ArticleCancer letters2014
Colon-specific tumorigenesis in mice driven by Cre-mediated inactivation of Apc and activation of mutant Kras.
Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Review
- Keystone pathobionts associated with colorectal cancer promote oncogenic reprograming.PloS one · 2024Article
- Advancing translational research for colorectal immuno-oncology.British journal of cancer · 2023Review
- Mouse models in colon cancer, inferences, and implications.iScience · 2023Review
- Keystone pathobionts associated with colorectal cancer promote oncogenic reprograming.bioRxiv : the preprint server for biology · 2023Article
- Article
- Mouse models of colorectal cancer: Past, present and future perspectives.World journal of gastroenterology · 2020Review
- APC gene 3'UTR SNPs and interactions with environmental factors are correlated with risk of colorectal cancer in Chinese Han population.Bioscience reports · 2020Article
- Multiple Roles of APC and its Therapeutic Implications in Colorectal Cancer.Journal of the National Cancer Institute · 2017Review
- Transplantation of engineered organoids enables rapid generation of metastatic mouse models of colorectal cancer.Nature biotechnology · 2017Article
- Mouse model of proximal colon-specific tumorigenesis driven by microsatellite instability-induced Cre-mediated inactivation of Apc and activation of Kras.Journal of gastroenterology · 2016Article
- Single and Multiple Gene Manipulations in Mouse Models of Human Cancer.Cancer growth and metastasis · 2015Review
- Colorectal cancer models for novel drug discovery.Expert opinion on drug discovery · 2015Review
- Zinc-α-2-glycoprotein: a candidate biomarker for colon cancer diagnosis in Chinese population.International journal of molecular sciences · 2014Article
- The utility of Apc-mutant rats in modeling human colon cancer.Disease models & mechanisms · 2014Review
- Animal models of gastrointestinal and liver diseases. New mouse models for studying dietary prevention of colorectal cancer.American journal of physiology. Gastrointestinal and liver physiology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Several genetically engineered mouse (GEM) models of colorectal cancer have been developed and are a mainstay in our efforts to identify means of preventing and treating this disease. Many of these models involve a germline disruption of the adenomatous polyposis coli (Apc) tumor suppressor gene and share the limitation that the great preponderance of tumors appear in the small rather than large intestine. In recent years efforts have been made to increase the similarity of these models to human sporadic colorectal cancer by disrupting Apc in a tissue-specific fashion using the Cre-Lox system so that the genetic aberrations are confined to the colonic epithelium. These models have shown great promise but reproducible and high penetrance colon-specific tumorigenesis has not yet been achieved without invasive techniques to introduce the Cre enzyme. We therefore sought to create a new model with high penetrance colon-specific tumorigenesis but without the need for exogenous Cre administration. We utilized existing mice possessing a conditional knock out for the Apc gene and a latent activated Kras allele and crossed them with mice expressing Cre recombinase solely in the large intestine. Using this approach we generated mice that developed 1-9 colonic adenomas per mouse (average 4.3) but without any tumors in the small intestine or cecum. No invasive tumors were observed. Despite the apparent lack of invasion, the geographical correctness, complete penetrance and intermediate tumor burden make this model a promising addition to our toolkit for the study of colorectal cancer treatment and prevention.
Indexed as
Identifiers
What OpenQuestion holds
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.