| First Author | Shoemaker AR | Year | 1997 |
| Journal | Cancer Res | Volume | 57 |
| Issue | 10 | Pages | 1999-2006 |
| PubMed ID | 9157997 | Mgi Jnum | J:40435 |
| Mgi Id | MGI:87779 | Citation | Shoemaker AR, et al. (1997) Somatic mutational mechanisms involved in intestinal tumor formation in Min mice. Cancer Res 57(10):1999-2006 |
| abstractText | 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. |
