Carcinogenesis, Vol 18, 2197-2203, Copyright © 1997 by Oxford University Press
CW van der Houven van Oordt, R Smits, SL Williamson, A Luz, PM Khan, R Fodde, AJ van der Eb and ML Breuer
Seven-week-old Apc1638N mice were exposed to a single dose of 5 Gy
total-body X-irradiation resulting in a 8-fold increase in the number of
intestinal tumors and a reduction of the lifespan to an average of 6
months. The distribution of tumors along the intestinal tract as well as
the adenoma/carcinoma ratio, were similar between non-irradiated and
irradiated animals. Semi-quantitative PCR analysis of intestinal-tumor DNA
revealed that 10 out of 14 tumors had lost the wild-type Apc allele.
However, in contrast to spontaneous Apc1638N intestinal tumors in which the
LOH event at the Apc locus involves the entire chromosome 18 (1), in 6 out
of 10 tumors derived from X-irradiated animals the Apc loss is associated
with only a partial intrachromosomal deletion. The remaining tumors have
lost all chromosome 18 markers tested. In addition to the intestinal
tumors, female Apc1638N mice are susceptible to the development of mammary
tumors. Upon X-irradiation, Apc1638N mice show a striking 15-fold increase
in mammary tumors. Moreover, Apc1638N mice spontaneously develop other
extra-intestinal neoplasia, such as desmoid-like lesions similar to those
associated with familial adenomatous polyposis (FAP), the human syndrome
caused by germline mutations in the APC gene. Spontaneous desmoid growth is
sex-dependent, as male Apc1638N mice develop 3-fold more desmoids than
female mice. Interestingly, X-irradiation seemed to increase the number of
desmoids per animal nearly twofold only in female Apc1638N mice. Five out
of 9 desmoids found in Apc1638N mice exposed to X-ray displayed loss of the
wild-type Apc allele.
ARTICLES
Intestinal and extra-intestinal tumor multiplicities in the Apc1638N mouse model after exposure to X-rays
Department of Molecular Carcinogenesis, Leiden University, The Netherlands.
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