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The genetic background modifies the spontaneous and X‐ray–induced tumor spectrum in the Apc 1638N mouse model
Author(s) -
van der Houven van Oordt C. Willemien,
Smits Ron,
Schouten Theo G.,
HouwingDuistermaat Jeanine J.,
Williamson Sophia L.H.,
Luz Arne,
Khan P. Meera,
van der Eb Alex J.,
Breuer Marco L.,
Fodde Riccardo
Publication year - 1999
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199903)24:3<191::aid-gcc3>3.0.co;2-l
Subject(s) - multiplicity (mathematics) , allele , biology , adenomatous polyposis coli , irradiation , broad spectrum , cancer research , genetics , chemistry , gene , colorectal cancer , cancer , mathematical analysis , physics , nuclear physics , combinatorial chemistry , mathematics
The effect of the genetic background on the tumor spectrum of Apc 1638N, a mouse model for attenuated familial adenomatous polyposis (FAP), has been investigated in X‐irradiated and untreated F1 hybrids between C57BL/6JIco‐ Apc 1638N (B6) and A/JCrlBR (A/J), BALB/cByJIco (C) or C3H/HeOuJIco (C3). Similar to the Apc Min model, the Apc 1638N intestinal tumor multiplicity seems to be modulated by Mom 1. Moreover, several additional (X‐ray–responsive) modifier loci appear also to affect the Apc 1638N intestinal tumor number. The genetic background did not significantly influence the number of spontaneous desmoids and cutaneous cysts in Apc 1638N. In general, X‐irradiation increased the desmoid multiplicity in Apc 1638N females but had no effect in males. The opposite was noted for the cyst multiplicity after X‐rays. Surprisingly, X‐irradiated CB6F1‐ Apc 1638N females were highly susceptible to the development of ovarian tumors, which displayed clear loss of the wild‐type Apc allele. Genes Chromosomes Cancer 24:191–198, 1999. © 1999 Wiley‐Liss, Inc.