellular oxidative stress and
cytotoxicity. In rat liver epithelial RL34 cells, a potent
electrophile HNE dramatically induced the productions of reactive
oxygen species (ROS), which correlated well with the reduction in cell
viability. We found that quercetin and tea polyphenols, such as
epigallocatechin gallate and theaflavins and their gallate esters,
significantly inhibited the HNE-induced ROS production and
cytotoxicity. In addition, HNE induced a transient decrease in the
mitochondrial membrane potential (delta psi), which was also retarded
by the antioxidants. These data suggest that the antioxidants, such as
quercetin and tea polyphenols, are inhibitors against mitochondrial
ROS production.

PMID: 11811529 [PubMed - indexed for MEDLINE]