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J Gastrointest Oncol. 2016 Dec;7(6):989-995. doi: 10.21037/jgo.2016.06.07.

Diminished expression of .

Journal of gastrointestinal oncology

Arif Akbar Bhat, Hilal Ahmad Wani, Ajaz Ahmad Waza, Rawoof Ahmad Malik, Akbar Masood, Showkat Jeelani, Showkat Kadla, Sabhiya Majid

Affiliations

  1. Department of Biochemistry, Government Medical College Srinagar (Research Centre University of Kashmir), Srinagar, India.
  2. Multidisciplinary Research Unit, Government Medical College Srinagar, Srinagar, India.
  3. Department of Biotechnology, University of Kashmir, Hazratbal Srinagar, India.
  4. Department of Human Genetics, Punjabi University Patiala, Punjab, India.
  5. Department of Biochemistry, University of Kashmir, Hazratbal Srinagar, Srinagar, India.

PMID: 28078123 PMCID: PMC5177594 DOI: 10.21037/jgo.2016.06.07

Abstract

BACKGROUND: Cancer initiation and progression are accompanied by profound changes in DNA. DNA methylation that was the first epigenetic alterations identified in cancer. DNA hypermethylation at promoter sites is closely associated with down regulation of protein and as major participant in the development and progression of series of human tumors. Therefore we hypothesized that promoter hypermethylation of

METHODS: A hospital based case-control study; including 200 GC cases and 200 matched controls from patients who went surgical resection. Promoter hypermethylation was determined by Methylation Specific Polymerase chain reaction. The expression of MGMT & RASSF1A protein was examined by Western blotting technique.

RESULTS: Frequency of promoter region hypermethylation of

CONCLUSIONS: These findings indicate that promoter hypermethylation at CpG island may be responsible for reduction of expression at protein level which may be an initial event in carcinogenesis and the progression of GC.

Keywords: CpG island; Methylation specific PCR; epigenetics, hypermethylation; gastric cancer (GC)

Conflict of interest statement

The authors have no conflicts of interest to declare.

References

  1. Int J Cancer. 2015 Mar 1;136(5):E359-86 - PubMed
  2. Cancer Res. 2001 Sep 15;61(18):6688-92 - PubMed
  3. Lab Invest. 2003 Apr;83(4):519-26 - PubMed
  4. Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 - PubMed
  5. Anticancer Res. 2009 Dec;29(12):5053-5 - PubMed
  6. World J Gastroenterol. 2008 May 21;14(19):3074-80 - PubMed
  7. Hum Mol Genet. 2001 Apr;10(7):687-92 - PubMed
  8. J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):297-307 - PubMed
  9. Int J Cancer. 2002 Dec 20;102(6):623-8 - PubMed
  10. PLoS One. 2012;7(5):e36780 - PubMed
  11. Nat Rev Genet. 2002 Jun;3(6):415-28 - PubMed
  12. J Med Genet. 2001 May;38(5):285-303 - PubMed
  13. Jpn J Clin Oncol. 2005 Jun;35(6):293-301 - PubMed
  14. J Natl Cancer Inst. 2001 May 2;93(9):691-9 - PubMed
  15. Oncogene. 2005 Nov 17;24(51):7630-4 - PubMed
  16. Breast Cancer Res Treat. 2011 Nov;130(1):109-17 - PubMed
  17. Int J Cancer. 2010 Apr 1;126(7):1630-9 - PubMed
  18. Cancer Res. 2005 May 1;65(9):3497-508 - PubMed
  19. Ann Surg Oncol. 2012 Jul;19(7):2088-94 - PubMed
  20. Carcinogenesis. 2011 Mar;32(3):411-6 - PubMed
  21. Carcinogenesis. 2003 Aug;24(8):1337-45 - PubMed
  22. Am J Pathol. 2002 Mar;160(3):787-94 - PubMed
  23. BMC Cancer. 2007 Jul 03;7:120 - PubMed
  24. Oncogene. 2004 Jan 8;23(1):1-8 - PubMed
  25. Br J Cancer. 2006 Oct 23;95(8):1101-7 - PubMed
  26. Am J Surg. 1996 Nov;172(5):473-6; discussion 476-7 - PubMed
  27. Cancer Res. 2001 Oct 1;61(19):7034-8 - PubMed
  28. Int J Cancer. 2010 Dec 15;127(12):2893-917 - PubMed
  29. Singapore Med J. 2014 Dec;55(12):621-8 - PubMed
  30. J Cancer Res Ther. 2012 Apr-Jun;8(2):243-6 - PubMed
  31. Int J Cancer. 2003 Nov 20;107(4):629-34 - PubMed
  32. Adv Exp Med Biol. 2003;532:39-49 - PubMed
  33. Clin Cancer Res. 2010 Apr 15;16(8):2418-26 - PubMed
  34. CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 - PubMed
  35. Cancer Res. 1999 Feb 15;59(4):793-7 - PubMed
  36. Mol Cell Biol. 2003 Jan;23 (1):206-15 - PubMed

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