Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype

Tetsuya Tsukamoto; Masami Yamamoto; Hiroko Fukami; Akemi Yoshikawa; Hiroki Sakai; Akihiro Hirata; Moriaki Kusakabe; Masae Tatematsu

doi:10.1016/j.canlet.2005.08.004

Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype

Tetsuya Tsukamoto, Masami Yamamoto, Hiroko Fukami, Akemi Yoshikawa, Hiroki Sakai, Akihiro Hirata, Moriaki Kusakabe, Masae Tatematsu

Research output: Contribution to journal › Article › peer-review

4 Citations (Scopus)

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.

Original language	English
Pages (from-to)	205-211
Number of pages	7
Journal	Cancer Letters
Volume	239
Issue number	2
DOIs	https://doi.org/10.1016/j.canlet.2005.08.004
Publication status	Published - 08-08-2006
Externally published	Yes

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

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title = "Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype",

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.",

author = "Tetsuya Tsukamoto and Masami Yamamoto and Hiroko Fukami and Akemi Yoshikawa and Hiroki Sakai and Akihiro Hirata and Moriaki Kusakabe and Masae Tatematsu",

year = "2006",

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doi = "10.1016/j.canlet.2005.08.004",

language = "English",

volume = "239",

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journal = "Cancer Letters",

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publisher = "Elsevier Ireland Ltd",

number = "2",

}

Susceptibility to colon carcinogenesis in C3H↔C57BL/6 chimeric mice reflects both tissue microenvironment and genotype. / Tsukamoto, Tetsuya; Yamamoto, Masami; Fukami, Hiroko; Yoshikawa, Akemi; Sakai, Hiroki; Hirata, Akihiro; Kusakabe, Moriaki; Tatematsu, Masae.

In: Cancer Letters, Vol. 239, No. 2, 08.08.2006, p. 205-211.

Research output: Contribution to journal › Article › peer-review

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

PY - 2006/8/8

Y1 - 2006/8/8

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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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