TY - JOUR
T1 - Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype
AU - Tsukamoto, Tetsuya
AU - Yamamoto, Masami
AU - Fukami, Hiroko
AU - Yoshikawa, Akemi
AU - Sakai, Hiroki
AU - Hirata, Akihiro
AU - Kusakabe, Moriaki
AU - Tatematsu, Masae
N1 - Funding Information:
The authors thank Dr Malcolm Moore for valuable discussion. This work was supported in part by Grants-in-Aid for Cancer Research from the Ministry of Health, Labour and Welfare and by Grants-in-Aid from the Ministry of Education, Science, Sports, Technology and Culture of Japan.
PY - 2006/8/8
Y1 - 2006/8/8
N2 - 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.
AB - 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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U2 - 10.1016/j.canlet.2005.08.004
DO - 10.1016/j.canlet.2005.08.004
M3 - Article
C2 - 16168562
AN - SCOPUS:33745666495
SN - 0304-3835
VL - 239
SP - 205
EP - 211
JO - Cancer Letters
JF - Cancer Letters
IS - 2
ER -
