Methylation status of p16 INK4A tumor suppressor gene in Iranian patients with sporadic breast cancer.

J Cancer Res Clin Oncol

Division of Genetics, Department of Biology, Faculty of Science, The University of Isfahan, Hezarjerib St., Isfahan, Islamic Republic of Iran.

Published: August 2009

AI Article Synopsis

  • p16(INK4A) is a tumor suppressor gene that inhibits Cdk4/6, and its inactivation can occur through various mechanisms such as promoter hypermethylation.
  • The study analyzed the methylation status of the p16(INK4A) gene in 70 Iranian breast cancer patients using methylation-specific PCR and other methods, finding significant hypermethylation in about 35.7% to 40% of samples.
  • Results suggest that the hypermethylation of the p16(INK4A) promoter may play a key role in the early stages of breast cancer development in these patients.

Article Abstract

Introduction: p16(INK4A) is a tumor suppressor encoding the Cdk inhibitor protein, which acts to repress Cdk4/6 and pRb phosphorylation. p16(INK4A) gene can be inactivated by a variety of events, including promoter hypermethylation.

Materials And Methods: To investigate the methylation status of the p16(INK4A) gene in Iranian patients with breast carcinoma, promoter methylation was studied by methylation-specific PCR (MSP) and restriction enzyme-related PCR (REP). In addition, p16(INK4A) promoter was analyzed by PCR-SSCP in order to detection of mutation and single nucleotide polymorphisms.

Results: Analysis of 70 patients by MPS and REP showed hypermethylation of p16(INK4A) promoter in 35.7% (25/70) and 40% (28/70) of samples, respectively. Comparison of the molecular data and pathological information of the samples suggested that p16(INK4A) gene might be inactivated at the early stages in breast cancer.

Conclusion: Therefore, it could be suggested that hypermethylation of p16(INK4A) promoter is one of the epigenetic factors affecting the progress of sporadic breast carcinogenesis in Iranian patients.

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Source
http://dx.doi.org/10.1007/s00432-008-0534-8DOI Listing

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