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Year : 2015  |  Volume : 52  |  Issue : 2  |  Page : 251-254

Heterozygosity of stromelysin-1 (rs3025058) promoter polymorphism is associated with gastric cancer

1 Department of Cell Biology, Institute of Genetics and Hospital for Genetic Diseases, Hyderabad, India
2 Department of Gastroenterology, Gandhi Hospital, Secunderabad, Andhra Pradesh, India
3 Department of Genetics, Osmania University, Hyderabad, India

Correspondence Address:
A Venkateshwari
Department of Cell Biology, Institute of Genetics and Hospital for Genetic Diseases, Hyderabad
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Source of Support: Financial support from University Grants Commission (Research Fellowship in Science for Meritorious Students to Krishnaveni D) is kindly acknowledged, Conflict of Interest: None

DOI: 10.4103/0019-509X.175806

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Background: Gastric cancer (GC) is the third most common cancer in India and is mediated by multiple genetic, epigenetic and environmental risk factors. A single nucleotide polymorphism rs3025058 at − 1171 of the stromelysin-1 (matrix metalloproteinase [MMP]-3) promoter is resulting due to insertion/deletion of adenine thought to have an impact on increasing the risk for tumor formation. Aim: This study is aimed to understand the role of stromelysin-1 rs3025058 (−1171, 5A/6A) promoter polymorphism in the etiology of GC in Indian population. Materials And Methods: Genomic DNA was isolated from blood samples of the GC patients and controls. The genotyping of stromelysin-1 rs3025058 (−1171, 5A/6A) promoter polymorphism was carried out by amplification refractory mutation system-polymerase chain reaction method followed by agarose gel electrophoresis. RESULTS: The frequency of 5A/5A, 5A/6A, and 6A/6A genotypes in GC patients were 7.69%, 76.92%, and 15.38%, while in controls were 5.31%, 86.73%, and7.96%, respectively. There was a significant difference in the distribution of 5A/6A genotype in patients compared to the controls (P < 0.05). Conclusion: This study showed an increased frequency of heterozygotes for stromelysin-1 rs3025058 and thought to be involved in the etiology of GC.


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