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Atkin NB: Chromosome 1 aberrations in cancer. Cancer Genet Cytogenet 1986;21:279–285. Atkin NB: Non-random chromosomal changes in human neoplasia; in Obe G (ed): Eukaryotic Chromosomes: Structural and Functional Aspects. New Dehli, Narosa, 1991, pp 153–164. Fabarius A, Willer A, Yerganian G, Hehlmann R, Duesberg P: Specific aneusomies in Chinese hamster cells at different stages of neoplastic transformation, initiated by nitrosomethylurea. Proc Natl Acad Sci USA 2002;99:6778–6783. Pejonic T, Heim S, Oerndal C, Jin Y, Mandahl N, Willen H, Mitelman F: Simple numerical chromosome aberrations in well-defined malignant epithelial tumors.
Contrary to the mutation hypothesis, many carcinogens are not mutagens, including some of the most potent ones. Examples are asbestos, tar, mineral oils, naphthalene, polycyclic aromatic hydrocarbons, butter yellow, urethane, dioxin, hormones, metal ions such as Ni, Cd, Cr, As, spindle blockers such as vincristine and colcemid, extranuclear radiation and solid plastic or metal implants [40, 44, 67, 70, 73, 158, 166, 168]. 2 No Transforming Genes. Despite years of efforts no genes or combinations of genes from cancers have been shown to transform normal cells to cancer cells [4, 5, 138] or mice carrying such genes in their germ lines into polyclonal tumors [1, 24, 56].
This evolution would be slow in the preneoplastic phase, because preneoplastic cells have no growth advantages over normal cells and because the degree of preneoplastic aneuploidy is typically low. By comparison the rate of karyotype variations of most cancer cells would be fast, because cancer cells form large populations by outgrowing normal cells and because the degrees of cancer-specific aneuploidy are typically high. Any kind of cancer could have as many specific aneusomies as there are chromosomes involved in the differentiation of its precursor cell in addition to random aneusomies.