| Literature DB >> 10451698 |
C W van der Houven van Oordt1, R Smits, T G Schouten, J J Houwing-Duistermaat, S L Williamson, A Luz, P Meera Khan, A J van der Eb, M L Breuer, R Fodde.
Abstract
The effect of the genetic background on the tumor spectrum of Apc1638N, a mouse model for attenuated familial adenomatous polyposis (FAP), has been investigated in X-irradiated and untreated F1 hybrids between C57BL/6JIco-Apc1638N (B6) and A/JCrIBR (A/J), BALB/cByJIco (C) or C3H/HeOuJIco (C3). Similar to the ApcMin model, the Apc1638N intestinal tumor multiplicity seems to be modulated by Mom1. Moreover, several additional (X-ray-responsive) modifier loci appear also to affect the Apc1638N intestinal tumor number. The genetic background did not significantly influence the number of spontaneous desmoids and cutaneous cysts in Apc1638N. In general, X-irradiation increased the desmoid multiplicity in Apc1638N females but had no effect in males. The opposite was noted for the cyst multiplicity after X-rays. Surprisingly, X-irradiated CB6F1-Apc1638N females were highly susceptible to the development of ovarian tumors, which displayed clear loss of the wild-type Apc allele.Entities:
Mesh:
Year: 1999 PMID: 10451698 DOI: 10.1002/(sici)1098-2264(199903)24:3<191::aid-gcc3>3.0.co;2-l
Source DB: PubMed Journal: Genes Chromosomes Cancer ISSN: 1045-2257 Impact factor: 5.006