ArticleProceedings of the National Academy of Sciences of the United States of America1998
A resistant genetic background leading to incomplete penetrance of intestinal neoplasia and reduced loss of heterozygosity in ApcMin/+ mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- Overview of research progress and application of experimental models of colorectal cancer.Frontiers in pharmacology · 2023Review
- The Effects of Genetic Background of Mouse Models of Cancer: Friend or Foe?Cold Spring Harbor protocols · 2016Article
- Genetic Manipulation of Homologous Recombination In Vivo Attenuates Intestinal Tumorigenesis.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- More than two decades of Apc modeling in rodents.Biochimica et biophysica acta · 2013Review
- Loss of HLTF function promotes intestinal carcinogenesis.Molecular cancer · 2012Article
- Monoallelic silencing and haploinsufficiency in early murine intestinal neoplasms.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Reduction of pancreatic acinar cell tumor multiplicity in Dnmt1 hypomorphic mice.Carcinogenesis · 2011Article
- Distinguishing between cancer driver and passenger gene alteration candidates via cross-species comparison: a pilot study.BMC cancer · 2010Article
- Enhanced intestinal tumor multiplicity and grade in vivo after HZE exposure: mouse models for space radiation risk estimates.Radiation and environmental biophysics · 2010Article
- Long-lived Min mice develop advanced intestinal cancers through a genetically conservative pathway.Cancer research · 2009Article
- APC and its modifiers in colon cancer.Advances in experimental medicine and biology · 2009Review
- Widespread hyperplasia induced by transgenic TGFalpha in ApcMin mice is associated with only regional effects on tumorigenesis.Carcinogenesis · 2008Article
- The pleiotropic phenotype of Apc mutations in the mouse: allele specificity and effects of the genetic background.Genetics · 2008Article
- Helicobacter hepaticus infection promotes colon tumorigenesis in the BALB/c-Rag2(-/-) Apc(Min/+) mouse.Infection and immunity · 2008Article
- Regulation of epithelial branching morphogenesis and cancer cell growth of the prostate by Wnt signaling.PloS one · 2008Article
- A protective role of mast cells in intestinal tumorigenesis.Carcinogenesis · 2008Article
- Article
- The modifier of Min 2 (Mom2) locus: embryonic lethality of a mutation in the Atp5a1 gene suggests a novel mechanism of polyp suppression.Genome research · 2007Article
- A target-selected Apc-mutant rat kindred enhances the modeling of familial human colon cancer.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Previous studies of Min/+ (multiple intestinal neoplasia) mice on a sensitive genetic background, C57BL/6 (B6), showed that adenomas have lost heterozygosity for the germ-line ApcMin mutation in the Apc (adenomatous polyposis coli) gene. We now report that on a strongly resistant genetic background, AKR/J (AKR), Min-induced adenoma multiplicity is reduced by about two orders of magnitude compared with that observed on the B6 background. Somatic treatment with a strong mutagen increases tumor number in AKR Min/+ mice in an age-dependent manner, similar to results previously reported for B6 Min/+ mice. Immunohistochemical analyses indicate that Apc expression is suppressed in all intestinal tumors from both untreated and treated AKR Min/+ mice. However, the mechanism of Apc inactivation in AKR Min/+ mice often differs from that observed for B6 Min/+ mice. Although loss of heterozygosity is observed in some tumors, a significant percentage of tumors showed neither loss of heterozygosity nor Apc truncation mutations. These results extend our understanding of the effects of genetic background on Min-induced tumorigenesis in several ways. First, the AKR strain carries modifiers of Min in addition to Mom1. This combination of AKR modifiers can almost completely suppress spontaneous intestinal tumorigenesis associated with the Min mutation. Second, even on such a highly resistant genetic background, tumor formation continues to involve an absence of Apc function. The means by which Apc function is inactivated is affected by genetic background. Possible scenarios are discussed.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.