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 – MGI References 9157997 – National Library of Medicine/PubMed |
| 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 |
|
Intestine |
very high |