ArticleCancer research2009
Long-lived Min mice develop advanced intestinal cancers through a genetically conservative pathway.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 38 citations in OpenAlex.
- BAMLET administration via drinking water inhibits intestinal tumor development and promotes long-term health.Scientific reports · 2024Article
- Mouse models in colon cancer, inferences, and implications.iScience · 2023Review
- Induction of colorectal carcinogenesis in the C57BL/6J and A/J mouse strains with a reduced DSS dose in the AOM/DSS model.Laboratory animal research · 2021Article
- Mouse models of colorectal cancer: Past, present and future perspectives.World journal of gastroenterology · 2020Review
- Natural Killer T-Cell Agonist α-Galactosylceramide and PD-1 Blockade Synergize to Reduce Tumor Development in a Preclinical Model of Colon Cancer.Frontiers in immunology · 2020Article
- Orange is the new black: Kinases are the new master regulators of tumor suppression.IUBMB life · 2019Review
- AIBP and APOA-I synergistically inhibit intestinal tumor growth and metastasis by promoting cholesterol efflux.Journal of translational medicine · 2019Article
- The path to metastatic mouse models of colorectal cancer.Oncogene · 2018Review
- Papilloma-pseudovirus eradicates intestinal tumours and triples the lifespan of ApcNature communications · 2017Article
- Dclk1, a tumor stem cell marker, regulates pro-survival signaling and self-renewal of intestinal tumor cells.Molecular cancer · 2017Article
- Cecal microbiota association with tumor load in a colorectal cancer mouse model.Microbial ecology in health and disease · 2017Article
- The Effects of Genetic Background of Mouse Models of Cancer: Friend or Foe?Cold Spring Harbor protocols · 2016Article
- Heterochromatin Protein 1 Binding Protein 3 Expression as a Candidate Marker of Intrinsic 5-Fluorouracil Resistance.Anticancer research · 2016Article
- Article
- Colon Tumors with the Simultaneous Induction of Driver Mutations in APC, KRAS, and PIK3CA Still Progress through the Adenoma-to-carcinoma Sequence.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- Mouse models of colorectal cancer as preclinical models.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
- Genetic Manipulation of Homologous Recombination In Vivo Attenuates Intestinal Tumorigenesis.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- DCLK1 facilitates intestinal tumor growth via enhancing pluripotency and epithelial mesenchymal transition.Oncotarget · 2014Article
- Human cancer xenografts in outbred nude mice can be confounded by polymorphisms in a modifier of tumorigenesis.Genetics · 2014Article
- Dynamic tumor growth patterns in a novel murine model of colorectal cancer.Cancer prevention research (Philadelphia, Pa.) · 2014Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
Abstract
C57BL/6J mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenomas along the entire length of the intestine and consequently die at an early age. This short lifespan would prevent the accumulation of somatic genetic mutations or epigenetic alterations necessary for tumor progression. To overcome this limitation, we generated F(1) Apc(Min/+) hybrids by crossing C57BR/cdcJ and SWR/J females to C57BL/6J Apc(Min/+) males. These hybrids developed few intestinal tumors and often lived longer than 1 year. Many of the tumors (24-87%) were invasive adenocarcinomas, in which neoplastic tissue penetrated through the muscle wall into the mesentery. In a few cases (3%), lesions metastasized by extension to regional lymph nodes. The development of these familial cancers does not require chromosomal gains or losses, a high level of microsatellite instability, or the presence of Helicobacter. To test whether genetic instability might accelerate tumor progression, we generated Apc(Min/+) mice homozygous for the hypomorphic allele of the Nijmegen breakage syndrome gene (Nbs1(DeltaB)) and also treated Apc(Min/+) mice with a strong somatic mutagen. These imposed genetic instabilities did not reduce the time required for cancers to form nor increase the percentage of cancers nor drive progression to the point of distant metastasis. In summary, we have found that the Apc(Min/+) mouse model for familial intestinal cancer can develop frequent invasive cancers in the absence of overt genomic instability. Possible factors that promote invasion include age-dependent epigenetic changes, conservative somatic recombination, or direct effects of alleles in the F(1) hybrid genetic background.
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Registered trials
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.