Allelic Imbalance at an 8q24 Oncogenic SNP is Involved in Activating MYC in Human Colorectal Cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2014-01-06

AUTHORS

Keishi Sugimachi, Atsushi Niida, Ken Yamamoto, Teppei Shimamura, Seiya Imoto, Hisae Iinuma, Yoshiaki Shinden, Hidetoshi Eguchi, Tomoya Sudo, Masahiko Watanabe, Junichi Tanaka, Shinei Kudo, Kazuo Hase, Masato Kusunoki, Kazutaka Yamada, Yasuhiro Shimada, Kenichi Sugihara, Yoshihiko Maehara, Satoru Miyano, Masaki Mori, Koshi Mimori

ABSTRACT

Background The rs6983267 at 8q24.21 has been established as a significant cancer-related single nucleotide polymorphism (SNP). The risk allele showed similarity to the binding site of transcription factor TCF4/LEF1 that activates transcription of MYC. However, little is known about the role of this SNP in increasing MYC activity in colorectal cancers (CRCs).MethodsThe genotypes of rs6983267 in peripheral blood and primary cancers, MYC activity and copy number (CN) alteration were examined in 107 CRCs. Next, we plotted the number of cancers cell lines exhibiting specific G/T genotypes in 746 cancer cell lines of the Sanger Institute database. Then we validated the relationship between the 8q24 SNP status and clinicopathologic parameters in 68 CRCs with loss of heterozygosity (LOH).ResultsThe MYC module activity was activated by either transcription in the risk allele (G) or by amplification in the non-risk allele (T). Then, we confirmed that the CN amplification dominantly occurred in the non-risk allele, whereas CN neutral LOH, which indicated uniparental disomy (UPD) was more frequently observed for the risk allele. Finally, we confirmed that risk allele dominant cases, either by amplification or by UPD, indicated a more malignant clinical phenotype than non-risk allele dominant cases.ConclusionsThe development of CRC requires MYC activation through retention of the risk allele, or amplification of the non-risk allele at the oncogenic SNP in the site of primary tumor. More... »

PAGES

515-521

Journal

TITLE

Annals of Surgical Oncology

ISSUE

Suppl 4

VOLUME

21

Identifiers

URI

http://scigraph.springernature.com/pub.10.1245/s10434-013-3468-6

DOI

http://dx.doi.org/10.1245/s10434-013-3468-6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027596302

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24390711


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    "description": "Background\nThe rs6983267 at 8q24.21 has been established as a significant cancer-related single nucleotide polymorphism (SNP). The risk allele showed similarity to the binding site of transcription factor TCF4/LEF1 that activates transcription of MYC. However, little is known about the role of this SNP in increasing MYC activity in colorectal cancers (CRCs).MethodsThe genotypes of rs6983267 in peripheral blood and primary cancers, MYC activity and copy number (CN) alteration were examined in 107 CRCs. Next, we plotted the number of cancers cell lines exhibiting specific G/T genotypes in 746 cancer cell lines of the Sanger Institute database. Then we validated the relationship between the 8q24 SNP status and clinicopathologic parameters in 68 CRCs with loss of heterozygosity (LOH).ResultsThe MYC module activity was activated by either transcription in the risk allele (G) or by amplification in the non-risk allele (T). Then, we confirmed that the CN amplification dominantly occurred in the non-risk allele, whereas CN neutral LOH, which indicated uniparental disomy (UPD) was more frequently observed for the risk allele. Finally, we confirmed that risk allele dominant cases, either by amplification or by UPD, indicated a more malignant clinical phenotype than non-risk allele dominant cases.ConclusionsThe development of CRC requires MYC activation through retention of the risk allele, or amplification of the non-risk allele at the oncogenic SNP in the site of primary tumor.", 
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