polyethylene glycol suppresses colon cancer

From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Sun Feb 13 2000 - 17:27:10 MST

  Parnaud G. Tache S. Peiffer G. Corpet DE.
  Securite des Aliments, Institut National de la Recherche Agronomique, Ecole
  Nationale Veterinaire de Toulouse, France.
  suppresses colon cancer and causes dose-dependent regression
  of azoxymethane-induced aberrant crypt foci in rats.
  Cancer Research. 59(20):5143-7, 1999 Oct 15.
  Dietary polyethylene-glycol (PEG) 8000, a
  nonfermented polymer laxative, strongly suppresses
  azoxymethane-induced aberrant crypt foci (ACF) in the colon of rats, as shown
  in a previous study (D. E. Corpet et al., Carcinogenesis (Lond.), 20:
  915-918, 1999). In the present study, we tested the effect of PEG
  administered during either initiation or postinitiation, the dose-response
  effect of PEG, the regressive effect of PEG on established ACF, and the
  preventive effect of PEG on colon cancers in rats. The general design was to
  initiate carcinogenesis in F344 rats by a single injection of azoxymethane
  (20 mg/kg) and to randomize the animals 7 days later to AIN-76 diets
  containing 5% PEG or no PEG (control). At termination, ACF and tumors were
  scored blindly by a single observer. The administration of 5% PEG for 32 days
  to groups of 10 female rats in either food or drinking water reduced the
  number of ACF by a factor of 8 (P = 0.0002) and reduced the number of large
  ACF by a factor of 20-30 (P = 0.002). No protection was afforded when PEG was
  given only during the initiation phase. Diets containing 0%, 0.5%, 2%, or 5%
  PEG fed for 35 days to four groups of male rats inhibited ACF in a
  dose-dependent manner (P < 0.0001). The administration of a 5% PEG diet for
  41 days, starting 42 days after carcinogen injection, led to a 73% decrease
  in the number of ACF (P < 0.0001). Dietary PEG thus caused the regression of
  established ACF. Macroscopic tumors were evaluated by histology in rats that
  had been fed a high-fat diet containing cooked casein to promote tumor growth
  for 81 days. In this accelerated model of carcinogenesis, dietary PEG
  suppressed the occurrence of colon adenomas and carcinomas: the incidence of
  tumors decreased from 70% to 10% (P = 0.005); and the multiplicity decreased
  from 2.1 to 0.1 tumor(s)/rat (P = 0.003). No cancer was detected in the
  PEG-fed rats. Taken together, these results suggest that PEG could be a
  potent anticancer agent in the postinitiation phase of carcinogenesis.
  Because PEG is a substance that is generally recognized as safe (GRAS list,
  Food and Drug Administration), its cancer-preventive features could be tested
  in humans.

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