TY - JOUR T1 - Analysis of <em>MSH2</em> Loss of Heterozygosity, Expression, and IVS10+12G&gt;A Polymorphism in Sporadic Colon Cancer JF - Anticancer Research JO - Anticancer Res SP - 2841 LP - 2848 VL - 38 IS - 5 AU - TAMARA CACEV AU - EMILIJA ZAPLETAL AU - VESNA MUSANI AU - IVANA RAKO AU - BOZO LONCAR AU - GORANA ARALICA AU - SANJA KAPITANOVIC Y1 - 2018/05/01 UR - http://ar.iiarjournals.org/content/38/5/2841.abstract N2 - Background: mutS homolog 2 (MSH2) deficiency may be involved in the development of microsatellite instability found in certain sporadic colorectal tumors. In addition to mutations or loss of heterozygosity resulting in complete loss of MSH2 function, polymorphisms affecting MSH2 expression have been also identified. Therefore, the aim of this study was to examine MSH2 status in sporadic colon cancer. Materials and Methods: MSH2 status was examined at the DNA, RNA and protein levels through loss of heterozygosity (LOH) analysis, quantitative real-time PCR and immunohistochemistry. MSH2 IVS10+12A&gt;G polymorphism was examined by real-time single nucleotide polymorphism genotyping. Results: MSH2 LOH was more frequent in tumors larger than 5 cm (p=0.032), mRNA expression was also significantly lower and the same expression pattern was present in the corresponding normal mucosa of the same patient (p=0.013 and p=0.008, respectively). No association was found between IVS10+12A&gt;G polymorphism and susceptibility to sporadic colon cancer. Conclusion: Altered MSH2 expression detected in sporadic colon tumors pointing to its role in colorectal tumorigenesis without a hereditary component. ER -