Cancro e sperimentazione: siamo davvero così simili agli animali?

Esistono spesso pubblicazioni, come le seguenti, che pur essendo di parte (pro-sperimentazione), ci danno spunti interessanti, forse inconsapevolmente, per capire quanto il modello animale – in questo caso nello studio del cancro – sia poco predittivo e soggetto a problemi metodologici:

“It is concluded that the lifetime feeding study has never been subjected to proper validation as an assay for human carcinogens. When an attempt is made to validate it on the basis of these reported studies and those in the literature, it appears to lack acceptable specificity and sensitivity. It is suggested that a drastically different design is needed and that such redesigning of the assay will require proper validation.”
[David Salsburg. The lifetime feeding study in mice and rats — An examination of its validity as a bioassay for human carcinogens. Fundamental and Applied Toxicology Volume 3, Issue 1, January–February 1983, Pages 63–67]

“The chemicals showing no or unclear carcinogenic effects in humans were more likely to show toxic side effects in the animal studies, indicating that the test concentrations were above the maximum tolerated dose. In addition, the animal experiments with these chemicals more often showed neoplastic effects on multiple sites than chemicals for which clear positive epidemiological studies are available. These findings may explain the existence of discrepancies between the outcomes of animal testing and human studies. They suggest that carcinogenic effects in multiple organs in animals could be seen as ultimate manifestations of the side effects of the testing method and that they have limited predictive value for the human situation.”
[Meijers JM, Swaen GM, Bloemen LJ. The predictive value of animal data in human cancer risk assessment. Regul Toxicol Pharmacol. 1997 Apr;25(2):94-102.]

“Furthermore, the value of the bioassay is itself questionable. The inconsistencies in tumor responses between rodent species and strains, the simultaneous tumor increase and decreases within a study and the susceptibility to tumorigenicity from non-genotoxic chemicals by mechanisms now shown to be of no relevance to humans, together make the use of rodents highly misleading as predictors of human cancer risk.”
[Monro A. Are lifespan rodent carcinogenicity studies defensible for pharmaceutical agents? Exp Toxicol Pathol. 1996 Feb;48(2-3):155-66.]

“Methodological issues in the interpretation of animal cancer tests: constraints on the estimation of carcinogenic potency and validity problems associated with using the limited data from bioassays to estimate human risk, reproducibility of results in carcinogenesis bioassays, comparison of lifetable and summary methods of analysis, and summarizing carcinogenic potency when multiple experiments on a chemical are positive.”
[Gold LS, Slone TH, Ames BN. What do animal cancer tests tell us about human cancer risk?: Overview of analyses of the carcinogenic potency database. Drug Metab Rev. 1998 May;30(2):359-404.]

“Cancer arises from a stepwise accumulation of genetic changes that liberates neoplastic cells from the homeostatic mechanisms that govern normal cell proliferation. In humans, at least four to six mutations are required to reach this state, but fewer seem to be required in mice.”
[Hahn WC, Weinberg RA. Modelling the molecular circuitry of cancer. Nat Rev Cancer. 2002 May;2(5):331-41.]



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