Mice Lacking a Myc Enhancer That Includes Human SNP rs6983267 Are Resistant to Intestinal Tumors

Author:

Sur Inderpreet Kaur12,Hallikas Outi3,Vähärautio Anna13,Yan Jian1,Turunen Mikko3,Enge Martin1,Taipale Minna13,Karhu Auli4,Aaltonen Lauri A.4,Taipale Jussi13

Affiliation:

1. Science for Life Center, Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.

2. Clinical Research Center, Karolinska University Hospital, Stockholm, Sweden.

3. Genome-Scale Biology Program, Institute of Biomedicine, University of Helsinki, Biomedicum, Post Office Box 63 (Haartmaninkatu 8), University of Helsinki, FI-00014 Helsinki, Finland.

4. Genome-Scale Biology Program, Department of Medical Genetics, University of Helsinki, Biomedicum, Post Office Box 63 (Haartmaninkatu 8), University of Helsinki, FI-00014 Helsinki, Finland.

Abstract

From Man to Mouse Genome-wide association studies of humans have identified single-nucleotide polymorphisms (SNPs) that increase an individual's risk of developing common diseases like cancer. Most of these SNPs have only a modest effect on risk, and many map to noncoding regions of the genome. Sur et al. (p. 1360 , published online 1 November; see the Perspective by Lewis and Tomlinson ) used a mouse model to study the functional impact of a particular SNP that resides 300 kilobases upstream of the MYC oncogene on human chromosome 8q24 and has been linked to cancer risk in humans. When a sequence encompassing this SNP was deleted in mice that were predisposed to develop intestinal tumors, the mice displayed fewer tumors than control mice. This SNP may thus play a causal role in human cancer, presumably through altered regulation of MYC.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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