ReviewOncogene1999
Mouse models for colorectal cancer.
Review in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 118 citations in OpenAlex.
- Article
- Novel read through agent: ZKN-0013 demonstrates efficacy in APCJournal of molecular medicine (Berlin, Germany) · 2023Article
- Tumor models to assess immune response and tumor-microbiome interactions in colorectal cancer.Pharmacology & therapeutics · 2022Review
- Statin Treatment as a Targeted Therapy for APC-Mutated Colorectal Cancer.Frontiers in oncology · 2022Article
- Recurrent Frameshift Neoantigen Vaccine Elicits Protective Immunity With Reduced Tumor Burden and Improved Overall Survival in a Lynch Syndrome Mouse Model.Gastroenterology · 2021Article
- Loss of enteric neuronal Ndrg4 promotes colorectal cancer via increased release of Nid1 and Fbln2.EMBO reports · 2021Article
- Genetic and biological hallmarks of colorectal cancer.Genes & development · 2021Review
- MMP7 as a potential biomarker of colon cancer and its prognostic value by bioinformatics analysis.Medicine · 2021Article
- Heterozygous APC germline mutations impart predisposition to colorectal cancer.Scientific reports · 2021Article
- Loss of mismatch repair signaling impairs the WNT-bone morphogenetic protein crosstalk and the colonic homeostasis.Journal of molecular cell biology · 2020Article
- Colorectal carcinogenesis: Insights into the cell death and signal transduction pathways: A review.World journal of gastrointestinal oncology · 2018Review
- Advantages of patient-derived orthotopic mouse models and genetic reporters for developing fluorescence-guided surgery.Journal of surgical oncology · 2018Review
- Development of Preclinical Models to Understand and Treat Colorectal Cancer.Clinics in colon and rectal surgery · 2018Review
- The effect of a germline mutation in the APC gene on β-catenin in human embryonic stem cells.BMC cancer · 2016Article
- Host-Protozoan Interactions Protect from Mucosal Infections through Activation of the Inflammasome.Cell · 2016Article
- Growth hormone is permissive for neoplastic colon growth.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The Innate Immune Receptor NLRX1 Functions as a Tumor Suppressor by Reducing Colon Tumorigenesis and Key Tumor-Promoting Signals.Cell reports · 2016Article
- A panoply of errors: polymerase proofreading domain mutations in cancer.Nature reviews. Cancer · 2016Review
- Mouse models for the discovery of colorectal cancer driver genes.World journal of gastroenterology · 2016Review
- The role of testosterone in colorectal carcinoma: pathomechanisms and open questions.The EPMA journal · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is one of the most common cancers in the Western world. Much has been learned about colorectal cancer from human inherited syndromes, such as familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC). Mouse models for CRC were generated by introducing mutations into the mouse genes, whose human counterparts were implicated in the onset and progression of CRC. Central among these are mice carrying mutations in the Adenomatous polyposis coli (Apc) gene. Although most of these Apc mutations share some common phenotypes as homozygous embryonic lethality and tumor predisposition, the severity of the tumor predisposition is variable. Mice with mutations in the mismatch repair genes, Msh2 and Mlh1, exhibit a mismatch repair defect and are predisposed to developing gastrointestinal cancer, lymphomas and tumors of other organ systems. Mice carrying a mutation in the Pms2 gene are predisposed to lymphomas and other tumors. Mice with a mutation in the Msh6 gene have a defect in base mismatch repair and show a tumor predisposition phenotype. Mice with mutations in Mlh1, Pms2 and Msh5 have defects in meiosis suggesting unique roles for these genes in gametogenesis.
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.