Reference SummaryShoemaker AR, Cancer Res 1997 May 15;57(10):1999-2006

Title

Somatic mutational mechanisms involved in intestinal tumor formation in Min mice.

Authors

Shoemaker AR; Luongo C; Moser AR; Marton LJ; Dove WF

Journal

Cancer Res

Volume

57

Issue

10

Year

1997

Pages

1999-2006

Abstract

We have demonstrated previously that intestinal tumor formation in B6 Min/+ mice is always accompanied by loss of the wild-type adenomatous polyoposis coli (Apc) allele and that intestinal tumor multiplicity in B6 Min/+ mice can be significantly increased by treatment with a single dose of N-ethyl-N-nitrosourea (ENU), Here, we show that some tumors from ENU-treated Min/+ mice can form without complete elimination of Apc(+). At least 25% of these tumors acquired somatic Apc truncation mutations, Interestingly, some ENU-induced tumors demonstrated loss of the Apc(+) allelic marker examined by the quantitative PCR assay used here, Using two methods of mutation detection, we identified no Apc mutations in at least 12% of the tumors from ENU-treated B6 Min/+ mice. Finally, no H- or K-ras-activating mutations were detected in intestinal tumors from either untreated or ENU-treated Min/+ mice, The majority of somatic human APC mutations in intestinal tumors lead to APC truncation. Our results demonstrate that somatic Apc truncation mutations also frequently occur in ENU-induced intestinal tumors in Min mice.

Links

J:40435 – Mouse Genome Informatics
9157997 – National Library of Medicine/PubMed

Models

Strain Model Name Treatment Agent(s) Organ Affected Frequency Model Details
AKB6F1-ApcMin/+ Intestine adenoma Intestine

observed

AKB6F1-ApcMin/+ Intestine carcinoma in situ Intestine

observed

C57BL/6J-ApcMin/+ Intestine tumor
  • N-ethyl-N-nitrosourea (N-nitrosoethylurea) (ENU)
Intestine

very high