Literature DB >> 19068450

Genetically modified mouse models in cancer studies.

Javier Santos1, Pablo Fernández-Navarro, María Villa-Morales, Laura González-Sánchez, José Fernández-Piqueras.   

Abstract

Genetically modified animals represent a resource of immense potential for cancer research. Classically, genetic modifications in mice were obtained through selected breeding experiments or treatments with powerful carcinogens capable of inducing random mutagenesis. A new era began in the early 1980s when genetic modifications by inserting foreign DNA genes into the cells of an animal allowed for the development of transgenic mice. Since that moment, genetic modifications have been able to be made in a predetermined way. Gene targeting emerged later as a method of in vivo mutagenesis whereby the sequence of a predetermined gene is selectively modified within an intact cell. In this review we focus on how genetically modified mice can be created to study tumour development, and how these models have contributed to an understanding of the genetic alterations involved in human cancer. We also discuss the strengths and weaknesses of the different mouse models for identifying cancer genes, and understanding the consequences of their alterations in order to obtain the maximum benefit for cancer patients.

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Year:  2008        PMID: 19068450     DOI: 10.1007/s12094-008-0292-8

Source DB:  PubMed          Journal:  Clin Transl Oncol        ISSN: 1699-048X            Impact factor:   3.405


  93 in total

Review 1.  Strategies for silencing human disease using RNA interference.

Authors:  Daniel H Kim; John J Rossi
Journal:  Nat Rev Genet       Date:  2007-03       Impact factor: 53.242

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Journal:  Nature       Date:  2007-03-08       Impact factor: 49.962

3.  Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras.

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Review 4.  Retroviral insertional mutagenesis: past, present and future.

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Journal:  Oncogene       Date:  2005-11-21       Impact factor: 9.867

Review 5.  Senescence, apoptosis and therapy--cutting the lifelines of cancer.

Authors:  Clemens A Schmitt
Journal:  Nat Rev Cancer       Date:  2003-04       Impact factor: 60.716

6.  Distinct epigenetic changes in the stromal cells of breast cancers.

Authors:  Min Hu; Jun Yao; Li Cai; Kurt E Bachman; Frédéric van den Brûle; Victor Velculescu; Kornelia Polyak
Journal:  Nat Genet       Date:  2005-07-10       Impact factor: 38.330

Review 7.  Cellular senescence as a tumor-suppressor mechanism.

Authors:  J Campisi
Journal:  Trends Cell Biol       Date:  2001-11       Impact factor: 20.808

8.  Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a.

Authors:  M Serrano; A W Lin; M E McCurrach; D Beach; S W Lowe
Journal:  Cell       Date:  1997-03-07       Impact factor: 41.582

9.  Frequent somatic mutations in PTEN and TP53 are mutually exclusive in the stroma of breast carcinomas.

Authors:  Keisuke Kurose; Kristie Gilley; Satoshi Matsumoto; Peter H Watson; Xiao-Ping Zhou; Charis Eng
Journal:  Nat Genet       Date:  2002-10-15       Impact factor: 38.330

10.  Pten is essential for embryonic development and tumour suppression.

Authors:  A Di Cristofano; B Pesce; C Cordon-Cardo; P P Pandolfi
Journal:  Nat Genet       Date:  1998-08       Impact factor: 38.330

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