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Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes
Cancer is caused by multiple genetic alterations leading to uncontrolled cell proliferation through multiple pathways. Malignant cells arise from a variety of genetic factors, such as mutations in tumor suppressor genes (TSGs) that are involved in regulating the cell cycle, apoptosis, or cell differ...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Libertas Academica
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3153120/ https://www.ncbi.nlm.nih.gov/pubmed/21836819 http://dx.doi.org/10.4137/CMO.S7516 |
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author | Taneja, Pankaj Zhu, Sinan Maglic, Dejan Fry, Elizabeth A. Kendig, Robert D. Inoue, Kazushi |
author_facet | Taneja, Pankaj Zhu, Sinan Maglic, Dejan Fry, Elizabeth A. Kendig, Robert D. Inoue, Kazushi |
author_sort | Taneja, Pankaj |
collection | PubMed |
description | Cancer is caused by multiple genetic alterations leading to uncontrolled cell proliferation through multiple pathways. Malignant cells arise from a variety of genetic factors, such as mutations in tumor suppressor genes (TSGs) that are involved in regulating the cell cycle, apoptosis, or cell differentiation, or maintenance of genomic integrity. Tumor suppressor mouse models are the most frequently used animal models in cancer research. The anti-tumorigenic functions of TSGs, and their role in development and differentiation, and inhibition of oncogenes are discussed. In this review, we summarize some of the important transgenic and knockout mouse models for TSGs, including Rb, p53, Ink4a/Arf, Brca1/2, and their related genes. |
format | Online Article Text |
id | pubmed-3153120 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Libertas Academica |
record_format | MEDLINE/PubMed |
spelling | pubmed-31531202011-08-11 Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes Taneja, Pankaj Zhu, Sinan Maglic, Dejan Fry, Elizabeth A. Kendig, Robert D. Inoue, Kazushi Clin Med Insights Oncol Review Cancer is caused by multiple genetic alterations leading to uncontrolled cell proliferation through multiple pathways. Malignant cells arise from a variety of genetic factors, such as mutations in tumor suppressor genes (TSGs) that are involved in regulating the cell cycle, apoptosis, or cell differentiation, or maintenance of genomic integrity. Tumor suppressor mouse models are the most frequently used animal models in cancer research. The anti-tumorigenic functions of TSGs, and their role in development and differentiation, and inhibition of oncogenes are discussed. In this review, we summarize some of the important transgenic and knockout mouse models for TSGs, including Rb, p53, Ink4a/Arf, Brca1/2, and their related genes. Libertas Academica 2011-07-28 /pmc/articles/PMC3153120/ /pubmed/21836819 http://dx.doi.org/10.4137/CMO.S7516 Text en © the author(s), publisher and licensee Libertas Academica Ltd. This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited. |
spellingShingle | Review Taneja, Pankaj Zhu, Sinan Maglic, Dejan Fry, Elizabeth A. Kendig, Robert D. Inoue, Kazushi Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes |
title | Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes |
title_full | Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes |
title_fullStr | Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes |
title_full_unstemmed | Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes |
title_short | Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes |
title_sort | transgenic and knockout mice models to reveal the functions of tumor suppressor genes |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3153120/ https://www.ncbi.nlm.nih.gov/pubmed/21836819 http://dx.doi.org/10.4137/CMO.S7516 |
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