ArticleClinical Medicine Insights. Oncology2013
Recent progress in mouse models for tumor suppressor genes and its implications in human cancer.
Article in Clinical Medicine Insights. Oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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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.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Genetically Modified Mouse Models for Sarcoma Research: A Comprehensive Review.Current oncology reports · 2025Review
- Diverse landscape of genetically engineered mouse models: Genomic and molecular insights into prostate cancer.Cancer letters · 2024Review
- PTEN Mouse Models of Cancer Initiation and Progression.Cold Spring Harbor perspectives in medicine · 2020Review
- Methylation and PTEN activation in dental pulp mesenchymal stem cells promotes osteogenesis and reduces oncogenesis.Nature communications · 2019Article
- c-MYB and DMTF1 in Cancer.Cancer investigation · 2019Review
- Functional link between plasma membrane spatiotemporal dynamics, cancer biology, and dietary membrane-altering agents.Cancer metastasis reviews · 2018Review
- Translocations involving ETS family proteins in human cancer.Integrative cancer science and therapeutics · 2018Article
- Expression of DNA doublestrand repair proteins in oral leukoplakia and the risk of malignant transformation.Oncology letters · 2018Article
- Cftr Modulates Wnt/β-Catenin Signaling and Stem Cell Proliferation in Murine Intestine.Cellular and molecular gastroenterology and hepatology · 2018Article
- Aberrant expression of ETS1 and ETS2 proteins in cancer.Cancer reports and reviews · 2018Article
- Tumor suppression by the EGR1, DMP1, ARF, p53, and PTEN Network.Cancer investigation · 2018Article
- Oncogenic and tumor-suppressive mouse models for breast cancer engaging HER2/neu.International journal of cancer · 2017Review
- AKT in cancer: new molecular insights and advances in drug development.British journal of clinical pharmacology · 2016Review
- Novel Molecular Markers for Breast Cancer.Biomarkers in cancer · 2016Review
- Clinical applications of mouse models for breast cancer engaging HER2/neu.Integrative cancer science and therapeutics · 2016Article
- The PTEN/PI3K/AKT Pathway in vivo, Cancer Mouse Models.Frontiers in oncology · 2014Review
- Haploinsufficient tumor suppressor genes.Advances in medicine and biologyArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Gain-of-function mutations in oncogenes and loss-of-function mutations in tumor suppressor genes (TSG) lead to cancer. In most human cancers, these mutations occur in somatic tissues. However, hereditary forms of cancer exist for which individuals are heterozygous for a germline mutation in a TSG locus at birth. The second allele is frequently inactivated by gene deletion, point mutation, or promoter methylation in classical TSGs that meet Knudson's two-hit hypothesis. Conversely, the second allele remains as wild-type, even in tumors in which the gene is haplo-insufficient for tumor suppression. This article highlights the importance of PTEN, APC, and other tumor suppressors for counteracting aberrant PI3K, β-catenin, and other oncogenic signaling pathways. We discuss the use of gene-engineered mouse models (GEMM) of human cancer focusing on Pten and Apc knockout mice that recapitulate key genetic events involved in initiation and progression of human neoplasia. Finally, the therapeutic potential of targeting these tumor suppressor and oncogene signaling networks is discussed.
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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.