Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2115754 | Cancer Letters | 2006 | 7 Pages |
Abstract
Considerable rodent strain differences have been documented with regard to susceptibility to colon carcinogens. To clarify mechanisms, chimeras of susceptible strain C3H and relatively resistant strain C57BL/6N (B6) mice were exposed to a colonotropic carcinogen, 1,2-dimethylhydrazine (DMH) and tumor incidence and multiplicity were assessed. In the chimeras, incidence was as high as the C3H level. Multiplicity of lesions of B6 cells was also increased (P<0.001), but maintenance of the strain difference. When tumor localization was analyzed, tumors of B6 genotype in chimeras demonstrated a greater spread of distribution than in the parental case. The chimeric environment may thus stimulate tumor initiation but cell autonomous suppressive factors may be retained.
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Authors
Tetsuya Tsukamoto, Masami Yamamoto, Hiroko Fukami, Akemi Yoshikawa, Hiroki Sakai, Akihiro Hirata, Moriaki Kusakabe, Masae Tatematsu,