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Polymorphism of the p38 beta gene in patients with colorectal cancer
Jönköping University, School of Health and Welfare, HHJ, Dep. of Natural Science and Biomedicine. Jönköping University, School of Health and Welfare, HHJ. Biomedical Platform.
Department of Laboratory Services, Ryhov County Hospital, Jönköping.
Clinical Microbiology, Ryhov County Hospital, Jönköping.
Department of Laboratory Services, Ryhov County Hospital, Jönköping.
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2014 (English)In: Oncology Letters, ISSN 1792-1074, E-ISSN 1792-1082, Vol. 8, 1093-1095 p.Article in journal (Refereed) Published
Abstract [en]

The p38 mitogen‑activated protein kinase (MAPK) signaling pathways have been proposed to participate in the pathological process of cancer by affecting inflammation, proliferation, metastasis and cell survival. A single nucleotide polymorphism (SNP; rs2235356, ‑1628A→G) in the promoter region of the p38β gene has been proposed as a genetic modifier for colorectal cancer (CRC) in a Chinese population. The present study evaluated the susceptibility of patients possessing this SNP to CRC, in addition to determining its association with clinical parameters in Swedish patients with CRC. Using the LightSNiP genotyping assay, this SNP was screened in 389 patients with CRC and 517 control subjects. No significant difference in the genotype distribution or in the allelic frequencies was identified between the two groups nor was any association identified with the clinical parameters. These findings indicate that the ‑1628A→G polymorphism of the p38β gene is not significantly associated with a susceptibility to CRC in a Swedish population.

Place, publisher, year, edition, pages
2014. Vol. 8, 1093-1095 p.
Keyword [en]
p38β, promoter region, single nucleotide polymorphism, colorectal cancer
National Category
Cancer and Oncology
Identifiers
URN: urn:nbn:se:hj:diva-24249DOI: 10.3892/ol.2014.2315ISI: 000340854600024OAI: oai:DiVA.org:hj-24249DiVA: diva2:734332
Available from: 2014-07-16 Created: 2014-07-16 Last updated: 2017-12-05Bibliographically approved

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